Antioxidant

Antioxidant
Antioxidants are compounds that inhibit oxidation (usually occurring as autoxidation), a

chemical reaction that can produce free radicals. Autoxidation leads to degradation of
organic compounds, including living matter. Antioxidants are frequently added to industrial
products, such as polymers, fuels, and lubricants, to extend their usable lifetimes.[1] Foods
are also treated with antioxidants to forestall spoilage, in particular the rancidification of
oils and fats. In cells, antioxidants such as glutathione, mycothiol or bacillithiol, and
enzyme systems like superoxide dismutase, can prevent damage from oxidative stress.[2]
Structure of the antioxidant, glutathione
Known dietary antioxidants are vitamins A, C, and E, but the term antioxidant has also
been applied to numerous other dietary compounds that only have antioxidant properties
in vitro, with little evidence for antioxidant properties in vivo.[3] Dietary supplements
marketed as antioxidants have not been shown to maintain health or prevent disease in
humans.[3][4]
History
As part of their adaptation from marine life, terrestrial plants began producing non-marine
antioxidants such as ascorbic acid (vitamin C), polyphenols and tocopherols. The evolution
of angiosperm plants between 50 and 200 million years ago resulted in the development
of many antioxidant pigments – particularly during the Jurassic period – as chemical
defences against reactive oxygen species that are byproducts of photosynthesis.[5]
Originally, the term antioxidant specifically referred to a chemical that prevented the
consumption of oxygen. In the late 19th and early 20th centuries, extensive study
concentrated on the use of antioxidants in important industrial processes, such as the
prevention of metal corrosion, the vulcanization of rubber, and the polymerization of fuels
in the fouling of internal combustion engines.[6]
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.[7] 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 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.[8][9] 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.[10] 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.[11]
Uses in technology
Food preservatives
Antioxidants 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.[12]
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.[13] 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).[14][15]
Unsaturated fats can be highly susceptible to oxidation, causing rancidification.[16]

Oxidized lipids are often discolored and can impart unpleasant tastes and flavors. 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. Metals catalyse oxidation. Some fatty foods such as olive
oil are partially protected from oxidation by their natural content of antioxidants. Fatty
foods are sensitive to photooxidation,[17] which forms hydroperoxides by oxidizing
unsaturated fatty acids and ester.[18] Exposure to ultraviolet (UV) radiation can cause
direct photooxidation and decompose peroxides and carbonyl molecules. These
molecules undergo free radical chain reactions, but antioxidants inhibit them by preventing
the oxidation processes.[18]
Cosmetics preservatives
Antioxidant stabilizers are also added to fat-based cosmetics such as lipstick and
moisturizers to prevent rancidity.[19] Antioxidants in cosmetic products prevent oxidation of
active ingredients and lipid content. For example, phenolic antioxidants such as stilbenes,
flavonoids, and hydroxycinnamic acid strongly absorb UV radiation due to the presence of
chromophores. They reduce oxidative stress from sun exposure by absorbing UV light.[20]
Industrial uses
Substituted phenols and derivatives of

phenylenediamine are common
antioxidants used to inhibit gum
formation in gasoline (petrol).
Antioxidants may be added to industrial products, such as stabilizers in fuels and additives
in lubricants, to prevent oxidation and polymerization that leads to the formation of
engine-fouling residues.[21]
Fuel
Components[22] Applications[22]
additive
N,N'-di-2-butyl-1,4- Turbine oils, transformer oils, hydraulic

AO-22
phenylenediamine fluids, waxes, and greases
N,N'-di-2-butyl-1,4-
AO-24 Low-temperature oils
phenylenediamine
2,6-di-tert-butyl-4-methylphenol Turbine oils, transformer oils, hydraulic

AO-29
(BHT) fluids, waxes, greases, and gasolines
Jet fuels and gasolines, including

AO-30 2,4-dimethyl-6-tert-butylphenol
aviation gasolines
Jet fuels and gasolines, including

AO-31 2,4-dimethyl-6-tert-butylphenol
aviation gasolines
2,4-dimethyl-6-tert-butylphenol and Jet fuels and gasolines, including

AO-32
2,6-di-tert-butyl-4-methylphenol aviation gasolines
Jet fuels and gasolines, widely

AO-37 2,6-di-tert-butylphenol
approved for aviation fuels
Antioxidant polymer stabilizers are widely used to prevent the degradation of polymers,
such as rubbers, plastics and adhesives, that causes a loss of strength and flexibility in
these materials.[23] Polymers containing double bonds in their main chains, such as natural
rubber and polybutadiene, are especially susceptible to oxidation and ozonolysis. They
can be protected by antiozonants. Oxidation can be accelerated by UV radiation in natural
sunlight to cause photo-oxidation. Various specialised light stabilisers, such as HALS may
be added to plastics to prevent this. Synthetic phenolic[24] and aminic[25] antioxidants are
increasingly being identified as potential human and environmental health hazards.
Environmental and health hazards

Synthetic phenolic antioxidants (SPAs) and aminic antioxidants have potential human and
environmental health hazards. SPAs are common in indoor dust, small air particles,
sediment, sewage, river water and wastewater.[26] They are synthesized from phenolic
compounds and include 2,6-di-tert-butyl-4-methylphenol (BHT), 2,6-di-tert-butyl-p-
benzoquinone (BHT-Q), 2,4-di-tert-butyl-phenol (DBP) and 3-tert-butyl-4-
hydroxyanisole (BHA). BHT can cause hepatotoxicity and damage to the endocrine system
and may increase tumor development rates due to 1,1-dimethylhydrazine.[27] BHT-Q can
cause DNA damage and mismatches[28] through the cleavage process, generating
superoxide radicals.[26] DBP is toxic to marine life if exposed long-term. Phenolic
antioxidants have low biodegradability, but they do not have severe toxicity toward aquatic
organisms at low concentrations. Another type of antioxidant, diphenylamine (DPA), is
commonly used in the production of commercial, industrial lubricants and rubber products
and it also acts as a supplement for automotive engine oils.[29]
Oxidative challenge in
biology
The structure of the antioxidant

vitamin ascorbic acid (vitamin C)
The vast majority of complex life on Earth requires oxygen for its metabolism, but this
same oxygen is a highly reactive element that can damage living organisms.[2][30]
Organisms contain chemicals and enzymes that minimize this oxidative damage without
interfering with the beneficial effect of oxygen.[31][32] In general, antioxidant systems either
prevent these reactive species from being formed, or remove them, thus minimizing their
damage.[30][31] Reactive oxygen species can have useful cellular functions, such as redox
signaling. Thus, ideally, antioxidant systems do not remove oxidants entirely, but maintain
them at some optimum concentration.[33]
Reactive oxygen species produced in cells include hydrogen peroxide (H2O2),

hypochlorous acid (HClO), and free radicals such as the hydroxyl radical (·OH) and the
superoxide anion (O2−).[34] 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.[35]
These oxidants can damage cells by starting chemical chain reactions such as lipid
peroxidation, or by oxidizing DNA or proteins.[31] Damage to DNA can cause mutations
and possibly cancer, if not reversed by DNA repair mechanisms,[36][37] while damage to
proteins causes enzyme inhibition, denaturation and protein degradation.[38]
The use of oxygen as part of the process for generating metabolic energy produces
reactive oxygen species.[39] In this process, the superoxide anion is produced as a by-
product of several steps in the electron transport chain.[40] 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.[41]
Peroxide is also produced from the oxidation of reduced flavoproteins, such as complex
I.[42] However, although these enzymes can produce oxidants, the relative importance of
the electron transfer chain to other processes that generate peroxide is unclear.[43][44] In
plants, algae, and cyanobacteria, reactive oxygen species are also produced during
photosynthesis,[45] particularly under conditions of high light intensity.[46] This effect is
partly offset by the involvement of carotenoids in photoinhibition, and in algae and
cyanobacteria, by large amount of iodide and selenium,[47] which involves these
antioxidants reacting with over-reduced forms of the photosynthetic reaction centres to
prevent the production of reactive oxygen species.[48][49]
Examples of bioactive antioxidant
compounds
Physiological antioxidants are classified into two broad divisions, depending on whether
they are soluble in water (hydrophilic) or in lipids (lipophilic). 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.[31] These compounds
may be synthesized in the body or obtained from the diet.[32] 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 systemically distributed (see table below). Some antioxidants are only found in a few
organisms, and can be pathogens or virulence factors.[50]
The interactions between these different antioxidants may be synergistic and

interdependent.[51][52] The action of one antioxidant may therefore depend on the proper
function of other members of the antioxidant system.[32] 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.[32]
Some compounds contribute to antioxidant defense by chelating transition metals and

preventing them from catalyzing the production of free radicals in the cell. The ability to
sequester iron for iron-binding proteins, such as transferrin and ferritin, is one such
function.[44] Selenium and zinc are commonly referred to as antioxidant minerals, but
these chemical elements have no antioxidant action themselves, but rather are required
for the activity of antioxidant enzymes, such as glutathione reductase and superoxide
dismutase. (See also selenium in biology and zinc in biology.)
Concentration in human Concentration in liver tissue
Antioxidant Solubility
serum (μM) (μmol/kg)
Ascorbic acid
Water 50–60[53] 260 (human)[54]
(vitamin C)
Glutathione Water 4[55] 6,400 (human)[54]
Lipoic acid Water 0.1–0.7[56] 4–5 (rat)[57]
Uric acid Water 200–400[58] 1,600 (human)[54]
β-carotene: 0.5–1[59]
5 (human, total
Carotenes Lipid [60]
retinol (vitamin A): 1–3 carotenoids)[61]
α-Tocopherol
Lipid 10–40[60] 50 (human)[54]
(vitamin E)
Ubiquinol
Lipid 5[62] 200 (human)[63]
(coenzyme Q)
Uric acid
Uric acid has the highest concentration of any blood antioxidant[58] and provides over half
of the total antioxidant capacity of human serum.[64] Uric acid's antioxidant activities are
also complex, given that it does not react with some oxidants, such as superoxide, but
does act against peroxynitrite,[65] peroxides, and hypochlorous acid.[66] Concerns over
elevated UA's contribution to gout must be considered one of many risk factors.[67] By
itself, UA-related risk of gout at high levels (415–530 μmol/L) is only 0.5% per year with
an increase to 4.5% per year at UA supersaturation levels (535+ μmol/L).[68] Many of
these aforementioned studies determined UA's antioxidant actions within normal
physiological levels,[69][65] and some found antioxidant activity at levels as high as 285
μmol/L.[70]
Vitamin C
Ascorbic acid or vitamin C, an oxidation-reduction (redox) catalyst found in both animals
and plants,[71] can reduce, and thereby neutralize, reactive oxygen species such as
hydrogen peroxide.[71][72] In addition to its direct antioxidant effects, ascorbic acid is also a
substrate for the redox enzyme ascorbate peroxidase, a function that is used in stress
resistance in plants.[73] Ascorbic acid is present at high levels in all parts of plants and can
reach concentrations of 20 millimolar in chloroplasts.[74]
Glutathione
The free radical mechanism of lipid

peroxidation
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.[75] 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.[76] In some organisms
glutathione is replaced by other thiols, such as by mycothiol in the Actinomycetes,
bacillithiol in some gram-positive bacteria,[77][78] or by trypanothione in the
Kinetoplastids.[79][80]
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.[81][82] Of these, α-tocopherol
has been most studied as it has the highest bioavailability, with the body preferentially
absorbing and metabolising this form.[83]
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.[81][84] 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.[85] 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.[86] 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,[87][88] 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.[89][90] The functions of the other forms of vitamin E are even less
well understood, although γ-tocopherol is a nucleophile that may react with electrophilic
mutagens,[83] and tocotrienols may be important in protecting neurons from damage.[91]
Pro-oxidant activities
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;[92] however, it will also reduce metal ions such as iron and copper[93] that
generate free radicals through the Fenton reaction.[35][94] While ascorbic acid is effective
antioxidant, it can also oxidatively change the flavor and color of food. With the presence
of transition metals, there are low concentrations of ascorbic acid that can act as a radical
scavenger in the Fenton reaction.[93]
2 Fe3+ + Ascorbate → 2 Fe2+ + Dehydroascorbate
2 Fe2+ + 2 H2O2 → 2 Fe3+ + 2 OH· + 2 OH−
The relative importance of the antioxidant and pro-oxidant activities of antioxidants is an

area of current research, but vitamin C, which exerts its effects as a vitamin by oxidizing
polypeptides, appears to have a mostly antioxidant action in the human body.[94]
Enzyme systems
Enzymatic pathway for detoxification of reactive oxygen species
As with the chemical antioxidants, cells are protected against oxidative stress by an
interacting network of antioxidant enzymes.[30][31] 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.[95]
Superoxide dismutase, catalase, and

peroxiredoxins
Superoxide dismutases (SODs) are a class of closely related enzymes that catalyze the
breakdown of the superoxide anion into oxygen and hydrogen peroxide.[96][97] SOD
enzymes are present in almost all aerobic cells and in extracellular fluids.[98] 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.[97] There also exists a third
form of SOD in extracellular fluids, which contains copper and zinc in its active sites.[99]
The mitochondrial isozyme seems to be the most biologically important of these three,
since mice lacking this enzyme die soon after birth.[100] 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).[95][101] 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.[102]
Catalases are enzymes that catalyse the conversion of hydrogen peroxide to water and
oxygen, using either an iron or manganese cofactor.[103][104] This protein is localized to
peroxisomes in most eukaryotic cells.[105] 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.[106] Despite its apparent
importance in hydrogen peroxide removal, humans with genetic deficiency of catalase —
"acatalasemia" — or mice genetically engineered to lack catalase completely, experience
few ill effects.[107][108]
Decameric structure of AhpC, a
bacterial 2-cysteine peroxiredoxin
from Salmonella typhimurium[109]
Peroxiredoxins are peroxidases that catalyze the reduction of hydrogen peroxide, organic
hydroperoxides, as well as peroxynitrite.[110] They are divided into three classes: typical 2-
cysteine peroxiredoxins; atypical 2-cysteine peroxiredoxins; and 1-cysteine
peroxiredoxins.[111] 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
acid by the peroxide substrate.[112] Over-oxidation of this cysteine residue in
peroxiredoxins inactivates these enzymes, but this can be reversed by the action of
sulfiredoxin.[113] Peroxiredoxins seem to be important in antioxidant metabolism, as mice
lacking peroxiredoxin 1 or 2 have shortened lifespans and develop hemolytic anaemia,
while plants use peroxiredoxins to remove hydrogen peroxide generated in
chloroplasts.[114][115][116]
Thioredoxin and glutathione systems

The thioredoxin system contains the 12-kDa protein thioredoxin and its companion
thioredoxin reductase.[117] Proteins related to thioredoxin are present in all sequenced
organisms. Plants, such as Arabidopsis thaliana, have a particularly great diversity of
isoforms.[118] 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.[119] After being oxidized, the active thioredoxin is regenerated by the action of
thioredoxin reductase, using NADPH as an electron donor.[120]
The glutathione system includes glutathione, glutathione reductase, glutathione
peroxidases, and glutathione S-transferases.[76] This system is found in animals, plants
and microorganisms.[76][121] 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.[122] 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,[123] but they are hypersensitive to induced oxidative
stress.[124] In addition, the glutathione S-transferases show high activity with lipid
peroxides.[125] These enzymes are at particularly high levels in the liver and also serve in
detoxification metabolism.[126]
Health research
Relation to diet
The dietary antioxidant vitamins A, C, and E are essential and required in specific daily
amounts to prevent diseases.[3][127][128] Polyphenols, which have antioxidant properties in
vitro due to their free hydroxy groups,[129] are extensively metabolized by catechol-O-
methyltransferase which methylates free hydroxyl groups, and thereby prevents them
from acting as antioxidants in vivo.[130][131]
Interactions
Common pharmaceuticals (and supplements) with antioxidant properties may interfere
with the efficacy of certain anticancer medication and radiation therapy.[132]
Pharmaceuticals and supplements that have antioxidant properties suppress the formation
of free radicals by inhibiting oxidation processes. Radiation therapy induce oxidative stress
that damages essential components of cancer cells, such as proteins, nucleic acids, and
lipids that comprise cell membranes.[133]
Adverse effects
Structure of the metal chelator

phytic 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.[134] Examples are oxalic acid, tannins and phytic acid, which are high in plant-
based diets.[135] 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. However, germination, soaking, or microbial
fermentation are all household strategies that reduce the phytate and polyphenol content
of unrefined cereal. Increases in Fe, Zn and Ca absorption have been reported in adults
fed dephytinized cereals compared with cereals containing their native phytate.[136]
Foods Reducing acid present
Cocoa bean and chocolate, spinach, turnip and rhubarb[137] Oxalic acid
Whole grains, maize, legumes[138] Phytic acid
Tea, beans, cabbage[137][139] Tannins

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.[140] Subsequent studies confirmed these adverse effects.[141] These harmful
effects may also be seen in non-smokers, as one 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.[142] No health risk was seen when all the randomized controlled studies were
examined together, but an increase in mortality was detected when only high-quality and
low-bias risk trials were examined separately.[143] As the majority of these low-bias trials
dealt with either elderly people, or people with disease, these results may not apply to the
general population.[144] This meta-analysis was later repeated and extended by the same
authors, confirming the previous results.[143] These two publications are consistent with
some previous meta-analyses that also suggested that vitamin E supplementation
increased mortality,[145] and that antioxidant supplements increased the risk of colon
cancer.[146] Beta-carotene may also increase lung cancer.[146][147] 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.[127][148][142]
Exercise and muscle soreness

A 2017 review showed that taking antioxidant dietary supplements before or after exercise
is unlikely to produce a noticeable reduction in muscle soreness after a person
exercises.[149]
Levels in food
Fruits and vegetables are

good sources of
antioxidant vitamins C and
E.
Antioxidant vitamins are found in vegetables, fruits, eggs, legumes and nuts. Vitamins A,
C, and E can be destroyed by long-term storage or prolonged cooking.[150] 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.[151] Processed food
contains fewer antioxidant vitamins than fresh and uncooked foods, as preparation
exposes food to heat and oxygen.[152]
Foods containing high levels of antioxidant

Antioxidant vitamins
vitamins[139][153][154]
Vitamin C (ascorbic acid) Fresh or frozen fruits and vegetables
Vitamin E (tocopherols,
Vegetable oils, nuts, and seeds
tocotrienols)
Carotenoids (carotenes as
Fruit, vegetables and eggs
provitamin A)
Other antioxidants are not obtained from the diet, but instead are made in the body. For
example, ubiquinol (coenzyme Q) is poorly absorbed from the gut and is made through the
mevalonate pathway.[63] 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 intake has little effect on the concentration of
glutathione in the body.[155][156] Although large amounts of sulfur-containing amino acids
such as acetylcysteine can increase glutathione,[157] no evidence exists that eating high
levels of these glutathione precursors is beneficial for healthy adults.[158]
Measurement and invalidation of

ORAC
Measurement of polyphenol and carotenoid content in food is not a straightforward
process, as antioxidants collectively are a diverse group of compounds with different
reactivities to various reactive oxygen species. In food science analyses in vitro, the
oxygen radical absorbance capacity (ORAC) was once an industry standard for estimating
antioxidant strength of whole foods, juices and food additives, mainly from the presence
of polyphenols.[159][160] Earlier measurements and ratings by the United States Department
of Agriculture were withdrawn in 2012 as biologically irrelevant to human health, referring
to an absence of physiological evidence for polyphenols having antioxidant properties in
vivo.[161] Consequently, the ORAC method, derived only from in vitro experiments, is no
longer considered relevant to human diets or biology, as of 2010.[161]
Alternative in vitro measurements of antioxidant content in foods – also based on the

presence of polyphenols – include the Folin-Ciocalteu reagent, and the Trolox equivalent
antioxidant capacity assay.[162]
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Further reading
Halliwell B, Gutteridge JM (2015). Free

Radicals in Biology and Medicine
(5th ed.). Oxford University Press.
ISBN 978-0-19-856869-8.
Lane N (2003). Oxygen: The Molecule
That Made the World. Oxford University
Press. ISBN 978-0-19-860783-0.
Pokorny J, Yanishlieva N, Gordon MH
(2001). Antioxidants in Food: Practical
Applications. CRC Press. ISBN 978-0-
8493-1222-9.
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Antioxidants are compounds that inhibit oxidation (usually occurring as autoxidation), a

Structure of the antioxidant, glutathione

Unsaturated fats can be highly susceptible to oxidation, causing rancidification.[16]

Substituted phenols and derivatives of

N,N'-di-2-butyl-1,4- Turbine oils, transformer oils, hydraulic

2,6-di-tert-butyl-4-methylphenol Turbine oils, transformer oils, hydraulic

Jet fuels and gasolines, including

Jet fuels and gasolines, including

2,4-dimethyl-6-tert-butylphenol and Jet fuels and gasolines, including

Jet fuels and gasolines, widely

Environmental and health hazards

The structure of the antioxidant

Reactive oxygen species produced in cells include hydrogen peroxide (H2O2),

The interactions between these different antioxidants may be synergistic and

Some compounds contribute to antioxidant defense by chelating transition metals and

Glutathione Water 4[55] 6,400 (human)[54]

Lipoic acid Water 0.1–0.7[56] 4–5 (rat)[57]

Uric acid Water 200–400[58] 1,600 (human)[54]

The free radical mechanism of lipid

2 Fe3+ + Ascorbate → 2 Fe2+ + Dehydroascorbate

2 Fe2+ + 2 H2O2 → 2 Fe3+ + 2 OH· + 2 OH−

The relative importance of the antioxidant and pro-oxidant activities of antioxidants is an

Enzymatic pathway for detoxification of reactive oxygen species

Superoxide dismutase, catalase, and

Thioredoxin and glutathione systems

Structure of the metal chelator

Foods Reducing acid present

Whole grains, maize, legumes[138] Phytic acid

Tea, beans, cabbage[137][139] Tannins

Exercise and muscle soreness

Fruits and vegetables are

Foods containing high levels of antioxidant

Vitamin C (ascorbic acid) Fresh or frozen fruits and vegetables

Measurement and invalidation of

Alternative in vitro measurements of antioxidant content in foods – also based on the

1 Klemchuk Peter P (2000)

Halliwell B, Gutteridge JM (2015). Free

Media related to Antioxidants at

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