text:
August 27, 2010 10:28 AMBlack Rice: Low-Cost Grain Packs Bigger Antioxidant Punch than Blueberries
Posted by Aina Hunter 1 comments
Black rice contains more antioxidants than blueberries, new research shows. (iStockphoto)
(CBS) Is black the new blue?
New research shows that black rice packs a bigger antioxidant punch even than blueberries, which have long been celebrated as antioxidant powerhouses.
And that's not the only advantage of the little-known grain.
"Just a spoonful of black rice bran contains more health promoting anthocyanin antioxidants than are found in a spoonful of blueberries, but with less sugar and more fiber and vitamin E antioxidants," researcher Dr. Zhimin Xu, associate professor of food science at Louisiana State University Agricultural Center in Baton Rouge, said in a written statement.
Black rice also costs less than blueberries or blackberries, another antioxidant-rich fruit.
Anthocyanin antioxidants - also found in red grapes, strawberries, red wine, red cabbage, red onion, and blood orange juice - have been shown to reduce the risk of heart disease and cancer.
Dr. Xu's research also showed that pigments in black rice bran can produce a variety of different colors, ranging from pink to black, and may provide a healthier alternative to artificial food colorings now used in some foods and beverages. Studies have linked some artificial colorants to cancer, behavioral problems in children, and other health problems.
Black rice is used mainly in Asia for food decoration, noodles, sushi, and pudding. Dr. Xu said that farmers are interested in growing black rice in Louisiana and that he would like to see people in the country embrace its use.
The Early Show
NEW YORK, Jan. 4, 2010Eating Antioxidants for a Better YouRegistered Dietician Keri Glassman Shares a Four-Day Cleanse to Kick Start Her Antioxidant Diet
Like this Story? Share it:
Play CBS Video Video The O2 DietRegistered dietitian Keri Glassman spoke to Maggie Rodriguez about her new book, "The O2 Diet," and how to lose up to five pounds in the first four days.
Registered dietician Keri Glassman recommends green tea and scrambled eggs on the four-day cleanse to kick off "The O2 Diet." (CBS)
(CBS) In "The Early Show" series, "New Year, New You," registered dietician Keri Glassman shared ideas for eating healthier from her new book, "The O2 Diet."
Read an excerpt of "The O2 Diet"
Glassman said, "Antioxidants are the superheroes that fight the bad-guy free radicals that are linked to heart disease, cancer, neuronal degeneration and aging."
In her book, Glassman outlines the ORAC scale, which measures a food's antioxidant power.
Glassman said, "(ORAC) measures how well a food mops up the free radicals in our bloodstream. Free radicals are the 'bad guys' roaming in your body or 'pinballs' in your body wreaking havoc on our cells. Think of antioxidants as little super heroes squashing these 'bad guys.'"
ORAC was developed in the early '90s at the National Institute on Aging and since then has been refined by the USDA and the Human Nutrition Research Center on Aging at Tufts University.
Glassman pointed out the ORAC value won't be on food labels. However, with Glassman's book you will be able to spot certain antioxidants, such as Vitamin C, that are clearly marked on nutritional labels.
But how is this diet different from others out there?
Glassman said, "I find that people know a lot about artificial sweeteners and the latest cholesterol lowering drug but they don't know the simple facts about what makes real food so powerful, and just how those foods work. When people understand this, they feel empowered to put the best foods in their body."
"This plan," she said, "helps change a person's outlook on food -- by focusing on putting more ORAC in your body -- you are inspired and want to be healthy versus feeling deprived and focusing on how little you can have or what you can't have."
The goal of this diet is to get more of the best foods -- not just focus on weight loss, she said.
"When you eat according to this plan you improve your skin, energy, heart health," she said. "The O2 Diet also focuses on managing stress, maximizing sleep and improving your environment."
In addition to mapping out antioxidant foods, Glassman lays out a diet in her book for four-day cleanse.
But why four days?
Glassman said the cleanse is long enough to help you make a difference in how you look and feel -- and give you enough time to change your mindset around food.
"You will feel empowered," she said. "The 'I want to put good things in my body feeling' will kick in. It is also enough time to lay the groundwork for some good habits that you continue on with during the plan."
On the cleanse, she added, you'll get a slightly higher antioxidants than you will on the rest of the plan. Glassman explained this is to give your body an antioxidant jumpstart.
Glassman's Four-Day Cleanse:
Scrambled eggs (1 whole egg omega 3 enriched, 3 whites)
1 tsp. dried basil
1 cup green tea
1 cup water with 1 oz. lemon juice
Eggs contain protein -- excellent to have at breakfast because provide a lot of satiety (keeps you full) through the day.
The omega 3 enriched is important because omega 3's are important for anti-inflammation, helping burn fat, heart health. Also, contain choline, important for healthy brain function.
Basil -- herbs and spices are an easy, calorie free way to up ORAC and add flavor to meals to make food more satisfying.
1 tsp. dried basil has 500 ORAC points.
Green tea -- I love almost as much as my children! 3,000 ORAC points per cup. Green tea is rich in the antioxidants catechins which may help burn fat. Buy in small quantities though -- green tea bags may lose up to 32 percent of its power in 6 months.
Lemon water -- There is an emotional component here. Think about being at a spa. What will make you feel healthier -- a Diet Coke or water with lemon? Starting your day with lemon water helps instill this feeling. Also, when properly hydrated you are less likely to eat for the wrong reasons. Often, people eat when they are thirsty. Staying hydrated from the moment you wake up helps prevent this. Plus, being properly hydrated is the easiest way to give your skin a boost.
Sliced Granny Smith apple with 1 tsp. cinnamon
Granny Smith apple -- 7,100 ORAC points -- Green apples are very satisfying, plus you are getting some fiber.
Cinnamon -- 1 tsp. 7,000 ORAC points -- also helps control blood sugar and researchers have found that just the smell of it may help reduce stress. It has been tested on stressed out commuters as they drove.
4 oz. Salmon
1 tsp. oregano
8 pecans
Any flavored vinegars on spinach such as raspberry, fig.
Water with lemon.
Spinach -- 1,300 ORAC points -- helps you fill up as well for little calories.
Salmon -- Protein is satisfying and salmon has the omega 3's I love.
Oregano -- 3,600 ORAC points (see comment about herbs and spices above)
Pecans -- A wonderful high ORAC nut! Just this small portion is enough to give you ORAC boost and help provide satiety. Also, contain plant sterols which help to lower cholesterol.
1 steamed artichoke or 1/2 cup artichoke hearts
We already know about green tea.
Artichokes one of my absolute fave foods. How fun are they to eat? Great for dieters because they are fun to eat and you can eat slow.
7,900 ORAC points. They contain compounds which may help lower cholesterol and act as an anti-inflammatory in the skin, making them a beauty food as well.
Large romaine salad with carrots, red bell peppers, tomatoes and olive oil and lemon to dress it
Steamed asparagus
4 oz. lean protein
water with lemon
Salad -- We know it is an easy low cal way to fill up. But research also suggests that women who ate leafy greens had brains that were 1-2 years younger in performance than those who didn't. Smart girls eat greens or girls who eat greens are smart? Either way eat up! Plus this salad is packed with more ORAC punch with the colorful veggies.
Olive oil -- Most of us know about the healthy fat but olive oil also has antioxidants in the form of polyphenols.
Asparagus -- 2,900 ORAC points. And, high in folate which is important for heart health. I always encourage two veggies (salad and another at dinner) to help fill you up and up antioxidants.
Lean protein -- Of course lean - we are dieting! Also, contain Co-Q10 which has antioxidant properties and helps with skin cell renewal.
Oregano -- 3,600 ORAC points (see above).
Blueberries -- 9,700 ORAC points per cup. All berries rock! Blueberries get their power from the anthocyanins which may lower LDL (bad) cholesterol and the pectin a fiber which helps keep you regular. Also, shown to boost memory and cognition.
Glassman says if you follow this cleanse for four days, you could lose two to five pounds, depending upon how the person is currently eating.
The benefits also are numerous, Glassman said.
"I have had clients say they felt 'euphoric,'" she said. "Aside from pants fitting a little better, I have clients tell me -- and I see -- how their skin glows a bit more, they have more energy -- often people work out more than they normally do. I also find that people sleep better and even feel more relaxed during these four days. They also feel excited about the changes they are making to their life and diet."
Why will people be successful on this four day cleanse?
Glassman said, "You are eating real food and you are not deprived and since you feel and see changes right away, you are inspired."
The cleanse also suggests the following for the four days:
• DRINK 8 glasses of water and the 2 cups of green tea
• SLEEP (AND HAVE SEX!) 7-8 hours per night -- even if you don't normally get this in make sure to for the next 4 nights. And, sex has health benefits.
• PAMPER -- cleanse your face and moisturize 2 times daily
• DESTRESS -- 15 minutes just for you each day
• EXERCISE -- 45 minutes per day
• IMPROVE YOUR ENVIRONMENT
Nov 2, 2007Antioxidants May Fight FatStudy: Antioxidants Called Flavonoids And Phenolic Acids May Cut Fatty Buildup In Fat Cells
Antioxidants found in many fruits, vegetables, nuts, tea, and wine may cut fatty buildup in fat cells, Taiwanese experiments show. (CBS/AP)
Quiz Are You Food Savvy?Have you consumed myths about diet and nutrition? Take these quizzes to find out.
Brits Weigh Weapons In Obesity Battle
Making The Best Bad Food Choices
Boiled Peanuts Whip Other PeanutsCapers: A Carnivore's Best BudBroccoli Protects Skin From Sun DamageWhy Garlic Is Good for YouSpoiled Produce Still Nutritious?
(WebMD) The benefits of antioxidants found in many fruits, vegetables, nuts, tea, and wine may include tinkering with fat cells in a way that curbs obesity and helps the heart.
A new study shows that, in test tubes, antioxidants called flavonoids and phenolic acids tweak fat cells from mice.
Those antioxidants didn't kill fat cells or slash the number of fat cells in the test tubes. Instead, they made fat cells cut their production of triglycerides, which are a heart hazard. The antioxidants did that by curbing an enzyme needed to make triglycerides, according to the study.
That particular enzyme was most effectively reduced by the phenolic acid o-coumaric acid and the flavonoid rutin, report the researchers.
They included Gow-Chin Yen, PhD, a professor in the department of food science and biotechnology at Taiwan's National Chung Hsing University.
It will take more work to find out if fat cells and antioxidants behave the same way in the human body. Meanwhile, reams of research support eating a healthy diet rich in produce.
The study appears in the Journal of Agricultural and Food Chemistry.
Diet Detective's Guide to Antioxidants -- What Are They Anyway?
By Charles Stuart Platkin
Story Published: Sep 23, 2010 at 7:36 PM PST
The term "antioxidant" is tossed around a lot these days, but many of you still are not sure exactly what antioxidants are or why they're important. The facts are that antioxidants are found in plant-based foods, and research has credited them with helping to minimize risk for many diseases, including cancer, cardiovascular disease and eye disease, and to improve overall health. Read on to find out more about antioxidants.
What is "oxidative stress"? Why does it occur? And what is an antioxidant?
Believe it or not, oxygen -- the very thing you need to survive  can actually harm you. Think of how the flesh of an apple browns when it's exposed to air. That's the effect of oxygen -- called oxidation. An antioxidant prevents oxidation. Dipping the cut apple in lemon juice prevents the browning. The lemon juice is an antioxidant. Oxidative stress occurs when someone has too many free radicals in his or her body and not enough antioxidants to combat them.
A free radical is a molecule that contains an oxygen atom that is missing an electron. In its effort to replace the missing electron, the free radical steals from another molecule, which then becomes a free radical itself. It's a vicious cycle. Antioxidants provide the free radical with its missing electron so that it doesn't have to steal one from another molecule, thus stopping the cycle.
Your body produces free radicals as byproducts of the many functions it performs, such as when you digest foods, when you exercise, or when you're exposed to tobacco and other environmental pollutants.
If there are too many free radicals and not enough antioxidants, the balance is off – there are not enough antioxidants to go around, and the damaged cells then become more susceptible to diseases such as cancer, heart disease, etc.
Is there a certain limit to how many free radicals a person should have?
"This is not known. However, some free radicals are needed because they are involved with normal cell signaling," says Victoria J. Drake, Ph.D., a researcher at the Linus Pauling Institute at Oregon State University. And just as not all free radicals are bad, some antioxidants might not be good: A recent study conducted at Kansas State University found that certain antioxidants can actually suppress key signaling mechanisms necessary for muscles to function effectively. But too many free radicals will cause cellular dysfunction, thereby leading to disease states, Drake adds.
What are some examples of antioxidants?
Antioxidants are found in plants -- they protect the plant from ultraviolet light and act as its immune system. Here are a few names you might have read or heard: beta carotene, flavonoids, lycopene, vitamin A, vitamin C, vitamin E and selenium.
Can we get antioxidants from a pill?
We're still learning what, if any, differences our bodies recognize when we take supplements instead of getting our antioxidants from foods. "Often there's no distinction between the form of antioxidant in a supplement and the form in a food," says Karen Collins, M.S., R.D., nutrition adviser to the American Institute for Cancer Research. "But sometimes the chemical form may change slightly. One concern about the use of supplements is the issue of synergy  how nutrients and phytochemicals work together differently from the way each one works on its own. (i.e., 1 + 1 = 3 instead of just 2.)"
There is something about the way nature packages fruits and vegetables -- the combination of chemicals in plants -- that causes them to fight off disease. "High intakes of fruits and vegetables have been associated with a reduced risk for several chronic diseases, including cardiovascular diseases, cancer, type 2 diabetes, osteoporosis and even eye-related disorders such as macular degeneration. Obtaining antioxidants from food is important because foods high in antioxidants also contain other micronutrients and phytochemicals that are important in preventing chronic disease," says Drake.
In addition, antioxidant supplements are often synthetic (man-made), and some of these synthetic forms may not have the same effects on the body as antioxidants that occur naturally in foods. But even if they are not synthetic, some beneficial properties may be lost when antioxidants are extracted from foods to manufacture supplements.
The other issue concerning supplements is the fact that there's still scientific ambiguity about what the correct dosage is for optimal effect – and whether or not that dosage changes for specific individuals. Some doctors, for example, have suggested that cancer patients who are following a course of treatment designed to increase the level of free radicals in their bodies may want to avoid antioxidants to help reduce cancer cells. "Correct dosage can be a problem with supplements, because it's easy to exceed healthy amounts and set the normal balance off," says Collins. "On the other hand, supplements might turn out to be helpful if it is found that larger amounts of particular phytochemicals do produce benefits. For now, consuming the large amounts possible with some supplements is a risky gamble."
According to National Institutes of Health's National Center for Complementary and Alternative Medicine, "Large, long-term studies (randomized, controlled trials) funded primarily by NIH have generally found that antioxidant supplements have no beneficial effects. For example:
The Physicians' Health Study II, which included more than 14,000 healthy male physicians 50 or older, found that neither vitamin E nor vitamin C supplements reduced the risk of major cardiovascular events (e.g., heart attack, stroke or death) or cancer.
The Selenium and Vitamin E Cancer Prevention Trial (SELECT)  a study of more than 35,000 healthy men 50 or older  found that selenium and vitamin E taken alone or together did not prevent prostate cancer. (Two earlier reviews suggested that preliminary evidence for selenium appeared promising.)
The Women's Health Study, which included almost 40,000 healthy women at least 45 years of age, found that, overall, vitamin E did not reduce the risk of death, major cardiovascular events (e.g., heart attack, stroke or death) or cancer. However, it was associated with reduced deaths from cardiovascular causes and also reduced major cardiovascular events in a subgroup of women 65 or older.
The Women's Antioxidant Cardiovascular Study found no beneficial effects of vitamin C, vitamin E or beta carotene on cardiovascular events (e.g., heart attack, stroke or death) in more than 8,000 female health professionals 40 years or older who were at high risk for cardiovascular disease."
Can taking supplements ever be harmful?
According toJanet Brill, Ph.D., R.D., a Florida-based nutrition expert, there have been thousands of well-designed clinical studies examining the effects of consuming isolated antioxidant supplements such as vitamin E, beta carotene and vitamin C on the development of chronic degenerative diseases. "While most have shown either beneficial or neutral effects, there is some concern over research demonstrating that higher doses can actually increasemyocardial events and promote cancer cell proliferation." For example, the CARET study (The Beta-Carotene and Retinol Efficacy Trial), which looked at more than 18,000 men and women who were smokers, former smokers or workers exposed to asbestos, found that at the end of four years lung cancer incidence was 28 percent higher in those subjects taking beta carotene supplements compared with those taking a placebo.
The Cochrane Library, a well-known scientific research collaboration among world scholars reviewed 67 randomized trials with a combined participation of 232,550 subjects to assess the effects of antioxidant supplements on mortality in primary or secondary prevention. The authors came to the conclusion that there is "no evidence to support antioxidant supplements for primary or secondary prevention." And, in fact, vitamin A, beta carotene and vitamin E may increase mortality. This review was controversial and disputed by supplement manufacturers and the food industry (specifically those food manufacturers that add supplements to foods).
I've seen the term ORAC associated with antioxidants -- what does that stand for?
Oxygen radical absorbance capacity. It is one method used to measure the amounts of antioxidants in foods. More specifically, it measures the degree of inhibition of peroxy-radical-induced oxidation of the compound being tested. Another method of testing antioxidant capacity is TAC or Total Antioxidant Capacity. According to Collins, "It's interesting to note that while there are different methods of measuring antioxidant power, they don't all come up with foods listed in the same order, which suggests that we still don't fully understand exactly which best measures the physiological antioxidant effects of foods." To see the United States Department of Agriculture's ORAC for selected foods go to: www .ars.usda.gov/sp2userfiles/place/12354500/data/orac/orac07.pdf
Where to you get the most antioxidant bang for your buck?
There's not a lot of research out there to point us decisively in the direction of a particular food. While we know that many vegetables and fruits are high in antioxidants, we don't have as much evidence to determine specific amounts in each food. And Collins points out that we need to think about foods a little differently from the way we have in the past – not in terms of rank but in terms of synergistic combinations. "In the old days we seemed to consider certain foods high in particular vitamins 'better' than others. Today we know that even when a fruit or vegetable is not a major source of vitamin C or A or antioxidants, for example, it can supply important phytochemicals that improve your overall health." And while fruits and vegetables are good sources, antioxidants are also found in other foods, including nuts, some seeds, legumes, coffee, tea and chocolate.
CHARLES STUART PLATKIN, Ph.D., M.P.H. is a nutrition and public health advocate and founder of DietDetective.com. Copyright 2010 by Charles Stuart Platkin. All rights reserved. Sign up for the free Diet Detective newsletter at www.DietDetective.co
New "best antioxidants" listOct, 2004 |
Finally--following what is likely the largest antioxidant study in history--the US Department of Agriculture (USDA) has produced a list of the 20 most antioxidant-rich foods. You may have guessed that blueberries rank high. But some of the findings will surprise you.
The study examined more than 100 types of fruits, vegetables, berries, nuts and spices. Winners included artichokes, russet potatoes and ground cloves, among other shockers, as top food sources of antioxidants. In the end, small red beans took the top spot, narrowly beating out wild blueberries as the food with the highest concentration of disease-fighting compounds per serving.
Most PopularCBS MoneyWatch.com Blogs
Holiday Non-Shopping: 7 Items Worth Waiting For
Black Friday Shoppers: Who's Naughty & Who's Nice
Food Prices Rising: Time to Go Vegan?
7 DIY Holiday Gift Ideas
Home Sales: NYC Apartment Sells for 88% Below Asking Price
A prevailing but controversial theory holds that antioxidants--non-vitamin nutrients that abound in some foods--may benefit the body by providing protection against oxidation, a process that may be linked to conditions such as cancer, heart disease and aging. Found most often in colorful produce, antioxidants are also available in powdered "green" supplements and pills.
The USDA study was published in the June 2004 issue of the Journal of Agricultural and Food Chemistry. Here's the full list, starting with the richest source of antioxidants:
* Small red beans (dried)
* Wild blueberries
* Red kidney beans
* Pinto beans
* Blueberries (cultivated)
* Cranberries
* Artichokes (cooked)
* Blackberries
* Prunes
* Raspberries
* Strawberries
* Red delicious apples
* Granny Smith apples
* Pecans
* Sweet cherries
* Black plums
* Russet potatoes (cooked)
* Black beans (dried)
* Plums
* Gala apples
COPYRIGHT 2004 PRIMEDIA Intertec, a PRIMEDIA Company. All Rights Reserved.
COPYRIGHT 2004 Gale Group
anti-aging with antioxidantsby Estitta Bushkin, Gary Bushkin | Feb, 2000 | 0 Comments
12 supplements that help us stay young and healthy
Do you know what epigallocatechin is? Or singlet oxygen and peroxynitrite? Ever heard of alpha-lipoic acid and ORACs? This seemingly foreign language is the key to your health. But it doesn't have to be foreign. What are these invisible friends and foes anyway?
Free radicals, the enemy within
Without the right protection, the Tin Man in the Wizard of Oz would have rusted away. And without antioxidants protecting us from the relentless attack of free radicals, we would rust on the inside, develop disease, and die young. While practically everyone wants something free, you certainly don't want these. Free radicals are vicious molecules missing an electron in their outer shell. Most are toxic forms of oxygen molecules. These unstable gangsters steal electrons from healthy cells, rendering them "biologically rusted," damaged, or destroyed. Free radicals spawn from environmental pollution, toxins, pesticides, chemicals, sunlight, radiation, food, drink, and metabolic activity in the body. These injurious free radicals destroy living tissue and fluids. They rapidly accelerate the aging process, severely damaging the ability of the immune system to battle unwanted pathogens (e.g. bacteria, viruses, and parasites) that enjoy invading your body. According to noted biochemist Richard Passwater, Ph.D., free radicals are "biological terrorists" of the human terrain.
Antioxidants are bio-police working 24/7
As free radical molecules cause oxidation, biological rusting continues inside the body. Antioxidants labor tirelessly to slow down and terminate this oxidation process. These kamikaze life-saver molecules continually seek and destroy free radicals, sacrificing themselves and self-destructing, to save other healthy cells from certain death. Catechins, which are abundant in green tea, are an example of antioxidants that readily allow themselves to be oxidized in place of more essential molecules in the body. Some antioxidants, like the proanthocyanidins (found in grapeseed and French maritime pine bark extracts) work to regenerate vitamin C, which then regenerates vitamin E.
Plants - where the antioxidant action is
The plant kingdom is home to thousands of body-friendly antioxidants identified by botanists, biologists, and biochemists. Thousands, perhaps millions more yet unknown, wait to be discovered. Appropriately dubbed phytonutrients ("phyto," meaning plant), these nutrients have names like bioflavonoids, polyphenols, and carotenoids.
12 dietary supplements that can keep you young and healthy
1. Alpha-lipoic acid is a unique water and fat-soluble antioxidant capable of quenching many more free radicals than only water or fat-soluble antioxidants. It recycles vitamins C and E, and glutathione, while scavenging and destroying free radicals.
2. Lycopene is the red carotenoid found in tomatoes, red grapefruit, apricots, and watermelon. This incredibly aggressive antioxidant has been the subject of much recent research positively validating its free radical quenching and cancer preventive abilities.
3. Indole carbinol 3 and sulforaphane stimulate the production of carcinogen killing enzymes. They are plentiful in Brussels sprouts, kale, collard greens, broccoli, mustard greens, cabbage, and cauliflower.
4. Alpha-tocopherol is commonly known as vitamin E, one of eight forms found in the vitamin E complex. Four are tocopherols, possessing antioxidant activity that has been validated in thousands of studies. Four are tocotrienols, cousins to vitamin E, which support the activity of alpha tocopherol. Olives, nuts, and seeds are rich sources.
5. Vitamin C, found in citrus fruits, tomatoes, peppers, broccoli and hot red peppers, is the primary water-soluble antioxidant in the body. Thousands of studies clearly support vitamin C's ability to protect against free radical damage. Because we cannot produce vitamin C internally, we must obtain it from food and supplemental sources.
6. Beta-carotene is one of over 600 carotenoids noted for their effectiveness at quenching singlet oxygen and other free radicals.
7. Vitamin A, the "anti-infective," maintains skin, respiratory tract surfaces, mucous membranes, and secretions, thereby reducing free radical activity generated by infection. Vitamin A converts from beta-carotene in the liver, stimulating production of white blood cells.
8. Lutein, discovered in marigolds, is best known as the eye antioxidant, preventing macular degeneration.
9. Beta 1,3-D glucan, a polysaccharide (sugar) found in yeast-cell walls and maitake mushrooms, stimulates free radical scavenging ability of natural killer cells and macrophages in the immune system.
10. NAC (n- acetyl cysteine) is an amino acid derivative that is a precursor to glutathione, the essential and most effective antioxidant in the liver.
11. SOD (superoxide dismutase), an antioxidant enzyme, prevents damage from the superoxide radical, the most common free radical we encounter.
12. Selenium is a trace mineral. Although, according to some purists, not technically an antioxidant, itself, it is generally considered one because it is essential to the formation and replenishment of the powerful free radical scavenger glutathione.
Don't forget these antioxidants
The anti-aging antioxidant ellagic acid is found in grapes, wine, berries, walnuts, apples, tea, and pomegranates. Bilberry is rich in blue-colored polyphenols that have exceptional antioxidant activity in the eyes. Epigallocatechin gallate, plentiful green tea, is perhaps more potent than any other antioxidant.
Stayin' alive with phytofood ORACs
Antioxidants are gifted with the unique ability to absorb and destroy free radicals, rendering them harmless. Breakthrough research at the USDA Human Nutrition Center for Aging at Tufts University in Boston, Massachusetts conducted by Ronald Prior, Ph.D., and his researchers uncovered and evaluated the specific free radical absorbing capacity of fruits and vegetables. This powerful capacity to absorb and neutralize free radicals was measured in what scientists call ORAC units (Oxygen Radical Absorbance Capacity). So what's the big deal? Specifically, this tells us how aggressively antioxidants in a fruit or vegetable destroy free radicals circulating throughout the body, and how effectively they prevent cell damage and anti-aging. Take our advice on this one -- eat and drink them every day!
There's more,
Garlic and onions are loaded with organosulfur compounds that stimulate the production of glutathione s-transferase, a powerful detoxifying enzyme in the liver.
Phytic acid found in rye, wheat, rice, lima beans, sesame seeds, peanuts, and soybeans is an intense free radical gobbler.
Barley grass juice, a super nutritious green beverage contains "2-O-GIV" (2-0-glycosylisovitexin), an aggressive inhibitor of lipid peroxidation (oxidation of fat). Other green juices, specifically wheat grass juice, teem with antioxidants that rival all the others. While antioxidants will not enable us to live forever, they can certainly increase our odds of living a long and healthy life. Get your fountain of youth arsenal together today. Head to the health food store for those turn-back-the-clock antioxidant supplements. Eat 5 to 10 servings of fruits and vegetables each day. Have a refreshing green drink. Munch on those prunes. And drink your grape juice. A glass a day keeps old age away!
Dorland's Medical Dictionary. Edition 28, Philadelphia, PA: W.B. Saunders Co., 1988.
Balch, James F., M.D. The Super Antioxidants. New York: M. Evans & Co., 1998.
Balch, James F., M.D., and Balch, Phyllis A. Prescription for Nutritional Healing. 2nd ed. Garden City Park, NY: Avery Publishing Group, 1997.
Packer, L., et al. "Alpha-lipoic acid as a biological antioxidant." Free Radical Biology and Medicine. 19(2):227-250, 1995.
Passwater, R. FAQ's - All About Pycnogenol, Garden City Park, NY: Avery Publishing Group, 1998.
Prior, R., et al. "Antioxidant Capacity of Fruits." Journal of Agriculture and Food Chemistry, 44(3):701-705, 1996.
Prior, R. and Cao, G. "Antioxidant Capacity and Polyphenolic Components of Teas: Implications for Altering In Vivo Antioxidant Status." P.S.E.B.M., 220:255-261, 1999.
Prior, R., et al. "Increases in human plasma antioxidant capacity after Consumption of controlled diets high in fruit and vegetables." Am J Clin Nutr, 68:1081-7, 1998.
Stryker, L. Biochemistry. 3rd Edition, New York, NY: W.H. Freeman and Co., 1988.
RELATED ARTICLE: Phytonutrients
Bioflavonoids. Previously collectively referred to as vitamin P, bioflavonoids enhance vitamin C absorption. Elderberry, hawthorn, horsetail, and rose hips are some supplements which are rich in bioflavonoids.
Carotenoids. The most famous of the carotenoids is, of course, beta-carotene. Rising stars in the carotenoid family include lutein, lycopene, and alpha-carotene.
Polyphenols. Super antioxidants which fall into the polyphenol family include flavonoids, which are found in such foods as soy and blueberries, as well as red wine and green tea, and the herbs feverfew and ginkgo.
RELATED ARTICLE: Grape juice = a fountain of youth
It's no secret that the French don't slouch when it comes to eating high-fat foods, or guzzling, perhaps, more wine than any culture in the world. Yet for years, significantly lower occurrence of heart disease in France vs. the United States remained a mystery. Why? Some experts call it the "French Paradox," although it should truly be called the "Mediterranean Paradox," since Spain, Portugal, Greece and a few other Mediterranean countries have similar diets that were studied along with the French.
Citing cardiovascular protection from its regular consumption, wine appears to dramatically lessen the incidence of heart attack and heart disease. We believe there's much more to it than that. Solid research indicates phytonutrients in the wine, not the alcohol, are the awesome antioxidant workers. Red wine and its non-alcoholic equal, purple grape juice, are brimming with the antioxidants resveratrol, grapeseed anthocyanidins, quercitin, ellagic acid, phenolic flavonoids, and epicatechin. Purple grape juice is, perhaps, the most powerful antioxidant food on earth, having demonstrated the highest ORAC rating of more than 40 fruits, vegetables, and juices tested in the lab!
RELATED ARTICLE: Nature's 12 Great Protectors
Your best defense against free radicals.
grape juice kale prunes spinach strawberries blueberries beets oranges cranberry juice red peppers cherries green tea
Gary Bushkin, MS, CNC, and Estitta Bushkin, MS, CNC, are co-authors of FAQ's - All About Green Food Supplements (Avery, Spring 1999) and FAQ's - All About Folic Acid (Avery, Spring 2000). They are consultants to the natural products industry.
Reviewed: 07/28/2004
Antioxidants protect cells from damage caused by unstable molecules known as free radicals (see Questions 1 and 3).
Laboratory and animal research have shown that antioxidants help prevent the free radical damage that is associated with cancer. However, results from recent studies in people (clinical trials) are not consistent (see Question 2).
Antioxidants are provided by a healthy diet that includes a variety of fruits and vegetables (see Question 4).
What are antioxidants?Antioxidants are substances that may protect cells from the damage caused by unstable molecules known as free radicals. Free radical damage may lead to cancer. Antioxidants interact with and stabilize free radicals and may prevent some of the damage free radicals might otherwise cause. Examples of antioxidants include beta-carotene, lycopene, vitamins C, E, and A, and other substances.
Can antioxidants prevent cancer?Considerable laboratory evidence from chemical, cell culture, and animal studies indicates that antioxidants may slow or possibly prevent the development of cancer. However, information from recent clinical trials is less clear. In recent years, large-scale, randomized clinical trials reached inconsistent conclusions.
What was shown in previously published large-scale clinical trials?Five large-scale clinical trials published in the 1990s reached differing conclusions about the effect of antioxidants on cancer. The studies examined the effect of beta-carotene and other antioxidants on cancer in different patient groups. However, beta-carotene appeared to have different effects depending upon the patient population. The conclusions of each study are summarized below.
The first large randomized trial on antioxidants and cancer risk was the Chinese Cancer Prevention Study, published in 1993. This trial investigated the effect of a combination of beta-carotene, vitamin E, and selenium on cancer in healthy Chinese men and women at high risk for gastric cancer. The study showed a combination of beta-carotene, vitamin E, and selenium significantly reducedincidence of both gastric cancer and cancer overall (1).
A 1994 cancer prevention study entitled the Alpha-Tocopherol (vitamin E)/ Beta-Carotene Cancer Prevention Study (ATBC) demonstrated that lung cancer rates of Finnish male smokers increased significantly with beta-carotene and were not affected by vitamin E (2).
Another 1994 study, the Beta-Carotene and Retinol (vitamin A) Efficacy Trial (CARET), also demonstrated a possible increase in lung cancer associated with antioxidants (3).
The 1996 Physicians' Health Study I (PHS) found no change in cancer rates associated with beta-carotene and aspirin taken by U.S. male physicians (4).
The 1999 Women's Health Study (WHS) tested effects of vitamin E and beta-carotene in the prevention of cancer and cardiovasculardisease among women age 45 years or older. Among apparently healthy women, there was no benefit or harm from beta-carotenesupplementation. Investigation of the effect of vitamin E is ongoing (5).
Are antioxidants under investigation in current large-scale clinical trials?Three large-scale clinical trials continue to investigate the effect of antioxidants on cancer. The objective of each of these studies is described below. More information about clinical trials can be obtained using http://www.cancer.gov/clinicaltrials, http://www.clinicaltrials.gov, or the RePORT Expenditures and Results (RePORTER) query tool at http://projectreporter.nih.gov/reporter.cfm on the Internet.
The Women's Health Study (WHS) is currently evaluating the effect of vitamin E in the primary prevention of cancer among U.S. female health professionals age 45 and older. The WHS is expected to conclude in August 2004.
The Selenium and Vitamin E Cancer Prevention Trial (SELECT) is taking place in the United States, Puerto Rico, and Canada. SELECT is trying to find out if taking selenium and/or vitamin E supplements can prevent prostate cancer in men age 50 or older. The SELECT trial is expected to stop recruiting patients in May 2006.
The Physicians' Health Study II (PHS II) is a follow up to the earlier clinical trial by the same name. The study is investigating the effects of vitamin E, C, and multivitamins on prostate cancer and total cancer incidence. The PHS II is expected to conclude in August 2007.
Will the National Cancer Institute (NCI) continue to investigate the effect of beta-carotene on cancer?Given the unexpected results of ATBC and CARET, and the finding of no effect of beta-carotene in the PHS and WHS, NCI will follow the people who participated in these studies and will examine the long-term health effects of beta-carotene supplements. Post-trial follow-up has already been funded by NCI for CARET, ATBC, the Chinese Cancer Prevention Study, and the two smaller trials of skin cancer and colonpolyps. Post-trial follow-up results have been published for ATBC, and as of July 2004 are in press for CARET and are in progress for the Chinese Cancer Prevention Study.
How might antioxidants prevent cancer?Antioxidants neutralize free radicals as the natural by-product of normal cell processes. Free radicals are molecules with incomplete electron shells which make them more chemically reactive than those with complete electron shells. Exposure to various environmental factors, including tobacco smoke and radiation, can also lead to free radical formation. In humans, the most common form of free radicals is oxygen. When an oxygen molecule (O2) becomes electrically charged or "radicalized" it tries to steal electrons from other molecules, causing damage to the DNA and other molecules. Over time, such damage may become irreversible and lead to disease including cancer. Antioxidants are often described as "mopping up" free radicals, meaning they neutralize the electrical charge and prevent the free radical from taking electrons from other molecules.
Which foods are rich in antioxidants?Antioxidants are abundant in fruits and vegetables, as well as in other foods including nuts, grains, and some meats, poultry, and fish. The list below describes food sources of common antioxidants.
Beta-carotene is found in many foods that are orange in color, including sweet potatoes, carrots, cantaloupe, squash, apricots, pumpkin, and mangos. Some green, leafy vegetables, including collard greens, spinach, and kale, are also rich in beta-carotene.
Lutein, best known for its association with healthy eyes, is abundant in green, leafy vegetables such as collard greens, spinach, and kale.
Lycopene is a potent antioxidant found in tomatoes, watermelon, guava, papaya, apricots, pink grapefruit, blood oranges, and other foods. Estimates suggest 85 percent of American dietary intake of lycopene comes from tomatoes and tomato products.
Selenium is a mineral, not an antioxidant nutrient. However, it is a component of antioxidant enzymes. Plant foods like rice and wheat are the major dietary sources of selenium in most countries. The amount of selenium in soil, which varies by region, determines the amount of selenium in the foods grown in that soil. Animals that eat grains or plants grown in selenium-rich soil have higher levels of selenium in their muscle. In the United States, meats and bread are common sources of dietary selenium. Brazil nuts also contain large quantities of selenium.
Vitamin A is found in three main forms: retinol (Vitamin A1), 3,4-didehydroretinol (Vitamin A2), and 3-hydroxy-retinol (Vitamin A3). Foods rich in vitamin A include liver, sweet potatoes, carrots, milk, egg yolks, and mozzarella cheese.
Vitamin C is also called ascorbic acid, and can be found in high abundance in many fruits and vegetables and is also found in cereals, beef, poultry, and fish.
Vitamin E, also known as alpha-tocopherol, is found in almonds, in many oils including wheat germ, safflower, corn, and soybeanoils, and is also found in mangos, nuts, broccoli, and other foods.
Blot WJ, Li JY, Taylor PR, et al. Nutrition intervention trials in Linxian, China: supplementation with specific vitamin/mineral combinations, cancer incidence, and disease-specific mortality in the general population. J Natl Cancer Inst 1993;85:1483–91.
The Alpha-Tocopherol, Beta Carotene Cancer Prevention Study Group. The effects of vitamin E and beta carotene on the incidence of lung cancer and other cancers in male smokers. N Engl J Med 1994;330:1029–35.
Omenn GS, Goodman G, Thomquist M, et al. The beta-carotene and retinol efficacy trial (CARET) for chemoprevention of lung cancer in high risk populations: smokers and asbestos-exposed workers. Cancer Res 1994;54(7 Suppl):2038s–43s.
Hennekens CH, Buring JE, Manson JE, Stampfer M, Rosner B, Cook NR, et al. Lack of effect of long-term supplementation with beta carotene on the incidence of malignant neoplasms and cardiovascular disease. N Engl J Med 1996;334:1145–9.
Lee IM, Cook NR, Manson JE. Beta-carotene supplementation and incidence of cancer and cardiovascular disease: Women's Health Study. J Natl Cancer Inst 1999;91:2102–6.
nts from Wikipedia encyclopedia
Space-filling model of the antioxidant metaboliteglutathione. The yellow sphere is the redox-active sulfur atom that provides antioxidant activity, while the red, blue, white, and dark grey spheres represent oxygen, nitrogen, hydrogen, and carbon atoms, respectively.
An antioxidant is a molecule capable of slowing or preventing the oxidation of other molecules. Oxidation is a chemical reaction that transferselectrons from a substance to an oxidizing agent. Oxidation reactions can produce free radicals, which start chain reactions that damage cells. Antioxidants terminate these chain reactions by removing free radical intermediates, and inhibit other oxidation reactions by being oxidized themselves. As a result, antioxidants are often reducing agents such as thiols, ascorbic acid or polyphenols.[1]
Although oxidation reactions are crucial for life, they can also be damaging; hence, plants and animals maintain complex systems of multiple types of antioxidants, such as glutathione, vitamin C, and vitamin E as well as enzymes such as catalase, superoxide dismutase and variousperoxidases. Low levels of antioxidants, or inhibition of the antioxidant enzymes, causes oxidative stress and may damage or kill cells.
As oxidative stress might be an important part of many human diseases, the use of antioxidants in pharmacology is intensively studied, particularly as treatments for stroke and neurodegenerative diseases. However, it is unknown whether oxidative stress is the cause or the consequence of disease. Antioxidants are also widely used as ingredients in dietary supplements in the hope of maintaining health and preventing diseases such as cancer and coronary heart disease. Although initial studies suggested that antioxidant supplements might promote health, later large clinical trials did not detect any benefit and suggested instead that excess supplementation may be harmful.[2] In addition to these uses of natural antioxidants in medicine, these compounds have many industrial uses, such as preservatives in food and cosmetics and preventing the degradation of rubber and gasoline.
HistoryThe term antioxidant originally was used to refer specifically to a chemical that prevented the consumption of oxygen. In the late 19th and early 20th century, extensive study was devoted to the uses of antioxidants in important industrial processes, such as the prevention of metal corrosion, thevulcanization of rubber, and the polymerization of fuels in the fouling of internal combustion engines.[3]
Early research on the role of antioxidants in biology focused on their use in preventing the oxidation of unsaturated fats, which is the cause of rancidity.[4] Antioxidant activity could be measured simply by placing the fat in a closed container with oxygen and measuring the rate of oxygen consumption. However, it was the identification of vitamins A, C, and E as antioxidants that revolutionized the field and led to the realization of the importance of antioxidants in the biochemistry of living organisms.[5][6]
The possible mechanisms of action of antioxidants were first explored when it was recognized that a substance with anti-oxidative activity is likely to be one that is itself readily oxidized.[7] Research into how vitamin E prevents the process of lipid peroxidation led to the identification of antioxidants as reducing agents that prevent oxidative reactions, often by scavenging reactive oxygen species before they can damage cells.[8]
The oxidative challenge in biology
Further information: Oxidative stress
The structure of the antioxidantvitamin ascorbic acid (vitamin C).
A paradox in metabolism is that while the vast majority of complex life on Earth requires oxygen for its existence, oxygen is a highly reactive molecule that damages living organisms by producing reactive oxygen species.[9] Consequently, organisms contain a complex network of antioxidantmetabolites and enzymes that work together to prevent oxidative damage to cellular components such as DNA, proteins and lipids.[1][10] In general, antioxidant systems either prevent these reactive species from being formed, or remove them before they can damage vital components of the cell.[1][9] However, since reactive oxygen species do have useful functions in cells, such as redox signaling, the function of antioxidant systems is not to remove oxidants entirely, but instead to keep them at an optimum level.[11]
The reactive oxygen species produced in cells include hydrogen peroxide (H2O2), hypochlorous acid (HOCl), and free radicals such as the hydroxyl radical (·OH) and the superoxide anion (O2−).[12] The hydroxyl radical is particularly unstable and will react rapidly and non-specifically with most biological molecules. This species is produced from hydrogen peroxide in metal-catalyzed redox reactions such as the Fenton reaction.[13] These oxidants can damage cells by starting chemical chain reactions such as lipid peroxidation, or by oxidizing DNA or proteins.[1] Damage to DNA can cause mutations and possibly cancer, if not reversed by DNA repair mechanisms,[14][15] while damage to proteins causes enzyme inhibition,denaturation and protein degradation.[16]
The use of oxygen as part of the process for generating metabolic energy produces reactive oxygen species.[17] In this process, the superoxide anion is produced as a by-product of several steps in the electron transport chain.[18] Particularly important is the reduction of coenzyme Q in complex III, since a highly reactive free radical is formed as an intermediate (Q·−). This unstable intermediate can lead to electron "leakage", when electrons jump directly to oxygen and form the superoxide anion, instead of moving through the normal series of well-controlled reactions of the electron transport chain.[19] Peroxide is also produced from the oxidation of reduced flavoproteins, such as complex I.[20] However, although these enzymes can produce oxidants, the relative importance of the electron transfer chain to other processes that generate peroxide is unclear.[21][22] Inplants, algae, and cyanobacteria, reactive oxygen species are also produced during photosynthesis,[23] particularly under conditions of high light intensity.[24] This effect is partly offset by the involvement of carotenoids in photoinhibition, which involves these antioxidants reacting with over-reduced forms of the photosynthetic reaction centres to prevent the production of reactive oxygen species.[25][26]
MetabolitesOverviewAntioxidants are classified into two broad divisions, depending on whether they are soluble in water (hydrophilic) or in lipids (hydrophobic). In general, water-soluble antioxidants react with oxidants in the cell cytosol and the blood plasma, while lipid-soluble antioxidants protect cell membranes from lipid peroxidation.[1] These compounds may be synthesized in the body or obtained from the diet.[10] The different antioxidants are present at a wide range of concentrations in body fluids and tissues, with some such as glutathione or ubiquinone mostly present within cells, while others such as uric acid are more evenly distributed (see table below). Some antioxidants are only found in a few organisms and these compounds can be important in pathogens and can be virulence factors.[27]
The relative importance and interactions between these different antioxidants is a very complex question, with the various metabolites and enzyme systems having synergistic and interdependent effects on one another.[28][29] The action of one antioxidant may therefore depend on the proper function of other members of the antioxidant system.[10] The amount of protection provided by any one antioxidant will also depend on its concentration, its reactivity towards the particular reactive oxygen species being considered, and the status of the antioxidants with which it interacts.[10]
Some compounds contribute to antioxidant defense by chelating transition metals and preventing them from catalyzing the production of free radicals in the cell. Particularly important is the ability to sequester iron, which is the function of iron-binding proteins such as transferrin and ferritin.[30] Selenium and zinc are commonly referred to as antioxidant nutrients, but these chemical elements have no antioxidant action themselves and are instead required for the activity of some antioxidant enzymes, as is discussed below.
Antioxidant metaboliteSolubilityConcentration in human serum (μM)[31]Concentration in liver tissue (μmol/kg)Ascorbic acid (vitamin C)Water50 – 60[32]260 (human)[33]GlutathioneWater4[34]6,400 (human)[33]Lipoic acidWater0.1 – 0.7[35]4 – 5 (rat)[36]Uric acidWater200 – 400[37]1,600 (human)[33]CarotenesLipidβ-carotene: 0.5 – 1[38]retinol (vitamin A): 1 – 3[39]
5 (human, total carotenoids)[40]α-Tocopherol (vitamin E)Lipid10 – 40[39]50 (human)[33]Ubiquinol (coenzyme Q)Lipid5[41]200 (human)[42]Ascorbic acidAscorbic acid or "vitamin C" is a monosaccharide antioxidant found in both animals and plants. As one of the enzymes needed to make ascorbic acid has been lost by mutation during human evolution, it must be obtained from the diet and is a vitamin.[43] Most other animals are able to produce this compound in their bodies and do not require it in their diets.[44] In cells, it is maintained in its reduced form by reaction with glutathione, which can be catalysed by protein disulfide isomerase and glutaredoxins.[45][46] Ascorbic acid is a reducing agent and can reduce, and thereby neutralize, reactive oxygen species such as hydrogen peroxide.[47] In addition to its direct antioxidant effects, ascorbic acid is also a substrate for the antioxidant enzyme ascorbate peroxidase, a function that is particularly important in stress resistance in plants.[48] Ascorbic acid is present at high levels in all parts of plants and can reach concentrations of 20 millimolar in chloroplasts.[49]
The free radical mechanism of lipid peroxidation.
Glutathione is a cysteine-containing peptide found in most forms of aerobic life.[50] It is not required in the diet and is instead synthesized in cells from its constituent amino acids.[51] Glutathione has antioxidant properties since the thiol group in its cysteine moiety is a reducing agent and can be reversibly oxidized and reduced. In cells, glutathione is maintained in the reduced form by the enzyme glutathione reductase and in turn reduces other metabolites and enzyme systems, such as ascorbate in the glutathione-ascorbate cycle, glutathione peroxidases and glutaredoxins, as well as reacting directly with oxidants.[45] Due to its high concentration and its central role in maintaining the cell's redox state, glutathione is one of the most important cellular antioxidants.[50] In some organisms glutathione is replaced by other thiols, such as by mycothiol in the Actinomycetes, or bytrypanothione in the Kinetoplastids.[52][53]
MelatoninMelatonin is a powerful antioxidant that can easily cross cell membranes and the blood-brain barrier.[54] Unlike other antioxidants, melatonin does not undergo redox cycling, which is the ability of a molecule to undergo repeated reduction and oxidation. Redox cycling may allow other antioxidants (such as vitamin C) to act as pro-oxidants and promote free radical formation. Melatonin, once oxidized, cannot be reduced to its former state because it forms several stable end-products upon reacting with free radicals. Therefore, it has been referred to as a terminal (or suicidal) antioxidant.[55]
Tocopherols and tocotrienols (vitamin E)Vitamin E is the collective name for a set of eight related tocopherols and tocotrienols, which are fat-soluble vitamins with antioxidant properties.[56][57] Of these, α-tocopherol has been most studied as it has the highest bioavailability, with the body preferentially absorbing and metabolising this form.[58]
It has been claimed that the α-tocopherol form is the most important lipid-soluble antioxidant, and that it protects membranes from oxidation by reacting with lipid radicals produced in the lipid peroxidation chain reaction.[56][59] This removes the free radical intermediates and prevents the propagation reaction from continuing. This reaction produces oxidised α-tocopheroxyl radicals that can be recycled back to the active reduced form through reduction by other antioxidants, such as ascorbate, retinol or ubiquinol.[60] This is in line with findings showing that α-tocopherol, but not water-soluble antioxidants, efficiently protects glutathione peroxidase 4 (GPX4)-deficient cells from cell death[61]. GPx4 is the only known enzyme that efficiently reduces lipid-hydroperoxides within biological membranes.
However, the roles and importance of the various forms of vitamin E are presently unclear,[62][63] and it has even been suggested that the most important function of α-tocopherol is as a signaling molecule, with this molecule having no significant role in antioxidant metabolism.[64][65] The functions of the other forms of vitamin E are even less well-understood, although γ-tocopherol is a nucleophile that may react with electrophilicmutagens,[58] and tocotrienols may be important in protecting neurons from damage.[66]
Pro-oxidant activities
Further information: Pro-oxidant
Antioxidants that are reducing agents can also act as pro-oxidants. For example, vitamin C has antioxidant activity when it reduces oxidizing substances such as hydrogen peroxide,[67] however, it will also reduce metal ions that generate free radicals through the Fenton reaction.[68][69]
2 Fe3+ + Ascorbate → 2 Fe2+ + Dehydroascorbate2 Fe2+ + 2 H2O2 → 2 Fe3+ + 2 OH· + 2 OH−The relative importance of the antioxidant and pro-oxidant activities of antioxidants are an area of current research, but vitamin C, for example, appears to have a mostly antioxidant action in the body.[68][70] However, less data is available for other dietary antioxidants, such as vitamin E,[71] or the polyphenols.[72]
Enzyme systems
Enzymatic pathway for detoxification of reactive oxygen species.
OverviewAs with the chemical antioxidants, cells are protected against oxidative stress by an interacting network of antioxidant enzymes.[1][9] Here, the superoxide released by processes such as oxidative phosphorylation is first converted to hydrogen peroxide and then further reduced to give water. This detoxification pathway is the result of multiple enzymes, with superoxide dismutases catalysing the first step and then catalases and various peroxidases removing hydrogen peroxide. As with antioxidant metabolites, the contributions of these enzymes to antioxidant defenses can be hard to separate from one another, but the generation of transgenic mice lacking just one antioxidant enzyme can be informative.[73]
Superoxide dismutase, catalase and peroxiredoxinsSuperoxide dismutases (SODs) are a class of closely related enzymes that catalyse the breakdown of the superoxide anion into oxygen and hydrogen peroxide.[74][75] SOD enzymes are present in almost all aerobic cells and in extracellular fluids.[76] Superoxide dismutase enzymes contain metal ion cofactors that, depending on the isozyme, can be copper, zinc, manganese or iron. In humans, the copper/zinc SOD is present in the cytosol, while manganese SOD is present in the mitochondrion.[75] There also exists a third form of SOD in extracellular fluids, which contains copper and zinc in its active sites.[77] The mitochondrial isozyme seems to be the most biologically important of these three, since mice lacking this enzyme die soon after birth.[78] In contrast, the mice lacking copper/zinc SOD (Sod1) are viable but have numerous pathologies and a reduced lifespan (see article on superoxide), while mice without the extracellular SOD have minimal defects (sensitive to hyperoxia).[73][79] In plants, SOD isozymes are present in the cytosol and mitochondria, with an iron SOD found in chloroplasts that is absent from vertebrates and yeast.[80]
Catalases are enzymes that catalyse the conversion of hydrogen peroxide to water and oxygen, using either an iron or manganese cofactor.[81][82]This protein is localized to peroxisomes in most eukaryotic cells.[83] Catalase is an unusual enzyme since, although hydrogen peroxide is its only substrate, it follows a ping-pong mechanism. Here, its cofactor is oxidised by one molecule of hydrogen peroxide and then regenerated by transferring the bound oxygen to a second molecule of substrate.[84] Despite its apparent importance in hydrogen peroxide removal, humans with genetic deficiency of catalase — "acatalasemia" — or mice genetically engineered to lack catalase completely, suffer few ill effects.[85][86]
Decameric structure of AhpC, a bacterial 2-cysteine peroxiredoxinfrom Salmonella typhimurium.[87]
Peroxiredoxins are peroxidases that catalyze the reduction of hydrogen peroxide, organic hydroperoxides, as well as peroxynitrite.[88] They are divided into three classes: typical 2-cysteine peroxiredoxins; atypical 2-cysteine peroxiredoxins; and 1-cysteine peroxiredoxins.[89] These enzymes share the same basic catalytic mechanism, in which a redox-active cysteine (the peroxidatic cysteine) in the active site is oxidized to a sulfenic acidby the peroxide substrate.[90] Over-oxidation of this cysteine residue in peroxiredoxins inactivates these enzymes, but this can be reversed by the action of sulfiredoxin.[91] Peroxiredoxins seem to be important in antioxidant metabolism, as mice lacking peroxiredoxin 1 or 2 have shortened lifespan and suffer from hemolytic anaemia, while plants use peroxiredoxins to remove hydrogen peroxide generated in chloroplasts.[92][93][94]
Thioredoxin and glutathione systemsThe thioredoxin system contains the 12-kDa protein thioredoxin and its companion thioredoxin reductase.[95] Proteins related to thioredoxin are present in all sequenced organisms with plants, such as Arabidopsis thaliana, having a particularly great diversity of isoforms.[96] The active site of thioredoxin consists of two neighboring cysteines, as part of a highly conserved CXXC motif, that can cycle between an active dithiol form (reduced) and an oxidized disulfide form. In its active state, thioredoxin acts as an efficient reducing agent, scavenging reactive oxygen species and maintaining other proteins in their reduced state.[97] After being oxidized, the active thioredoxin is regenerated by the action of thioredoxin reductase, using NADPH as an electron donor.[98]
The glutathione system includes glutathione, glutathione reductase, glutathione peroxidases and glutathione S-transferases.[50] This system is found in animals, plants and microorganisms.[50][99] Glutathione peroxidase is an enzyme containing four selenium-cofactors that catalyzes the breakdown of hydrogen peroxide and organic hydroperoxides. There are at least four different glutathione peroxidase isozymes in animals.[100]Glutathione peroxidase 1 is the most abundant and is a very efficient scavenger of hydrogen peroxide, while glutathione peroxidase 4 is most active with lipid hydroperoxides. Surprisingly, glutathione peroxidase 1 is dispensable, as mice lacking this enzyme have normal lifespans,[101] but they are hypersensitive to induced oxidative stress.[102] In addition, the glutathione S-transferases show high activity with lipid peroxides.[103] These enzymes are at particularly high levels in the liver and also serve in detoxification metabolism.[104]
Oxidative stress in disease
Further information: Pathology, Free-radical theory of aging
Oxidative stress is thought to contribute to the development of a wide range of diseases including Alzheimer's disease,[105][106] Parkinson's disease,[107] the pathologies caused by diabetes,[108][109] rheumatoid arthritis,[110] and neurodegeneration in motor neuron diseases.[111] In many of these cases, it is unclear if oxidants trigger the disease, or if they are produced as a secondary consequence of the disease and from general tissue damage;[12] One case in which this link is particularly well-understood is the role of oxidative stress in cardiovascular disease. Here, low density lipoprotein (LDL) oxidation appears to trigger the process of atherogenesis, which results in atherosclerosis, and finally cardiovascular disease.[112][113]
A low calorie diet extends median and maximum lifespan in many animals. This effect may involve a reduction in oxidative stress.[114] While there is some evidence to support the role of oxidative stress in aging in model organisms such as Drosophila melanogaster and Caenorhabditis elegans,[115][116] the evidence in mammals is less clear.[117][118][119] Indeed, a 2009 review of experiments in mice concluded that almost all manipulations of antioxidant systems had no effect on aging.[120] Diets high in fruit and vegetables, which are high in antioxidants, promote health and reduce the effects of aging, however antioxidant vitamin supplementation has no detectable effect on the aging process, so the effects of fruit and vegetables may be unrelated to their antioxidant contents.[121][122] One reason for this might be the fact that consuming antioxidant molecules such as polyphenols and vitamin E will produce changes in other parts of metabolism, so it may be these other effects that are the real reason these compunds are important in human nutrition.[64][123]
Health effectsDisease treatmentThe brain is uniquely vulnerable to oxidative injury, due to its high metabolic rate and elevated levels of polyunsaturated lipids, the target of lipid peroxidation.[124] Consequently, antioxidants are commonly used as medications to treat various forms of brain injury. Here, superoxide dismutase mimetics,[125] sodium thiopental and propofol are used to treat reperfusion injury and traumatic brain injury,[126] while the experimental drug NXY-059[127][128] and ebselen[129] are being applied in the treatment of stroke. These compounds appear to prevent oxidative stress in neurons and prevent apoptosis and neurological damage. Antioxidants are also being investigated as possible treatments for neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis,[130][131] and as a way to prevent noise-induced hearing loss.[132]
Structure of the polyphenol antioxidant resveratrol.
Antioxidants can cancel out the cell-damaging effects of free radicals.[1] Furthermore, people who eat fruits and vegetables, which happen to be good sources of antioxidants, have a lower risk of heart disease and some neurological diseases,[133] and there is evidence that some types of vegetables, and fruits in general, protect against a number of cancers.[134] These observations suggested the idea that antioxidants might help prevent these conditions. However, this hypothesis has now been tested in many clinical trials and does not seem to be true, since antioxidant supplements have no clear effect on the risk of chronic diseases such as cancer and heart disease.[133][135] This suggests that other substances in fruit and vegetables (possibly flavonoids), or a complex mix of substances, may contribute to the better cardiovascular health of those who consume more fruit and vegetables.[136][137] However, there is some evidence that antioxidants might help prevent other diseases such as macular degeneration,[138] suppressed immunity due to poor nutrition,[139] and neurodegeneration.[140]
It is thought that oxidation of low density lipoprotein in the blood contributes to heart disease, and initial observational studies found that people taking Vitamin E supplements had a lower risk of developing heart disease.[141] Consequently, at least seven large clinical trials were conducted to test the effects of antioxidant supplement with Vitamin E, in doses ranging from 50 to 600 mg per day. However, none of these trials found astatistically significant effect of Vitamin E on overall number of deaths or on deaths due to heart disease.[142] Further studies have also been negative.[143][144] It is not clear if the doses used in these trials or in most dietary supplements are capable of producing any significant decrease in oxidative stress.[145] Overall, despite the clear role of oxidative stress in cardiovascular disease, controlled studies using antioxidant vitamins have observed no reduction in either the risk of developing heart disease, or the rate of progression of existing disease.[146][147]
While several trials have investigated supplements with high doses of antioxidants, the "Supplémentation en Vitamines et Mineraux Antioxydants" (SU.VI.MAX) study tested the effect of supplementation with doses comparable to those in a healthy diet.[148] Over 12,500 French men and women took either low-dose antioxidants (120 mg of ascorbic acid, 30 mg of vitamin E, 6 mg of beta carotene, 100 μg of selenium, and 20 mg of zinc) orplacebo pills for an average of 7.5 years. The investigators found there was no statistically significant effect of the antioxidants on overall survival, cancer, or heart disease. However, in a post-hoc analysis they found a 31% reduction in the risk of cancer in men, but not women.
Many nutraceutical and health food companies sell formulations of antioxidants as dietary supplements and these are widely used in industrialized countries.[149] These supplements may include specific antioxidant chemicals, like resveratrol (from grape seeds or knotweed roots),[150]combinations of antioxidants, like the "ACES" products that contain beta carotene (provitamin A), vitamin C, vitamin E and Selenium, or herbs that contain antioxidants - such as green tea and jiaogulan. Although some levels of antioxidant vitamins and minerals in the diet are required for good health, there is considerable doubt as to whether these antioxidant supplements are beneficial or harmful, and if they are actually beneficial, which antioxidant(s) are needed and in what amounts.[133][135][151] Indeed, some authors argue that the hypothesis that antioxidants could prevent chronic diseases has now been disproven and that the idea was misguided from the beginning.[152]
For overall life expectancy, it has even been suggested that moderate levels of oxidative stress may increase lifespan in the worm Caenorhabditis elegans, by inducing a protective response to increased levels of reactive oxygen species.[153] However, the suggestion that increased life expectancy comes from increased oxidative stress conflicts with results seen in the yeast Saccharomyces cerevisiae,[154] and the situation in mammals is even less clear.[117][118][119] Nevertheless, antioxidant supplements do not appear to increase life expectancy in humans.[155]
Physical exerciseDuring exercise, oxygen consumption can increase by a factor of more than 10.[156] This leads to a large increase in the production of oxidants and results in damage that contributes to muscular fatigue during and after exercise. The inflammatory response that occurs after strenuous exercise is also associated with oxidative stress, especially in the 24 hours after an exercise session. The immune system response to the damage done by exercise peaks 2 to 7 days after exercise, which is the period during which most of the adaptation that leads to greater fitness occurs. During this process, free radicals are produced by neutrophils to remove damaged tissue. As a result, excessive antioxidant levels may inhibit recovery and adaptation mechanisms.[157] Antioxidant supplements may also prevent any of the health gains that normally come from exercise, such as increased insulin sensitivity.[158]
The evidence for benefits from antioxidant supplementation in vigorous exercise is mixed. There is strong evidence that one of the adaptations resulting from exercise is a strengthening of the body's antioxidant defenses, particularly the glutathione system, to regulate the increased oxidative stress.[159] This effect may be to some extent protective against diseases which are associated with oxidative stress, which would provide a partial explanation for the lower incidence of major diseases and better health of those who undertake regular exercise.[160]
However, no benefits for physical performance to athletes are seen with vitamin E supplementation.[161] Indeed, despite its key role in preventinglipid membrane peroxidation, 6 weeks of vitamin E supplementation had no effect on muscle damage in ultramarathon runners.[162] Although there appears to be no increased requirement for vitamin C in athletes, there is some evidence that vitamin C supplementation increased the amount of intense exercise that can be done and vitamin C supplementation before strenuous exercise may reduce the amount of muscle damage.[163][164]However, other studies found no such effects, and some research suggests that supplementation with amounts as high as 1000 mg inhibits recovery.[165]
Further information: Micronutrients
Structure of the metal chelatorphytic acid.
Relatively strong reducing acids can have antinutrient effects by binding to dietary minerals such as iron and zinc in the gastrointestinal tract and preventing them from being absorbed.[166] Notable examples are oxalic acid, tannins and phytic acid, which are high in plant-based diets.[167]Calcium and iron deficiencies are not uncommon in diets in developing countries where less meat is eaten and there is high consumption of phytic acid from beans and unleavened whole grain bread.[168]
FoodsReducing acid presentCocoa and chocolate, spinach, turnip and rhubarb.[169]Oxalic acidWhole grains, maize, legumes.[170]Phytic acidTea, beans, cabbage.[169][171]TanninsNonpolar antioxidants such as eugenol—a major component of oil of cloves—have toxicity limits that can be exceeded with the misuse of undilutedessential oils.[172] Toxicity associated with high doses of water-soluble antioxidants such as ascorbic acid are less of a concern, as these compounds can be excreted rapidly in urine.[173] More seriously, very high doses of some antioxidants may have harmful long-term effects. The beta-Carotene and Retinol Efficacy Trial (CARET) study of lung cancer patients found that smokers given supplements containing beta-carotene and vitamin A had increased rates of lung cancer.[174] Subsequent studies confirmed these adverse effects.[175]
These harmful effects may also be seen in non-smokers, as a recent meta-analysis including data from approximately 230,000 patients showed that β-carotene, vitamin A or vitamin E supplementation is associated with increased mortality but saw no significant effect from vitamin C.[176] No health risk was seen when all the randomized controlled studies were examined together, but an increase in mortality was detected only when the high-quality and low-bias risk trials were examined separately. However, as the majority of these low-bias trials dealt with either elderly people, or people already suffering disease, these results may not apply to the general population.[177] This meta-analysis was later repeated and extended by the same authors, with the new analysis published by the Cochrane Collaboration; confirming the previous results.[178] These two publications are consistent with some previous meta-analyzes that also suggested that Vitamin E supplementation increased mortality,[179] and that antioxidant supplements increased the risk of colon cancer.[180] However, the results of this meta-analysis are inconsistent with other studies such as the SU.VI.MAX trial, which suggested that antioxidants have no effect on cause-all mortality.[148][181][182][183] Overall, the large number of clinical trials carried out on antioxidant supplements suggest that either these products have no effect on health, or that they cause a small increase in mortality in elderly or vulnerable populations.[133][135][176]
While antioxidant supplementation is widely used in attempts to prevent the development of cancer, it has been proposed that antioxidants may, paradoxically, interfere with cancer treatments.[184] This was thought to occur since the environment of cancer cells causes high levels of oxidative stress, making these cells more susceptible to the further oxidative stress induced by treatments. As a result, by reducing the redox stress in cancer cells, antioxidant supplements could decrease the effectiveness of radiotherapy and chemotherapy.[185][186] On the other hand, other reviews have suggested that antioxidants could reduce side effects or increase survival times.[187][188]
Measurement and levels in food
Further information: List of antioxidants in food, Polyphenol antioxidants
Fruits and vegetables are good sources of antioxidants.
Measurement of antioxidants is not a straightforward process, as this is a diverse group of compounds with different reactivities to different reactive oxygen species. In food science, the oxygen radical absorbance capacity (ORAC) has become the current industry standard for assessing antioxidant strength of whole foods, juices and food additives.[189][190] Other measurement tests include the Folin-Ciocalteu reagent, and the Trolox equivalent antioxidant capacity assay.[191] The CAP-e assay measures antioxidants that are available to enter and protect live cells.[192]
Antioxidants are found in varying amounts in foods such as vegetables, fruits, grain cereals, eggs, meat, legumes and nuts. Some antioxidants such as lycopene and ascorbic acid can be destroyed by long-term storage or prolonged cooking.[193][194] Other antioxidant compounds are more stable, such as the polyphenolic antioxidants in foods such as whole-wheat cereals and tea.[195][196] The effects of cooking and food processing are complex, as these processes can also increase the bioavailability of antioxidants, such as some carotenoids in vegetables.[197] In general, processed foods contain fewer antioxidants than fresh and uncooked foods, since the preparation processes may expose the food to oxygen.[198]
Antioxidant compoundsFoods containing high levels of these antioxidants[171][199][200]Vitamin C (ascorbic acid)Fruits and vegetablesVitamin E (tocopherols, tocotrienols)Vegetable oilsPolyphenolic antioxidants (resveratrol, flavonoids)Tea, coffee, soy, fruit, olive oil, chocolate, cinnamon, oregano and red wineCarotenoids (lycopene, carotenes, lutein)Fruit, vegetables and eggs.[201]Other antioxidants are not vitamins and are instead made in the body. For example, ubiquinol (coenzyme Q) is poorly absorbed from the gut and is made in humans through the mevalonate pathway.[42] Another example is glutathione, which is made from amino acids. As any glutathione in the gut is broken down to free cysteine, glycine and glutamic acid before being absorbed, even large oral doses have little effect on the concentration of glutathione in the body.[202][203] Although large amounts of sulfur-containing amino acids such as acetylcysteine can increase glutathione,[204] no evidence exists that eating high levels of these glutathione precursors is beneficial for healthy adults.[205] Supplying more of these precursors may be useful as part of the treatment of some diseases, such as acute respiratory distress syndrome, protein-energy malnutrition, or preventing the liver damage produced by paracetamol overdose.[204][206]
Other compounds in the diet can alter the levels of antioxidants by acting as pro-oxidants. Here, consuming the compound causes oxidative stress, which the body responds to by inducing higher levels of antioxidant defenses such as antioxidant enzymes.[152] Some of these compounds, such as isothiocyanates and curcumin, may be chemopreventive agents that either block the transformation of abnormal cells into cancerous cells, or even kill existing cancer cells.[152][207]
Uses in technologyFood preservativesAntioxidants are used as food additives to help guard against food deterioration. Exposure to oxygen and sunlight are the two main factors in the oxidation of food, so food is preserved by keeping in the dark and sealing it in containers or even coating it in wax, as with cucumbers. However, as oxygen is also important for plant respiration, storing plant materials in anaerobic conditions produces unpleasant flavors and unappealing colors.[208] Consequently, packaging of fresh fruits and vegetables contains an ~8% oxygen atmosphere. Antioxidants are an especially important class of preservatives as, unlike bacterial or fungal spoilage, oxidation reactions still occur relatively rapidly in frozen or refrigerated food.[209] These preservatives include natural antioxidants such as ascorbic acid (AA, E300) and tocopherols (E306), as well as synthetic antioxidants such as propyl gallate (PG, E310), tertiary butylhydroquinone (TBHQ), butylated hydroxyanisole (BHA, E320) and butylated hydroxytoluene (BHT, E321).[210][211]
The most common molecules attacked by oxidation are unsaturated fats; oxidation causes them to turn rancid.[212] Since oxidized lipids are often discolored and usually have unpleasant tastes such as metallic or sulfurous flavors, it is important to avoid oxidation in fat-rich foods. Thus, these foods are rarely preserved by drying; instead, they are preserved by smoking, salting or fermenting. Even less fatty foods such as fruits are sprayed with sulfurous antioxidants prior to air drying. Oxidation is often catalyzed by metals, which is why fats such as butter should never be wrapped inaluminium foil or kept in metal containers. Some fatty foods such as olive oil are partially protected from oxidation by their natural content of antioxidants, but remain sensitive to photooxidation.[213] Antioxidant preservatives are also added to fat-based cosmetics such as lipstick andmoisturizers to prevent rancidity.
Industrial uses
Antioxidants are frequently added to industrial products. A common use is as stabilizers in fuels and lubricants to prevent oxidation, and in gasolines to prevent the polymerization that leads to the formation of engine-fouling residues.[214]
They are widely used to prevent the oxidative degradation of polymers such as rubbers, plastics and adhesives that causes a loss of strength and flexibility in these materials.[215] Polymers containing double bonds in their main chains are especially susceptible to oxidation and ozonolysis. Solid polymer products start to crack on exposed surfaces as the material degrades and the chains unzip. The mode of cracking varies between oxygen and ozone attack, the former causing a "crazy paving" effect, while ozone attack produces deeper cracks aligned at right angles to the tensile strain in the product. Ozone cracking is especially damaging to elastomers such as natural rubber, polybutadiene and other double-bonded rubbers. They can be protected by antiozonants. Oxidation and UV degradation are also frequently linked, mainly because UV radiation creates free radicals by bond breakage. The free radicals then react with oxygen to produce peroxy radicals which cause yet further damage, often in a chain reaction. Other polymers suceptible to oxidation include polypropylene and polyethylene. The former is more sensitive owing to the presence of secondary carbon atoms present in every repeat unit. Attack occurs at this point because the free radical formed is more stable than one formed on a primary carbon atom. Oxidation of polyethylene tends to occur at weak links in the chain, such as branch points in low density polyethylene.
Fuel additiveComponents[216]Applications[216]AO-22N,N'-di-2-butyl-1,4-phenylenediamineTurbine oils, transformer oils, hydraulic fluids, waxes, andgreasesAO-24N,N'-di-2-butyl-1,4-phenylenediamineLow-temperature oilsAO-292,6-di-tert-butyl-4-methylphenolTurbine oils, transformer oils, hydraulic fluids, waxes, greases, and gasolinesAO-302,4-dimethyl-6-tert-butylphenolJet fuels and gasolines, including aviation gasolinesAO-312,4-dimethyl-6-tert-butylphenolJet fuels and gasolines, including aviation gasolinesAO-322,4-dimethyl-6-tert-butylphenol and 2,6-di-tert-butyl-4-methylphenolJet fuels and gasolines, including aviation gasolinesAO-372,6-di-tert-butylphenolJet fuels and gasolines, widely approved for aviation fuelsSee alsoPharmacy and Pharmacology portal
Free radical theory
Phytochemical
Mitohormesis
Polymer degradation
Antiozonant
Evolution of dietary antioxidants
Superdrink
Nick Lane Oxygen: The Molecule That Made the World (Oxford University Press, 2003) ISBN 0-198-60783-0
Barry Halliwell and John M.C. Gutteridge Free Radicals in Biology and Medicine(Oxford University Press, 2007) ISBN 0-198-56869-X
Jan Pokorny, Nelly Yanishlieva and Michael H. Gordon Antioxidants in Food: Practical Applications (CRC Press Inc, 2001) ISBN 0-849-31222-1
^ a b c d e f g Sies H (1997). "Oxidative stress: oxidants and antioxidants" (PDF). Exp Physiol 82 (2): 291–5. PMID 9129943.http://ep.physoc.org/cgi/reprint/82/2/291.pdf.
^ Bjelakovic G, et al. (2007). "Mortality in randomized trials of antioxidant supplements for primary and secondary prevention: systematic review and meta-analysis". JAMA 297 (8): 842–57. doi:10.1001/jama.297.8.842. PMID 17327526.
^ Matill HA (1947). Antioxidants. Annu Rev Biochem 16: 177–192.
^ German J (1999). "Food processing and lipid oxidation". Adv Exp Med Biol 459: 23–50. PMID 10335367.
^ Jacob R (1996). "Three eras of vitamin C discovery". Subcell Biochem 25: 1–16. PMID 8821966.
^ Knight J (1998). "Free radicals: their history and current status in aging and disease". Ann Clin Lab Sci 28 (6): 331–46. PMID 9846200.
^ Moreau and Dufraisse, (1922) Comptes Rendus des Séances et Mémoires de la Société de Biologie, 86, 321.
^ Wolf G (01 Mar 2005). "The discovery of the antioxidant function of vitamin E: the contribution of Henry A. Mattill". J Nutr 135 (3): 363–6. PMID 15735064. http://jn.nutrition.org/cgi/content/full/135/3/363.
^ a b c Davies K (1995). "Oxidative stress: the paradox of aerobic life". Biochem Soc Symp 61: 1–31. PMID 8660387.
^ a b c d Vertuani S, Angusti A, Manfredini S (2004). "The antioxidants and pro-antioxidants network: an overview". Curr Pharm Des 10 (14): 1677–94. doi:10.2174/1381612043384655. PMID 15134565.
^ Rhee SG (June 2006). "Cell signaling. H2O2, a necessary evil for cell signaling". Science (journal) 312 (5782): 1882–3.doi:10.1126/science.1130481. PMID 16809515.
^ a b Valko M, Leibfritz D, Moncol J, Cronin M, Mazur M, Telser J (2007). "Free radicals and antioxidants in normal physiological functions and human disease". Int J Biochem Cell Biol 39 (1): 44–84. doi:10.1016/j.biocel.2006.07.001. PMID 16978905.
^ Stohs S, Bagchi D (1995). "Oxidative mechanisms in the toxicity of metal ions". Free Radic Biol Med 18 (2): 321–36. doi:10.1016/0891-5849(94)00159-H. PMID 7744317.
^ Nakabeppu Y, Sakumi K, Sakamoto K, Tsuchimoto D, Tsuzuki T, Nakatsu Y (2006). "Mutagenesis and carcinogenesis caused by the oxidation of nucleic acids". Biol Chem 387 (4): 373–9. doi:10.1515/BC.2006.050. PMID 16606334.
^ Valko M, Izakovic M, Mazur M, Rhodes C, Telser J (2004). "Role of oxygen radicals in DNA damage and cancer incidence". Mol Cell Biochem266 (1–2): 37–56. doi:10.1023/B:MCBI.0000049134.69131.89. PMID 15646026.
^ Stadtman E (1992). "Protein oxidation and aging". Science 257 (5074): 1220–4. doi:10.1126/science.1355616. PMID 1355616.
^ Raha S, Robinson B (2000). "Mitochondria, oxygen free radicals, disease and aging". Trends Biochem Sci 25 (10): 502–8.doi:10.1016/S0968-0004(00)01674-1. PMID 11050436.
^ Lenaz G (2001). "The mitochondrial production of reactive oxygen species: mechanisms and implications in human pathology". IUBMB Life52 (3–5): 159–64. doi:10.1080/15216540152845957. PMID 11798028.
^ Finkel T, Holbrook NJ (2000). "Oxidants, oxidative stress and the biology of aging". Nature 408 (6809): 239–47. doi:10.1038/35041687.PMID 11089981.
^ Hirst J, King MS, Pryde KR (October 2008). "The production of reactive oxygen species by complex I". Biochem. Soc. Trans. 36 (Pt 5): 976–80. doi:10.1042/BST0360976. PMID 18793173.
^ Seaver LC, Imlay JA (November 2004). "Are respiratory enzymes the primary sources of intracellular hydrogen peroxide?". J. Biol. Chem.279 (47): 48742–50. doi:10.1074/jbc.M408754200. PMID 15361522. http://www.jbc.org/cgi/pmidlookup?view=long&pmid=15361522.
^ Imlay JA (2003). "Pathways of oxidative damage". Annu. Rev. Microbiol. 57: 395–418. doi:10.1146/annurev.micro.57.030502.090938. PMID 14527285.
^ Demmig-Adams B, Adams WW (December 2002). "Antioxidants in photosynthesis and human nutrition". Science (journal) 298 (5601): 2149–53. doi:10.1126/science.1078002. PMID 12481128.
^ Krieger-Liszkay A (2005). "Singlet oxygen production in photosynthesis". J Exp Bot 56 (411): 337–46. doi:10.1093/jxb/erh237. PMID 15310815. http://jxb.oxfordjournals.org/cgi/content/full/56/411/337.
^ Szabó I, Bergantino E, Giacometti G (2005). "Light and oxygenic photosynthesis: energy dissipation as a protection mechanism against photo-oxidation". EMBO Rep 6 (7): 629–34. doi:10.1038/sj.embor.7400460. PMID 15995679.
^ Kerfeld CA (October 2004). "Water-soluble carotenoid proteins of cyanobacteria". Arch. Biochem. Biophys. 430 (1): 2–9.doi:10.1016/j.abb.2004.03.018. PMID 15325905.
^ Miller RA, Britigan BE (January 1997). "Role of oxidants in microbial pathophysiology". Clin. Microbiol. Rev. 10 (1): 1–18. PMID 8993856.PMC: 172912. http://cmr.asm.org/cgi/pmidlookup?view=long&pmid=8993856.
^ Chaudière J, Ferrari-Iliou R (1999). "Intracellular antioxidants: from chemical to biochemical mechanisms". Food Chem Toxicol 37 (9–10): 949 – 62. doi:10.1016/S0278-6915(99)00090-3. PMID 10541450.
^ Sies H (1993). "Strategies of antioxidant defense". Eur J Biochem 215 (2): 213 – 9. doi:10.1111/j.1432-1033.1993.tb18025.x. PMID 7688300.
^ Imlay J (2003). "Pathways of oxidative damage". Annu Rev Microbiol 57: 395–418. doi:10.1146/annurev.micro.57.030502.090938. PMID 14527285.
^ Ames B, Cathcart R, Schwiers E, Hochstein P (1981). "Uric acid provides an antioxidant defense in humans against oxidant- and radical-caused aging and cancer: a hypothesis". Proc Natl Acad Sci USA 78 (11): 6858–62. doi:10.1073/pnas.78.11.6858. PMID 6947260.
^ Khaw K, Woodhouse P (1995). "Interrelation of vitamin C, infection, haemostatic factors, and cardiovascular disease". BMJ 310 (6994): 1559 – 63. PMID 7787643. http://www.bmj.com/cgi/content/full/310/6994/1559.
^ a b c d Evelson P, Travacio M, Repetto M, Escobar J, Llesuy S, Lissi E (2001). "Evaluation of total reactive antioxidant potential (TRAP) of tissue homogenates and their cytosols". Arch Biochem Biophys 388 (2): 261 – 6. doi:10.1006/abbi.2001.2292. PMID 11368163.
^ Morrison JA, Jacobsen DW, Sprecher DL, Robinson K, Khoury P, Daniels SR (30 November 1999). "Serum glutathione in adolescent males predicts parental coronary heart disease". Circulation 100 (22): 2244–7. PMID 10577998. http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=10577998.
^ Teichert J, Preiss R (1992). "HPLC-methods for determination of lipoic acid and its reduced form in human plasma". Int J Clin Pharmacol Ther Toxicol 30 (11): 511 – 2. PMID 1490813.
^ Akiba S, Matsugo S, Packer L, Konishi T (1998). "Assay of protein-bound lipoic acid in tissues by a new enzymatic method". Anal Biochem258 (2): 299 – 304. doi:10.1006/abio.1998.2615. PMID 9570844.
^ Glantzounis G, Tsimoyiannis E, Kappas A, Galaris D (2005). "Uric acid and oxidative stress". Curr Pharm Des 11 (32): 4145 – 51.doi:10.2174/138161205774913255. PMID 16375736.
^ El-Sohemy A, Baylin A, Kabagambe E, Ascherio A, Spiegelman D, Campos H (2002). "Individual carotenoid concentrations in adipose tissue and plasma as biomarkers of dietary intake". Am J Clin Nutr 76 (1): 172 – 9. PMID 12081831.
^ a b Sowell A, Huff D, Yeager P, Caudill S, Gunter E (1994). "Retinol, alpha-tocopherol, lutein/zeaxanthin, beta-cryptoxanthin, lycopene, alpha-carotene, trans-beta-carotene, and four retinyl esters in serum determined simultaneously by reversed-phase HPLC with multiwavelength detection". Clin Chem 40 (3): 411 – 6. PMID 8131277. http://www.clinchem.org/cgi/reprint/40/3/411.pdf?ijkey=12d7f1fb0a06f27c93b282ad4ea3435c0fb78f7e.
^ Stahl W, Schwarz W, Sundquist A, Sies H (1992). "cis-trans isomers of lycopene and beta-carotene in human serum and tissues". Arch Biochem Biophys 294 (1): 173 – 7. doi:10.1016/0003-9861(92)90153-N. PMID 1550343.
^ Zita C, Overvad K, Mortensen S, Sindberg C, Moesgaard S, Hunter D (2003). "Serum coenzyme Q10 concentrations in healthy men supplemented with 30 mg or 100 mg coenzyme Q10 for two months in a randomised controlled study". Biofactors 18 (1 – 4): 185 – 93.doi:10.1002/biof.5520180221. PMID 14695934.
^ a b Turunen M, Olsson J, Dallner G (2004). "Metabolism and function of coenzyme Q". Biochim Biophys Acta 1660 (1 – 2): 171 – 99.doi:10.1016/j.bbamem.2003.11.012. PMID 14757233.
^ Smirnoff N (2001). "L-ascorbic acid biosynthesis". Vitam Horm 61: 241 – 66. doi:10.1016/S0083-6729(01)61008-2. PMID 11153268.
^ Linster CL, Van Schaftingen E (2007). "Vitamin C. Biosynthesis, recycling and degradation in mammals". Febs J. 274 (1): 1–22.doi:10.1111/j.1742-4658.2006.05607.x. PMID 17222174.
^ a b Meister A (1994). "Glutathione-ascorbic acid antioxidant system in animals". J Biol Chem 269 (13): 9397 – 400. PMID 8144521.
^ Wells W, Xu D, Yang Y, Rocque P (15 Sep 1990). "Mammalian thioltransferase (glutaredoxin) and protein disulfide isomerase have dehydroascorbate reductase activity". J Biol Chem 265 (26): 15361 – 4. PMID 2394726. http://www.jbc.org/cgi/reprint/265/26/15361.
^ Padayatty S, Katz A, Wang Y, Eck P, Kwon O, Lee J, Chen S, Corpe C, Dutta A, Dutta S, Levine M (01 Feb 2003). "Vitamin C as an antioxidant: evaluation of its role in disease prevention". J Am Coll Nutr 22 (1): 18 – 35. PMID 12569111.http://www.jacn.org/cgi/content/full/22/1/18.
^ Shigeoka S, Ishikawa T, Tamoi M, Miyagawa Y, Takeda T, Yabuta Y, Yoshimura K (2002). "Regulation and function of ascorbate peroxidase isoenzymes". J Exp Bot 53 (372): 1305 – 19. doi:10.1093/jexbot/53.372.1305. PMID 11997377.http://jxb.oxfordjournals.org/cgi/content/full/53/372/1305.
^ Smirnoff N, Wheeler GL (2000). "Ascorbic acid in plants: biosynthesis and function". Crit. Rev. Biochem. Mol. Biol. 35 (4): 291–314.doi:10.1080/10409230008984166. PMID 11005203.
^ a b c d Meister A, Anderson M (1983). "Glutathione". Annu Rev Biochem 52: 711 – 60. doi:10.1146/annurev.bi.52.070183.003431. PMID 6137189.
^ Meister A (1988). "Glutathione metabolism and its selective modification" (PDF). J Biol Chem 263 (33): 17205 – 8.doi:10.1073/pnas.0508621102. PMID 3053703. http://www.jbc.org/cgi/reprint/263/33/17205.pdf.
^ Fahey RC (2001). "Novel thiols of prokaryotes". Annu. Rev. Microbiol. 55: 333–56. doi:10.1146/annurev.micro.55.1.333. PMID 11544359.
^ Fairlamb AH, Cerami A (1992). "Metabolism and functions of trypanothione in the Kinetoplastida". Annu. Rev. Microbiol. 46: 695–729.doi:10.1146/annurev.mi.46.100192.003403. PMID 1444271.
^ Reiter RJ, Carneiro RC, Oh CS (1997). "Melatonin in relation to cellular antioxidative defense mechanisms". Horm. Metab. Res. 29 (8): 363–72. doi:10.1055/s-2007-979057. PMID 9288572.
^ Tan DX, Manchester LC, Reiter RJ, Qi WB, Karbownik M, Calvo JR (2000). "Significance of melatonin in antioxidative defense system: reactions and products". Biological signals and receptors 9 (3–4): 137–59. doi:10.1159/000014635. PMID 10899700.
^ a b Herrera E, Barbas C (2001). "Vitamin E: action, metabolism and perspectives". J Physiol Biochem 57 (2): 43 – 56. PMID 11579997.
^ Packer L, Weber SU, Rimbach G (01 Feb 2001). "Molecular aspects of alpha-tocotrienol antioxidant action and cell signalling". J. Nutr. 131(2): 369S–73S. PMID 11160563. http://jn.nutrition.org/cgi/content/full/131/2/369S.
^ a b Brigelius-Flohé R, Traber M (01 Jul 1999). "Vitamin E: function and metabolism". Faseb J 13 (10): 1145 – 55. PMID 10385606.http://www.fasebj.org/cgi/content/full/13/10/1145.
^ Traber MG, Atkinson J (2007). "Vitamin E, antioxidant and nothing more". Free Radic. Biol. Med. 43 (1): 4–15.doi:10.1016/j.freeradbiomed.2007.03.024. PMID 17561088.
^ Wang X, Quinn P (1999). "Vitamin E and its function in membranes". Prog Lipid Res 38 (4): 309 – 36. doi:10.1016/S0163-7827(99)00008-9.PMID 10793887.
^ Seiler A, Schneider M, F�rster H, Roth S, Wirth EK, Culmsee C, Plesnila N, Kremmer E, R�dmark O, Wurst W, Bornkamm GW, Schweizer U, Conrad M (September 2008). "Glutathione peroxidase 4 senses and translates oxidative stress into 12/15-lipoxygenase dependent- and AIF-mediated cell death". Cell Metab. 8 (3): 237–48. doi:10.1016/j.cmet.2008.07.005. PMID 18762024.
^ Brigelius-Flohé R, Davies KJ (2007). "Is vitamin E an antioxidant, a regulator of signal transduction and gene expression, or a 'junk' food? Comments on the two accompanying papers: "Molecular mechanism of alpha-tocopherol action" by A. Azzi and "Vitamin E, antioxidant and nothing more" by M. Traber and J. Atkinson". Free Radic. Biol. Med. 43 (1): 2–3. PMID 17561087.
^ Atkinson J, Epand RF, Epand RM (2007). "Tocopherols and tocotrienols in membranes: A critical review". Free Radic. Biol. Med. 44 (5): 739–764. doi:10.1016/j.freeradbiomed.2007.11.010. PMID 18160049.
^ a b Azzi A (2007). "Molecular mechanism of alpha-tocopherol action". Free Radic. Biol. Med. 43 (1): 16–21.doi:10.1016/j.freeradbiomed.2007.03.013. PMID 17561089.
^ Zingg JM, Azzi A (2004). "Non-antioxidant activities of vitamin E". Curr. Med. Chem. 11 (9): 1113–33. PMID 15134510.
^ Sen C, Khanna S, Roy S (2006). "Tocotrienols: Vitamin E beyond tocopherols". Life Sci 78 (18): 2088–98. doi:10.1016/j.lfs.2005.12.001.PMID 16458936.
^ Duarte TL, Lunec J (2005). "Review: When is an antioxidant not an antioxidant? A review of novel actions and reactions of vitamin C". Free Radic. Res. 39 (7): 671–86. doi:10.1080/10715760500104025. PMID 16036346.
^ a b Carr A, Frei B (01 Jun 1999). "Does vitamin C act as a pro-oxidant under physiological conditions?". Faseb J. 13 (9): 1007–24. PMID 10336883. http://www.fasebj.org/cgi/content/full/13/9/1007.
^ Stohs SJ, Bagchi D (1995). "Oxidative mechanisms in the toxicity of metal ions". Free Radic. Biol. Med. 18 (2): 321–36. doi:10.1016/0891-5849(94)00159-H. PMID 7744317.
^ Valko M, Morris H, Cronin MT (2005). "Metals, toxicity and oxidative stress". Curr. Med. Chem. 12 (10): 1161–208.doi:10.2174/0929867053764635. PMID 15892631.
^ Schneider C (2005). "Chemistry and biology of vitamin E". Mol Nutr Food Res 49 (1): 7–30. doi:10.1002/mnfr.200400049. PMID 15580660.
^ Halliwell, B. (2008). "Are polyphenols antioxidants or pro-oxidants? What do we learn from cell culture and in vivo studies?". Archives of Biochemistry and Biophysics 476 (2): 107–112. doi:10.1016/j.abb.2008.01.028.
^ a b Ho YS, Magnenat JL, Gargano M, Cao J (October 1998). "The nature of antioxidant defense mechanisms: a lesson from transgenic studies". Environ. Health Perspect. 106 (Suppl 5): 1219–28. doi:10.2307/3433989. PMID 9788901.
^ Zelko I, Mariani T, Folz R (2002). "Superoxide dismutase multigene family: a comparison of the CuZn-SOD (SOD1), Mn-SOD (SOD2), and EC-SOD (SOD3) gene structures, evolution, and expression". Free Radic Biol Med 33 (3): 337–49. doi:10.1016/S0891-5849(02)00905-X.PMID 12126755.
^ a b Bannister J, Bannister W, Rotilio G (1987). "Aspects of the structure, function, and applications of superoxide dismutase". CRC Crit Rev Biochem 22 (2): 111–80. doi:10.3109/10409238709083738. PMID 3315461.
^ Johnson F, Giulivi C (2005). "Superoxide dismutases and their impact upon human health". Mol Aspects Med 26 (4–5): 340–52.doi:10.1016/j.mam.2005.07.006. PMID 16099495.
^ Nozik-Grayck E, Suliman H, Piantadosi C (2005). "Extracellular superoxide dismutase". Int J Biochem Cell Biol 37 (12): 2466–71.doi:10.1016/j.biocel.2005.06.012. PMID 16087389.
^ Melov S, Schneider J, Day B, Hinerfeld D, Coskun P, Mirra S, Crapo J, Wallace D (1998). "A novel neurological phenotype in mice lacking mitochondrial manganese superoxide dismutase". Nat Genet 18 (2): 159–63. doi:10.1038/ng0298-159. PMID 9462746.
^ Reaume A, Elliott J, Hoffman E, Kowall N, Ferrante R, Siwek D, Wilcox H, Flood D, Beal M, Brown R, Scott R, Snider W (1996). "Motor neurons in Cu/Zn superoxide dismutase-deficient mice develop normally but exhibit enhanced cell death after axonal injury". Nat Genet 13(1): 43–7. doi:10.1038/ng0596-43. PMID 8673102.
^ Van Camp W, Inzé D, Van Montagu M (1997). "The regulation and function of tobacco superoxide dismutases". Free Radic Biol Med 23 (3): 515–20. doi:10.1016/S0891-5849(97)00112-3. PMID 9214590.
^ Chelikani P, Fita I, Loewen P (2004). "Diversity of structures and properties among catalases". Cell Mol Life Sci 61 (2): 192–208.doi:10.1007/s00018-003-3206-5. PMID 14745498.
^ Zámocký M, Koller F (1999). "Understanding the structure and function of catalases: clues from molecular evolution and in vitromutagenesis". Prog Biophys Mol Biol 72 (1): 19–66. doi:10.1016/S0079-6107(98)00058-3. PMID 10446501.
^ del Río L, Sandalio L, Palma J, Bueno P, Corpas F (1992). "Metabolism of oxygen radicals in peroxisomes and cellular implications". Free Radic Biol Med 13 (5): 557–80. doi:10.1016/0891-5849(92)90150-F. PMID 1334030.
^ Hiner A, Raven E, Thorneley R, García-Cánovas F, Rodríguez-López J (2002). "Mechanisms of compound I formation in heme peroxidases". J Inorg Biochem 91 (1): 27–34. doi:10.1016/S0162-0134(02)00390-2. PMID 12121759.
^ Mueller S, Riedel H, Stremmel W (15 Dec 1997). "Direct evidence for catalase as the predominant H2O2 -removing enzyme in human erythrocytes". Blood 90 (12): 4973–8. PMID 9389716. http://www.bloodjournal.org/cgi/content/full/90/12/4973.
^ Ogata M (1991). "Acatalasemia". Hum Genet 86 (4): 331–40. doi:10.1007/BF00201829. PMID 1999334.
^ Parsonage D, Youngblood D, Sarma G, Wood Z, Karplus P, Poole L (2005). "Analysis of the link between enzymatic activity and oligomeric state in AhpC, a bacterial peroxiredoxin". Biochemistry 44 (31): 10583–92. doi:10.1021/bi050448i. PMID 16060667. PDB 1YEX
^ Rhee S, Chae H, Kim K (2005). "Peroxiredoxins: a historical overview and speculative preview of novel mechanisms and emerging concepts in cell signaling". Free Radic Biol Med 38 (12): 1543–52. doi:10.1016/j.freeradbiomed.2005.02.026. PMID 15917183.
^ Wood Z, Schr�der E, Robin Harris J, Poole L (2003). "Structure, mechanism and regulation of peroxiredoxins". Trends Biochem Sci 28 (1): 32–40. doi:10.1016/S0968-0004(02)00003-8. PMID 12517450.
^ Claiborne A, Yeh J, Mallett T, Luba J, Crane E, Charrier V, Parsonage D (1999). "Protein-sulfenic acids: diverse roles for an unlikely player in enzyme catalysis and redox regulation". Biochemistry 38 (47): 15407–16. doi:10.1021/bi992025k. PMID 10569923.
^ J�nsson TJ, Lowther WT (2007). "The peroxiredoxin repair proteins". Sub-cellular biochemistry 44: 115–41. doi:10.1007/978-1-4020-6051-9_6. PMID 18084892.
^ Neumann C, Krause D, Carman C, Das S, Dubey D, Abraham J, Bronson R, Fujiwara Y, Orkin S, Van Etten R (2003). "Essential role for the peroxiredoxin Prdx1 in erythrocyte antioxidant defence and tumour suppression". Nature 424 (6948): 561–5. doi:10.1038/nature01819. PMID 12891360.
^ Lee T, Kim S, Yu S, Kim S, Park D, Moon H, Dho S, Kwon K, Kwon H, Han Y, Jeong S, Kang S, Shin H, Lee K, Rhee S, Yu D (2003). "Peroxiredoxin II is essential for sustaining life span of erythrocytes in mice". Blood 101 (12): 5033–8. doi:10.1182/blood-2002-08-2548. PMID 12586629. http://www.bloodjournal.org/cgi/content/full/101/12/5033.
^ Dietz K, Jacob S, Oelze M, Laxa M, Tognetti V, de Miranda S, Baier M, Finkemeier I (2006). "The function of peroxiredoxins in plant organelle redox metabolism". J Exp Bot 57 (8): 1697–709. doi:10.1093/jxb/erj160. PMID 16606633.
^ Nordberg J, Arner ES (2001). "Reactive oxygen species, antioxidants, and the mammalian thioredoxin system". Free Radic Biol Med 31(11): 1287–312. doi:10.1016/S0891-5849(01)00724-9. PMID 11728801.
^ Vieira Dos Santos C, Rey P (2006). "Plant thioredoxins are key actors in the oxidative stress response". Trends Plant Sci 11 (7): 329–34.doi:10.1016/j.tplants.2006.05.005. PMID 16782394.
^ Arnér E, Holmgren A (2000). "Physiological functions of thioredoxin and thioredoxin reductase". Eur J Biochem 267 (20): 6102–9.doi:10.1046/j.1432-1327.2000.01701.x. PMID 11012661. http://www.blackwell-synergy.com/doi/full/10.1046/j.1432-1327.2000.01701.x.
^ Mustacich D, Powis G (2000). "Thioredoxin reductase". Biochem J 346 (Pt 1): 1–8. doi:10.1042/0264-6021:3460001. PMID 10657232.
^ Creissen G, Broadbent P, Stevens R, Wellburn A, Mullineaux P (1996). "Manipulation of glutathione metabolism in transgenic plants".Biochem Soc Trans 24 (2): 465–9. PMID 8736785.
^ Brigelius-Flohé R (1999). "Tissue-specific functions of individual glutathione peroxidases". Free Radic Biol Med 27 (9–10): 951–65.doi:10.1016/S0891-5849(99)00173-2. PMID 10569628.
^ Ho Y, Magnenat J, Bronson R, Cao J, Gargano M, Sugawara M, Funk C (1997). "Mice deficient in cellular glutathione peroxidase develop normally and show no increased sensitivity to hyperoxia". J Biol Chem 272 (26): 16644–51. doi:10.1074/jbc.272.26.16644. PMID 9195979.http://www.jbc.org/cgi/content/full/272/26/16644.
^ de Haan J, Bladier C, Griffiths P, Kelner M, O'Shea R, Cheung N, Bronson R, Silvestro M, Wild S, Zheng S, Beart P, Hertzog P, Kola I (1998). "Mice with a homozygous null mutation for the most abundant glutathione peroxidase, Gpx1, show increased susceptibility to the oxidative stress-inducing agents paraquat and hydrogen peroxide". J Biol Chem 273 (35): 22528–36. doi:10.1074/jbc.273.35.22528. PMID 9712879.http://www.jbc.org/cgi/content/full/273/35/22528.
^ Sharma R, Yang Y, Sharma A, Awasthi S, Awasthi Y (2004). "Antioxidant role of glutathione S-transferases: protection against oxidant toxicity and regulation of stress-mediated apoptosis". Antioxid Redox Signal 6 (2): 289–300. doi:10.1089/152308604322899350. PMID 15025930.
^ Hayes J, Flanagan J, Jowsey I (2005). "Glutathione transferases". Annu Rev Pharmacol Toxicol 45: 51–88.doi:10.1146/annurev.pharmtox.45.120403.095857. PMID 15822171.
^ Christen Y (01 Feb 2000). "Oxidative stress and Alzheimer disease". Am J Clin Nutr 71 (2): 621S–629S. PMID 10681270.http://www.ajcn.org/cgi/content/full/71/2/621s.
^ Nunomura A, Castellani R, Zhu X, Moreira P, Perry G, Smith M (2006). "Involvement of oxidative stress in Alzheimer disease". J Neuropathol Exp Neurol 65 (7): 631–41. doi:10.1097/01.jnen.0000228136.58062.bf. PMID 16825950.
^ Wood-Kaczmar A, Gandhi S, Wood N (2006). "Understanding the molecular causes of Parkinson's disease". Trends Mol Med 12 (11): 521–8. doi:10.1016/j.molmed.2006.09.007. PMID 17027339.
^ Davì G, Falco A, Patrono C (2005). "Lipid peroxidation in diabetes mellitus". Antioxid Redox Signal 7 (1–2): 256–68.doi:10.1089/ars.2005.7.256. PMID 15650413.
^ Giugliano D, Ceriello A, Paolisso G (1996). "Oxidative stress and diabetic vascular complications". Diabetes Care 19 (3): 257–67.doi:10.2337/diacare.19.3.257. PMID 8742574.
^ Hitchon C, El-Gabalawy H (2004). "Oxidation in rheumatoid arthritis". Arthritis Res Ther 6 (6): 265–78. doi:10.1186/ar1447. PMID 15535839.
^ Cookson M, Shaw P (1999). "Oxidative stress and motor neurone disease". Brain Pathol 9 (1): 165–86. PMID 9989458.
^ Van Gaal L, Mertens I, De Block C (2006). "Mechanisms linking obesity with cardiovascular disease". Nature 444 (7121): 875–80.doi:10.1038/nature05487. PMID 17167476.
^ Aviram M (2000). "Review of human studies on oxidative damage and antioxidant protection related to cardiovascular diseases". Free Radic Res 33 Suppl: S85–97. PMID 11191279.
^ G. López-Lluch, N. Hunt, B. Jones, M. Zhu, H. Jamieson, S. Hilmer, M. V. Cascajo, J. Allard, D. K. Ingram, P. Navas, and R. de Cabo (2006). "Calorie restriction induces mitochondrial biogenesis and bioenergetic efficiency". Proc Natl Acad Sci USA 103 (6): 1768 – 1773.doi:10.1073/pnas.0510452103. PMID 16446459.
^ Larsen P (1993). "Aging and resistance to oxidative damage in Caenorhabditis elegans". Proc Natl Acad Sci USA 90 (19): 8905–9.doi:10.1073/pnas.90.19.8905. PMID 8415630.
^ Helfand S, Rogina B (2003). "Genetics of aging in the fruit fly, Drosophila melanogaster". Annu Rev Genet 37: 329–48.doi:10.1146/annurev.genet.37.040103.095211. PMID 14616064.
^ a b Sohal R, Mockett R, Orr W (2002). "Mechanisms of aging: an appraisal of the oxidative stress hypothesis". Free Radic Biol Med 33 (5): 575–86. doi:10.1016/S0891-5849(02)00886-9. PMID 12208343.
^ a b Sohal R (2002). "Role of oxidative stress and protein oxidation in the aging process". Free Radic Biol Med 33 (1): 37–44.doi:10.1016/S0891-5849(02)00856-0. PMID 12086680.
^ a b Rattan S (2006). "Theories of biological aging: genes, proteins, and free radicals". Free Radic Res 40 (12): 1230–8.doi:10.1080/10715760600911303. PMID 17090411.
^ Pérez, Viviana I.; Alex Bokov, Holly Van Remmen, James Mele, Qitao Ran, Yuji Ikeno, Arlan Richardson (2009). "Is the oxidative stress theory of aging dead?". Biochimica et Biophysica Acta (BBA) - General Subjects 1790 (10): 1005-1014. doi:10.1016/j.bbagen.2009.06.003.PMID 19524016. http://www.sciencedirect.com/science/article/B6T1W-4WH2KYY-3/2/3b2909c65fa19256ae2436cb8c143471. Retrieved 2009-09-14.
^ Thomas D (2004). "Vitamins in health and aging". Clin Geriatr Med 20 (2): 259–74. doi:10.1016/j.cger.2004.02.001. PMID 15182881.
^ Ward J (1998). "Should antioxidant vitamins be routinely recommended for older people?". Drugs Aging 12 (3): 169–75.doi:10.2165/00002512-199812030-00001. PMID 9534018.
^ Aggarwal BB, Shishodia S (2006). "Molecular targets of dietary agents for prevention and therapy of cancer". Biochem. Pharmacol. 71 (10): 1397–421. doi:10.1016/j.bcp.2006.02.009. PMID 16563357.
^ Reiter R (1995). "Oxidative processes and antioxidative defense mechanisms in the aging brain" (PDF). Faseb J 9 (7): 526–33. PMID 7737461. http://www.fasebj.org/cgi/reprint/9/7/526.pdf.
^ Warner D, Sheng H, Batinic-Haberle I (2004). "Oxidants, antioxidants and the ischemic brain". J Exp Biol 207 (Pt 18): 3221–31.doi:10.1242/jeb.01022. PMID 15299043. http://jeb.biologists.org/cgi/content/full/207/18/3221.
^ Wilson J, Gelb A (2002). "Free radicals, antioxidants, and neurologic injury: possible relationship to cerebral protection by anesthetics". J Neurosurg Anesthesiol 14 (1): 66–79. doi:10.1097/00008506-200201000-00014. PMID 11773828.
^ Lees K, Davalos A, Davis S, Diener H, Grotta J, Lyden P, Shuaib A, Ashwood T, Hardemark H, Wasiewski W, Emeribe U, Zivin J (2006). "Additional outcomes and subgroup analyses of NXY-059 for acute ischemic stroke in the SAINT I trial". Stroke 37 (12): 2970–8.doi:10.1161/01.STR.0000249410.91473.44. PMID 17068304.
^ Lees K, Zivin J, Ashwood T, Davalos A, Davis S, Diener H, Grotta J, Lyden P, Shuaib A, H�rdemark H, Wasiewski W (2006). "NXY-059 for acute ischemic stroke". N Engl J Med 354 (6): 588–600. doi:10.1056/NEJMoa052980. PMID 16467546.
^ Yamaguchi T, Sano K, Takakura K, Saito I, Shinohara Y, Asano T, Yasuhara H (01 Jan 1998). "Ebselen in acute ischemic stroke: a placebo-controlled, double-blind clinical trial. Ebselen Study Group". Stroke 29 (1): 12–7. PMID 9445321.http://stroke.ahajournals.org/cgi/content/full/29/1/12.
^ Di Matteo V, Esposito E (2003). "Biochemical and therapeutic effects of antioxidants in the treatment of Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis". Curr Drug Targets CNS Neurol Disord 2 (2): 95–107. doi:10.2174/1568007033482959. PMID 12769802.
^ Rao A, Balachandran B (2002). "Role of oxidative stress and antioxidants in neurodegenerative diseases". Nutr Neurosci 5 (5): 291–309.doi:10.1080/1028415021000033767. PMID 12385592.
^ Kopke RD, Jackson RL, Coleman JK, Liu J, Bielefeld EC, Balough BJ (2007). "NAC for noise: from the bench top to the clinic". Hear. Res.226 (1-2): 114–25. doi:10.1016/j.heares.2006.10.008. PMID 17184943.
^ a b c d Stanner SA, Hughes J, Kelly CN, Buttriss J (2004). "A review of the epidemiological evidence for the 'antioxidant hypothesis'". Public Health Nutr 7 (3): 407–22. doi:10.1079/PHN2003543. PMID 15153272.
^ Food, Nutrition, Physical Activity, and the Prevention of Cancer: a Global Perspective. World Cancer Research Fund (2007). ISBN 978-0-9722522-2-5.
^ a b c Shenkin A (2006). "The key role of micronutrients". Clin Nutr 25 (1): 1–13. doi:10.1016/j.clnu.2005.11.006. PMID 16376462.
^ Cherubini A, Vigna G, Zuliani G, Ruggiero C, Senin U, Fellin R (2005). "Role of antioxidants in atherosclerosis: epidemiological and clinical update". Curr Pharm Des 11 (16): 2017–32. doi:10.2174/1381612054065783. PMID 15974956.
^ Lotito SB, Frei B (2006). "Consumption of flavonoid-rich foods and increased plasma antioxidant capacity in humans: cause, consequence, or epiphenomenon?". Free Radic. Biol. Med. 41 (12): 1727–46. doi:10.1016/j.freeradbiomed.2006.04.033. PMID 17157175.
^ Bartlett H, Eperjesi F (2003). "Age-related macular degeneration and nutritional supplementation: a review of randomised controlled trials".Ophthalmic Physiol Opt 23 (5): 383–99. doi:10.1046/j.1475-1313.2003.00130.x. PMID 12950886.
^ Wintergerst E, Maggini S, Hornig D (2006). "Immune-enhancing role of vitamin C and zinc and effect on clinical conditions". Ann Nutr Metab50 (2): 85–94. doi:10.1159/000090495. PMID 16373990.
^ Wang J, Wen L, Huang Y, Chen Y, Ku M (2006). "Dual effects of antioxidants in neurodegeneration: direct neuroprotection against oxidative stress and indirect protection via suppression of glia-mediated inflammation". Curr Pharm Des 12 (27): 3521–33.doi:10.2174/138161206778343109. PMID 17017945.
^ Rimm EB, Stampfer MJ, Ascherio A, Giovannucci E, Colditz GA, Willett WC (1993). "Vitamin E consumption and the risk of coronary heart disease in men". N Engl J Med 328 (20): 1450–6. doi:10.1056/NEJM199305203282004. PMID 8479464.
^ Vivekananthan DP, Penn MS, Sapp SK, Hsu A, Topol EJ (2003). "Use of antioxidant vitamins for the prevention of cardiovascular disease: meta-analysis of randomised trials". Lancet 361 (9374): 2017–23. doi:10.1016/S0140-6736(03)13637-9. PMID 12814711.
^ Sesso HD, Buring JE, Christen WG, et al. (November 2008). "Vitamins E and C in the prevention of cardiovascular disease in men: the Physicians' Health Study II randomized controlled trial". JAMA 300 (18): 2123–33. doi:10.1001/jama.2008.600. PMID 18997197.http://jama.ama-assn.org/cgi/pmidlookup?view=long&pmid=18997197.
^ Lee IM, Cook NR, Gaziano JM, et al. (July 2005). "Vitamin E in the primary prevention of cardiovascular disease and cancer: the Women's Health Study: a randomized controlled trial". JAMA 294 (1): 56–65. doi:10.1001/jama.294.1.56. PMID 15998891. http://jama.ama-assn.org/cgi/pmidlookup?view=long&pmid=15998891.
^ Roberts LJ, Oates JA, Linton MF, et al. (2007). "The relationship between dose of vitamin E and suppression of oxidative stress in humans". Free Radic. Biol. Med. 43 (10): 1388–93. doi:10.1016/j.freeradbiomed.2007.06.019. PMID 17936185.
^ Bleys J, Miller E, Pastor-Barriuso R, Appel L, Guallar E (2006). "Vitamin-mineral supplementation and the progression of atherosclerosis: a meta-analysis of randomized controlled trials". Am. J. Clin. Nutr. 84 (4): 880–7; quiz 954–5. PMID 17023716.
^ Cook NR, Albert CM, Gaziano JM, et al. (2007). "A randomized factorial trial of vitamins C and E and beta carotene in the secondary prevention of cardiovascular events in women: results from the Women's Antioxidant Cardiovascular Study". Arch. Intern. Med. 167 (15): 1610–8. doi:10.1001/archinte.167.15.1610. PMID 17698683.
^ a b Hercberg S, Galan P, Preziosi P, Bertrais S, Mennen L, Malvy D, Roussel AM, Favier A, Briancon S (2004). "The SU.VI.MAX Study: a randomized, placebo-controlled trial of the health effects of antioxidant vitamins and minerals". Arch Intern Med 164 (21): 2335–42.doi:10.1001/archinte.164.21.2335. PMID 15557412.
^ Radimer K, Bindewald B, Hughes J, Ervin B, Swanson C, Picciano M (2004). "Dietary supplement use by US adults: data from the National Health and Nutrition Examination Survey, 1999–2000". Am J Epidemiol 160 (4): 339–49. doi:10.1093/aje/kwh207. PMID 15286019.http://aje.oxfordjournals.org/cgi/content/full/160/4/339.
^ Latruffe N, Delmas D, Jannin B, Cherkaoui Malki M, Passilly-Degrace P, Berlot JP (December 2002). "Molecular analysis on the chemopreventive properties of resveratrol, a plant polyphenol microcomponent". Int. J. Mol. Med. 10 (6): 755–60. PMID 12430003.
^ Woodside J, McCall D, McGartland C, Young I (2005). "Micronutrients: dietary intake v. supplement use". Proc Nutr Soc 64 (4): 543–53.doi:10.1079/PNS2005464. PMID 16313697.
^ a b c Hail N, Cortes M, Drake EN, Spallholz JE (July 2008). "Cancer chemoprevention: a radical perspective". Free Radic. Biol. Med. 45 (2): 97–110. doi:10.1016/j.freeradbiomed.2008.04.004. PMID 18454943.
^ Schulz TJ, Zarse K, Voigt A, Urban N, Birringer M, Ristow M (2007). "Glucose Restriction Extends Caenorhabditis elegans Life Span by Inducing Mitochondrial Respiration and Increasing Oxidative Stress". Cell Metab. 6 (4): 280–93. doi:10.1016/j.cmet.2007.08.011. PMID 17908557.
^ Barros MH, Bandy B, Tahara EB, Kowaltowski AJ (2004). "Higher respiratory activity decreases mitochondrial reactive oxygen release and increases life span in Saccharomyces cerevisiae". J. Biol. Chem. 279 (48): 49883–8. doi:10.1074/jbc.M408918200. PMID 15383542.
^ Green GA (December 2008). "Review: antioxidant supplements do not reduce all-cause mortality in primary or secondary prevention". Evid Based Med 13 (6): 177. doi:10.1136/ebm.13.6.177. PMID 19043035.
^ Dekkers J, van Doornen L, Kemper H (1996). "The role of antioxidant vitamins and enzymes in the prevention of exercise-induced muscle damage". Sports Med 21 (3): 213–38. doi:10.2165/00007256-199621030-00005. PMID 8776010.
^ Tiidus P (1998). "Radical species in inflammation and overtraining". Can J Physiol Pharmacol 76 (5): 533–8. doi:10.1139/cjpp-76-5-533.PMID 9839079. http://article.pubs.nrc-cnrc.gc.ca/ppv/RPViewDoc?issn=0008-4212&volume=76&issue=5&startPage=533.
^ Ristow M, Zarse K, Oberbach A, et al. (May 2009). "Antioxidants prevent health-promoting effects of physical exercise in humans". Proc. Natl. Acad. Sci. U.S.A.. doi:10.1073/pnas.0903485106. PMID 19433800.
^ Leeuwenburgh C, Fiebig R, Chandwaney R, Ji L (1994). "Aging and exercise training in skeletal muscle: responses of glutathione and antioxidant enzyme systems". Am J Physiol 267 (2 Pt 2): R439–45. PMID 8067452. http://ajpregu.physiology.org/cgi/reprint/267/2/R439.
^ Leeuwenburgh C, Heinecke J (2001). "Oxidative stress and antioxidants in exercise". Curr Med Chem 8 (7): 829–38. PMID 11375753.
^ Takanami Y, Iwane H, Kawai Y, Shimomitsu T (2000). "Vitamin E supplementation and endurance exercise: are there benefits?". Sports Med 29 (2): 73–83. doi:10.2165/00007256-200029020-00001. PMID 10701711.
^ Mastaloudis A, Traber M, Carstensen K, Widrick J (2006). "Antioxidants did not prevent muscle damage in response to an ultramarathon run". Med Sci Sports Exerc 38 (1): 72–80. doi:10.1249/01.mss.0000188579.36272.f6. PMID 16394956.
^ Peake J (2003). "Vitamin C: effects of exercise and requirements with training". Int J Sport Nutr Exerc Metab 13 (2): 125–51. PMID 12945825.
^ Jakeman P, Maxwell S (1993). "Effect of antioxidant vitamin supplementation on muscle function after eccentric exercise". Eur J Appl Physiol Occup Physiol 67 (5): 426–30. doi:10.1007/BF00376459. PMID 8299614.
^ Close G, Ashton T, Cable T, Doran D, Holloway C, McArdle F, MacLaren D (2006). "Ascorbic acid supplementation does not attenuate post-exercise muscle soreness following muscle-damaging exercise but may delay the recovery process". Br J Nutr 95 (5): 976–81.doi:10.1079/BJN20061732. PMID 16611389.
^ Hurrell R (01 Sep 2003). "Influence of vegetable protein sources on trace element and mineral bioavailability". J Nutr 133 (9): 2973S–7S.PMID 12949395. http://jn.nutrition.org/cgi/content/full/133/9/2973S.
^ Hunt J (01 Sep 2003). "Bioavailability of iron, zinc, and other trace minerals from vegetarian diets". Am J Clin Nutr 78 (3 Suppl): 633S–639S.PMID 12936958. http://www.ajcn.org/cgi/content/full/78/3/633S.
^ Gibson R, Perlas L, Hotz C (2006). "Improving the bioavailability of nutrients in plant foods at the household level". Proc Nutr Soc 65 (2): 160–8. doi:10.1079/PNS2006489. PMID 16672077.
^ a b Mosha T, Gaga H, Pace R, Laswai H, Mtebe K (1995). "Effect of blanching on the content of antinutritional factors in selected vegetables".Plant Foods Hum Nutr 47 (4): 361–7. doi:10.1007/BF01088275. PMID 8577655.
^ Sandberg A (2002). "Bioavailability of minerals in legumes". Br J Nutr 88 (Suppl 3): S281–5. doi:10.1079/BJN/2002718. PMID 12498628.
^ a b Beecher G (01 Oct 2003). "Overview of dietary flavonoids: nomenclature, occurrence and intake". J Nutr 133 (10): 3248S–3254S. PMID 14519822. http://jn.nutrition.org/cgi/content/full/133/10/3248S.
^ Prashar A, Locke I, Evans C (2006). "Cytotoxicity of clove (Syzygium aromaticum) oil and its major components to human skin cells". Cell Prolif 39 (4): 241–8. doi:10.1111/j.1365-2184.2006.00384.x. PMID 16872360.
^ Hornig D, Vuilleumier J, Hartmann D (1980). "Absorption of large, single, oral intakes of ascorbic acid". Int J Vitam Nutr Res 50 (3): 309–14.PMID 7429760.
^ Omenn G, Goodman G, Thornquist M, Balmes J, Cullen M, Glass A, Keogh J, Meyskens F, Valanis B, Williams J, Barnhart S, Cherniack M, Brodkin C, Hammar S (1996). "Risk factors for lung cancer and for intervention effects in CARET, the Beta-Carotene and Retinol Efficacy Trial". J Natl Cancer Inst 88 (21): 1550–9. doi:10.1093/jnci/88.21.1550. PMID 8901853.
^ Albanes D (01 Jun 1999). "Beta-carotene and lung cancer: a case study". Am J Clin Nutr 69 (6): 1345S–50S. PMID 10359235.http://www.ajcn.org/cgi/content/full/69/6/1345S.
^ a b Bjelakovic G, Nikolova D, Gluud L, Simonetti R, Gluud C (2007). "Mortality in Randomized Trials of Antioxidant Supplements for Primary and Secondary Prevention: Systematic Review and Meta-analysis". JAMA 297 (8): 842–57. doi:10.1001/jama.297.8.842. PMID 17327526.http://jama.ama-assn.org/cgi/content/abstract/297/8/842.
^ Study Citing Antioxidant Vitamin Risks Based On Flawed Methodology, Experts Argue News release from Oregon State Universitypublished on ScienceDaily, Accessed 19 April 2007
^ Bjelakovic G, Nikolova D, Gluud LL, Simonetti RG, Gluud C (2008). "Antioxidant supplements for prevention of mortality in healthy participants and patients with various diseases". Cochrane Database of Systematic Reviews (2): CD007176.doi:10.1002/14651858.CD007176.
^ Miller E, Pastor-Barriuso R, Dalal D, Riemersma R, Appel L, Guallar E (2005). "Meta-analysis: high-dosage vitamin E supplementation may increase all-cause mortality". Ann Intern Med 142 (1): 37–46. PMID 15537682.
^ Bjelakovic G, Nagorni A, Nikolova D, Simonetti R, Bjelakovic M, Gluud C (2006). "Meta-analysis: antioxidant supplements for primary and secondary prevention of colorectal adenoma". Aliment Pharmacol Ther 24 (2): 281–91. doi:10.1111/j.1365-2036.2006.02970.x. PMID 16842454.
^ Caraballoso M, Sacristan M, Serra C, Bonfill X (2003). "Drugs for preventing lung cancer in healthy people". Cochrane Database Syst Rev: CD002141. doi:10.1002/14651858.CD002141. PMID 12804424.
^ Bjelakovic G, Nagorni A, Nikolova D, Simonetti R, Bjelakovic M, Gluud C (2006). "Meta-analysis: antioxidant supplements for primary and secondary prevention of colorectal adenoma". Aliment. Pharmacol. Ther. 24 (2): 281–91. doi:10.1111/j.1365-2036.2006.02970.x. PMID 16842454.
^ Coulter I, Hardy M, Morton S, Hilton L, Tu W, Valentine D, Shekelle P (2006). "Antioxidants vitamin C and vitamin e for the prevention and treatment of cancer". Journal of general internal medicine: official journal of the Society for Research and Education in Primary Care Internal Medicine 21 (7): 735–44. PMID 16808775.
^ Schumacker P (2006). "Reactive oxygen species in cancer cells: Live by the sword, die by the sword". Cancer Cell 10 (3): 175–6.doi:10.1016/j.ccr.2006.08.015. PMID 16959608.
^ Seifried H, McDonald S, Anderson D, Greenwald P, Milner J (01 Aug 2003). "The antioxidant conundrum in cancer". Cancer Res 63 (15): 4295–8. PMID 12907593. http://cancerres.aacrjournals.org/cgi/content/full/63/15/4295.
^ Lawenda BD, Kelly KM, Ladas EJ, Sagar SM, Vickers A, Blumberg JB (June 2008). "Should supplemental antioxidant administration be avoided during chemotherapy and radiation therapy?". J. Natl. Cancer Inst. 100 (11): 773–83. doi:10.1093/jnci/djn148. PMID 18505970.
^ Block KI, Koch AC, Mead MN, Tothy PK, Newman RA, Gyllenhaal C (September 2008). "Impact of antioxidant supplementation on chemotherapeutic toxicity: a systematic review of the evidence from randomized controlled trials". Int. J. Cancer 123 (6): 1227–39.doi:10.1002/ijc.23754. PMID 18623084.
^ Block KI, Koch AC, Mead MN, Tothy PK, Newman RA, Gyllenhaal C (August 2007). "Impact of antioxidant supplementation on chemotherapeutic efficacy: a systematic review of the evidence from randomized controlled trials". Cancer Treat. Rev. 33 (5): 407–18.doi:10.1016/j.ctrv.2007.01.005. PMID 17367938.
^ Cao G, Alessio H, Cutler R (1993). "Oxygen-radical absorbance capacity assay for antioxidants". Free Radic Biol Med 14 (3): 303–11.doi:10.1016/0891-5849(93)90027-R. PMID 8458588.
^ Ou B, Hampsch-Woodill M, Prior R (2001). "Development and validation of an improved oxygen radical absorbance capacity assay using fluorescein as the fluorescent probe". J Agric Food Chem 49 (10): 4619–26. doi:10.1021/jf010586o. PMID 11599998.
^ Prior R, Wu X, Schaich K (2005). "Standardized methods for the determination of antioxidant capacity and phenolics in foods and dietary supplements". J Agric Food Chem 53 (10): 4290–302. doi:10.1021/jf0502698. PMID 15884874.
^ Honzel D, Carter SG, Redman KA, Schauss AG, Endres JR, Jensen GS (2008). "Comparison of chemical and cell-based antioxidant methods for evaluation of foods and natural products: generating multifaceted data by parallel testing using erythrocytes and polymorphonuclear cells.". J Agric Food Chem 56 (18): 8319–25. doi:10.1021/jf800401d. PMID 18717566.
^ Xianquan S, Shi J, Kakuda Y, Yueming J (2005). "Stability of lycopene during food processing and storage". J Med Food 8 (4): 413–22.doi:10.1089/jmf.2005.8.413. PMID 16379550.
^ Rodriguez-Amaya D (2003). "Food carotenoids: analysis, composition and alterations during storage and processing of foods". Forum Nutr56: 35–7. PMID 15806788.
^ Baublis A, Lu C, Clydesdale F, Decker E (01 Jun 2000). "Potential of wheat-based breakfast cereals as a source of dietary antioxidants". J Am Coll Nutr 19 (3 Suppl): 308S–311S. PMID 10875602. http://www.jacn.org/cgi/content/full/19/suppl_3/308S.
^ Rietveld A, Wiseman S (01 Oct 2003). "Antioxidant effects of tea: evidence from human clinical trials". J Nutr 133 (10): 3285S–3292S. PMID 14519827. http://jn.nutrition.org/cgi/content/full/133/10/3285S.
^ Maiani G, Periago Castón MJ, Catasta G, et al. (November 2008). "Carotenoids: Actual knowledge on food sources, intakes, stability and bioavailability and their protective role in humans". Mol Nutr Food Res 53. doi:10.1002/mnfr.200800053. PMID 19035552.
^ Henry C, Heppell N (2002). "Nutritional losses and gains during processing: future problems and issues". Proc Nutr Soc 61 (1): 145–8.doi:10.1079/PNS2001142. PMID 12002789. http://journals.cambridge.org/production/action/cjoGetFulltext?fulltextid=804076.
^ "Antioxidants and Cancer Prevention: Fact Sheet". National Cancer Institute.http://www.cancer.gov/cancertopics/factsheet/antioxidantsprevention. Retrieved 2007-02-27.
^ Ortega RM (2006). "Importance of functional foods in the Mediterranean diet". Public Health Nutr 9 (8A): 1136–40.doi:10.1017/S1368980007668530. PMID 17378953.
^ Goodrow EF, Wilson TA, Houde SC, et al. (October 2006). "Consumption of one egg per day increases serum lutein and zeaxanthin concentrations in older adults without altering serum lipid and lipoprotein cholesterol concentrations". J. Nutr. 136 (10): 2519–24. PMID 16988120.
^ Witschi A, Reddy S, Stofer B, Lauterburg B (1992). "The systemic availability of oral glutathione". Eur J Clin Pharmacol 43 (6): 667–9.doi:10.1007/BF02284971. PMID 1362956.
^ Flagg EW, Coates RJ, Eley JW, et al. (1994). "Dietary glutathione intake in humans and the relationship between intake and plasma total glutathione level". Nutr Cancer 21 (1): 33–46. PMID 8183721.
^ a b Dodd S, Dean O, Copolov DL, Malhi GS, Berk M (December 2008). "N-acetylcysteine for antioxidant therapy: pharmacology and clinical utility". Expert Opin Biol Ther 8 (12): 1955–62. doi:10.1517/14728220802517901. PMID 18990082.
^ van de Poll MC, Dejong CH, Soeters PB (June 2006). "Adequate range for sulfur-containing amino acids and biomarkers for their excess: lessons from enteral and parenteral nutrition". J. Nutr. 136 (6 Suppl): 1694S–1700S. PMID 16702341.
^ Wu G, Fang YZ, Yang S, Lupton JR, Turner ND (March 2004). "Glutathione metabolism and its implications for health". J. Nutr. 134 (3): 489–92. PMID 14988435.
^ Pan MH, Ho CT (November 2008). "Chemopreventive effects of natural dietary compounds on cancer development". Chem Soc Rev 37(11): 2558–74. doi:10.1039/b801558a. PMID 18949126.
^ Kader A, Zagory D, Kerbel E (1989). "Modified atmosphere packaging of fruits and vegetables". Crit Rev Food Sci Nutr 28 (1): 1–30. PMID 2647417.
^ Zallen E, Hitchcock M, Goertz G (1975). "Chilled food systems. Effects of chilled holding on quality of beef loaves". J Am Diet Assoc 67 (6): 552–7. PMID 1184900.
^ Iverson F (1995). "Phenolic antioxidants: Health Protection Branch studies on butylated hydroxyanisole". Cancer Lett 93 (1): 49–54.doi:10.1016/0304-3835(95)03787-W. PMID 7600543.
^ "E number index". UK food guide. http://www.ukfoodguide.net/enumeric.htm#antioxidants. Retrieved 2007-03-05.
^ Robards K, Kerr A, Patsalides E (1988). "Rancidity and its measurement in edible oils and snack foods. A review". Analyst 113 (2): 213–24.doi:10.1039/an9881300213. PMID 3288002.
^ Del Carlo M, Sacchetti G, Di Mattia C, Compagnone D, Mastrocola D, Liberatore L, Cichelli A (2004). "Contribution of the phenolic fraction to the antioxidant activity and oxidative stability of olive oil". J Agric Food Chem 52 (13): 4072–9. doi:10.1021/jf049806z. PMID 15212450.
^ CE Boozer, GS Hammond, CE Hamilton (1955) "Air Oxidation of Hydrocarbons. The Stoichiometry and Fate of Inhibitors in Benzene and Chlorobenzene". Journal of the American Chemical Society, 3233–3235
^ "Why use Antioxidants?". SpecialChem Adhesives. http://www.specialchem4adhesives.com/tc/antioxidants/index.aspx?id=. Retrieved 2007-02-27.
^ a b "Fuel antioxidants". Innospec Chemicals. http://www.innospecinc.com/americas/products/fuel_antitoxidants.cfm. Retrieved 2007-02-27.
Any contents taken from Wikipedia encyclopedia conform to Share—to copy, distribute and transmit the work, and to Remix—to adapt the work