Antioxidants are molecules that inhibit the oxidation of other molecules. Oxidation is a chemical reaction that can produce free radicals, causing chain reactions that can damage cells. Antioxidants such as thiols or ascorbic acid (vitamin C) terminate this chain reaction. The term "antioxidants" is primarily used for two different groups of substances: industrial chemicals added to products to prevent oxidation, and natural chemicals found in foods and tissues that are said to have beneficial health effects.
To balance the oxidative state, plants and animals maintain an overlapping system of antioxidant complexes, such as glutathione and enzymes (eg, catalase and superoxide dismutase) produced internally or dietary antioxidants: vitamin A, vitamin C, and vitamin E.
Antioxidant dietary supplements do not improve health or are effective in preventing disease. These include beta-carotene supplements, vitamin A, and vitamin E which have no effect on mortality or cancer risk. Supplementation with selenium or vitamin E does not reduce the risk of cardiovascular disease.
Industrial antioxidants have various uses, including preservatives in foods and cosmetics, and oxidation inhibitors in fuel.
Video Antioxidant
Health effects
Relationship to diet
Although the level of certain antioxidant vitamins in the diet is necessary for good health, there is a great debate about whether antioxidant-rich foods or supplements have anti-disease activity. In addition, if they are truly beneficial, it is not known which antioxidants are needed from the diet and how much outside of normal dietary intake. Some authors have denied the hypothesis that antioxidant vitamins can prevent chronic illness, while others maintain such possibility as unproven and misdirected right from the start.
Polyphenols, which often have in vitro antioxidant properties, are not always antioxidants in vivo because of their extensive metabolism. In many polyphenols, catechol groups act as electron acceptor and are therefore responsible for antioxidant activity. However, this catechol group undergoes extensive metabolism after taking up the human body, for example by catechol-O-methyl transferase, and is therefore no longer capable of acting as an electron acceptor. Many polyphenols may have non-antioxidant roles in minute concentrations that affect cell-to-cell signaling, receptor sensitivity, inflammatory enzyme activity or gene regulation.
Although dietary antioxidants have been studied for potential effects on neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis, this study can not be concluded.
Candidate drug
Tirilazad is a steroid derivative of antioxidants that inhibit lipid peroxidation that is believed to play a key role in neuronal death in stroke and head injury. This shows activity in animal models of stroke, but human trials show no effect on mortality or other outcomes in subarachnoid hemorrhage and worsening outcomes in ischemic stroke.
Likewise, the antioxidant designed by NXY-059 demonstrates the efficacy of animal models, but fails to correct stroke results in clinical trials. In November 2014, other antioxidants are being studied as potential neuroprotectants.
Common drugs (and supplements) with antioxidant properties can interfere with the effectiveness of certain anticancer drugs and radiation.
A systematic review of 2016 examines antioxidant drugs, such as allopurinol and acetylcysteine, in addition to treatment for schizophrenia. Evidence is not enough to determine the benefits and there are potential side effects.
Physical training
A 2000 review reported that vitamin E supplementation did not provide benefits to physical performance among athletes. Antioxidant supplementation may reduce the benefits of cardiovascular exercise.
Adverse effects
Relatively strong reducing acids can have antinutrient effects by binding mineral minerals such as iron and zinc in the digestive tract and preventing them from being absorbed. Important examples are oxalic acid, tannin and phytic acid, which are high in the plant-based diet. Iron and calcium deficiency is not uncommon in diets in developing countries where fewer meat is eaten and there is a high consumption of phytic acid from nuts and unleavened whole wheat bread.
Nonpolar antioxidants such as eugenol - the main component of clove oil - have a toxicity limit that can be exceeded by the misuse of pure essential oils. Toxicities associated with high doses of water-soluble antioxidants such as ascorbic acid are underestimated, as these compounds can be excreted rapidly in the urine. More seriously, the very high doses of some antioxidants may have long-term harmful effects. Beta-carotene and Retinol Efficacy Trial (CARET) trials in lung cancer patients found that smokers supplemented with beta-carotene and vitamin A had increased lung cancer rates. Further studies confirm this adverse effect.
This harmful effect can also be seen in non-smokers, because the latest meta-analysis including data from about 230,000 patients suggests that supplements? -carotene, vitamin A or vitamin E are associated with increased mortality but do not see any significant effect of vitamin C. No health risk is seen when all randomized controlled trials are examined together, but mortality increases are detected when only high-quality risk trials and low-risk bias examined separately. Since the majority of these low-bias trials are associated with elderly people, or people with illness, these results may not apply to the general population. This meta-analysis is then repeated and extended by the same author, with a new analysis published by Cochrane Collaboration; This analysis confirms the previous results. Both of these publications are consistent with some previous meta-analyzes that also suggest that vitamin E supplements increase mortality, and antioxidant supplements increase the risk of colon cancer. Beta-carotene can also increase lung cancer. Overall, a large number of clinical trials conducted on antioxidant supplements show that neither of these products have any health effect, nor that they cause a small increase in mortality in an elderly or vulnerable population.
While antioxidant supplementation is widely used in an effort to prevent the development of cancer, antioxidants can interfere with cancer treatment, because the environment of cancer cells causes high levels of oxidative stress, making these cells more susceptible to further oxidative stress caused by treatment. As a result, by reducing redox stress in cancer cells, antioxidant supplements (and medications) can decrease the effectiveness of radiotherapy and chemotherapy. On the other hand, other reviews suggest that antioxidants may reduce side effects or improve survival time.
Maps Antioxidant
Oxidative challenge in biology
The paradox in metabolism is that, while most of the complex life on Earth requires oxygen for its existence, oxygen is a highly reactive molecule that destroys living organisms by producing reactive oxygen species. As a result, the organism contains a complex network of antioxidant metabolites and enzymes that work together to prevent oxidative damage to cellular components such as DNA, proteins, and lipids. In general, the antioxidant system prevents this reactive species from forming, or removing it before it can damage the vital components of the cell. However, reactive oxygen species also have useful cellular functions, such as redox signaling. Thus, the function of the antioxidant system is not to remove oxidants completely, but rather to keep them at an optimum level.
Reactive oxygen species produced in cells include hydrogen peroxide (H 2 O 2 ), hypochlorite acid (HClO), and free radicals such as hydroxyl radicals (Ã, Â · OH) and superoxide anions (O 2 - ). The hydroxyl radicals are highly unstable and will react quickly and are not specific to most biological molecules. This species is produced from hydrogen peroxide in a metal-catalyzed redox reaction such as a Fenton reaction. These oxidants can damage cells by initiating chemical chain reactions such as lipid peroxidation, or by oxidising DNA or proteins. DNA damage can cause mutations and possible cancer, if not inversely with DNA repair mechanisms, while damage to proteins causes inhibition of enzymes, denaturation and degradation of proteins.
The use of oxygen as part of the process to produce metabolic energy produces reactive oxygen species. In this process, superoxide anions are produced as a by-product of several steps in the electron transport chain. Most important is the reduction of coenzyme Q in complex III, because highly reactive free radicals are formed as intermediates (Q Ã, Â · - ). This unstable middle can cause "leakage" of electrons, when electrons jump directly into oxygen and form superoxide anions instead of moving through normal circuits of electron-controlled transport chain reaction. Peroxides are also produced from the oxidation of flavoprotein reduction, such as complex I. However, although this enzyme can produce oxidants, the relative importance of the electron transfer chain to other processes that produce peroxide is unclear. In plants, algae, and cyanobacteria, reactive oxygen species are also produced during photosynthesis, especially under conditions of high light intensity. This effect is partially offset by carotenoid involvement in photographs, and in algae and cyanobacteria, by large quantities of iodide and selenium, which involve these antioxidants reacting with excessive forms of photosynthetic reaction centers to prevent the production of reactive oxygen species..
Metabolites
Antioxidants are classified into two broad divisions, depending on whether they are water soluble (hydrophilic) or lipid (lipophilic). In general, water-soluble antioxidants react with oxidants in the cell cytosol and blood plasma, while fat-soluble antioxidants protect the cell membranes from lipid peroxidation. These compounds can be synthesized in the body or obtained from the diet. Different antioxidants are present in various concentrations in body fluids and tissues, with some like glutathione or ubiquinone mostly present in cells, while others such as uric acid are more evenly distributed (see table below). Some antioxidants are found only in some organisms and these compounds can be important in pathogens and can be a virulence factor.
The relative importance and interaction between these different antioxidants is a very complex question, with various metabolites and enzyme systems having synergistic and interdependent effects on one another. Therefore, the action of one antioxidant depends on the proper functioning of other members of the antioxidant system. The amount of protection provided by an antioxidant will also depend on its concentration, its reactivity to certain species of reactive oxygen being considered, and the antioxidant status that it interacts with.
Some compounds contribute to the defense of antioxidants by chelating transition metals and prevent them from catalyzing the production of free radicals in cells. Most important is the ability to confiscate iron, which is a function of iron-binding proteins such as transferrin and ferritin. Selenium and zinc are often referred to as antioxidant nutrients , but these chemical elements do not have their own antioxidant action and are otherwise required for the activity of some antioxidant enzymes, as discussed below.
Uric acid
Uric acid is the highest concentration antioxidant in human blood. Uric acid (UA) is an oxypurine antioxidant produced from xanthine by xanthine oxidase enzyme, and is a product between purine metabolism. In almost all terrestrial animals, urate oxidase further catalyzes the oxidation of uric acid into allantoin, but in humans and the highest primates, the urinary oxidase gene does not work, so UA does not break down further. The reason for the evolution of the loss of urate conversion to allantoin remains a topic of active speculation. The antioxidant effects of uric acid have led researchers to suggest these mutations are beneficial to primates and early humans. The study of altitude acclimatization supports the hypothesis that the veins act as antioxidants by reducing oxidative stress caused by high altitude hypoxia.
Uric acid has the highest concentration of any antioxidant blood and provides more than half of the total capacity of human serum antioxidants. The antioxidant activity of uric acid is also complex, given that it does not react with some oxidants, such as superoxide, but acts against peroxinitrics, peroxides, and hypochlorite acids. Concerns about the increased contribution of UA to gout should be regarded as one of many risk factors. By itself, UA risk associated with UA at high levels (415-530? Mol/L) is only 0.5% per year with an increase of up to 4.5% per year at UA supersaturation level (535 μm/L). Many of the studies mentioned above that determine UA's antioxidant action in normal physiological levels, and some find antioxidant activity at levels as high as 285? Mol/L.
Vitamin C
Ascorbic acid or "vitamin C" is a monosaccharide oxidation reduction catalyst (redox) found in animals and plants. As one of the enzymes necessary to make ascorbic acid lost due to mutations during the evolution of primates, humans must obtain it from food; therefore it is a vitamin. Most other animals can produce these compounds in their bodies and do not need them in their diet. Ascorbic acid is required for the conversion of procollagen into collagen by oxidizing proline residues to hydroxyproline. In other cells, it is maintained in a form that is reduced by reaction with glutathione, which can be catalyzed by the protein disulfide isomerase and glutaredoxins. Ascorbic acid is a redox catalyst that can reduce, and thus neutralize, reactive oxygen species such as hydrogen peroxide. In addition to the direct antioxidant effect, ascorbic acid is also a substrate for the ascorbic peroxidase redox enzyme, a very important function in plant stress resistance. Ascorbic acid is present at high levels in all parts of the plant and can reach a concentration of 20 millimolar in chloroplasts.
Glutathione
Glutathione is a cysteine-containing peptide found in most aerobic life forms. It is not needed in the diet and is instead synthesized in the cell from its constituent amino acids. Glutathione has antioxidant properties because the thiol group in its cysteine ​​part is a reducing agent and can be oxidized and reduced reversibly. In cells, glutathione is preserved in reduced form by the enzyme glutathione reductase and in turn reduces metabolites and other enzyme systems, such as ascorbate in the glutathione-ascorbate cycle, glutathione peroxidases and glutaredoxins, and reacts directly with oxidants. Because of its high concentration and its central role in maintaining the cell redox state, glutathione is one of the most important cellular antioxidants. In some organisms glutathione is replaced by other thiols, such as by mycothiol in Actinomycetes, bacillithiol in some Gram-positive bacteria, or by trypanothione in Kinetoplastids.
Melatonin
Melatonin is a powerful antioxidant. Melatonin readily crosses cell membranes and blood-brain barriers. Unlike other antioxidants, melatonin does not undergo a redox cycle, which is the ability of molecules to experience repeated reduction and oxidation. Redox cycling allows other antioxidants (such as vitamin C) to act as a pro-oxidant and increase the formation of free radicals. Melatonin, once oxidized, can not be reduced to its original form as it forms some stable final product after reacting with free radicals. Therefore, it has been termed as a terminal antioxidant (or suicide).
Vitamin E
Vitamin E is the collective name for a set of eight tocopherols and tocotrienols, which is a fat-soluble vitamin with antioxidant properties. Of this amount ,? -tocopherol has been most studied for having the highest bioavailability, with a special body absorbing and metabolizing this form.
It has been claimed that the form of tocopherol is the most important antioxidant that is soluble in fat, and protects the membrane from oxidation by reacting with the lipid radicals produced in the lipid peroxidation chain reaction. This eliminates free radical intermediates and prevents the propagation reaction from continuing. This reaction produces oxidation - a tracokoksil radical that can be recycled back to the reduced active form by reduction by other antioxidants, such as ascorbate, retinol or ubiquinol. This is in line with the findings that show that? -tocopherol, but not a water-soluble antioxidant, efficiently protects glutathione peroxidase 4 (GPX4) -the cellular deficiency of cell death. GPx4 is the only known enzyme that efficiently reduces the lipid-hydroperoxides in the biological membrane.
However, the role and importance of various forms of vitamin E today is not clear, and even has suggested that the most important function of? α-tocopherol is as a signal molecule, with these molecules having no important role in antioxidant metabolism. The other form functions of vitamin E are even poorly understood, though? -tocopherol is a nucleophile that can react with electrophilic mutagens, and tocotrienol may be important in protecting neurons from damage.
Pro-oxidant activity
Antioxidants that reduce agents can also act as pro-oxidants. For example, vitamin C has antioxidant activity when reducing oxidizing agents such as hydrogen peroxide; however, it also reduces the metal ions that produce free radicals through the Fenton reaction.
- 2 Fe 3 Askorbat -> 2 Fe 2 Dehydroascorbate
- 2 Fe 2 2 H 2 O 2 -> 2 Fe 3 2 OH < b> Ã, Â · 2 OH -
The relative importance of antioxidant activity and antioxidant pro-oxidants is the current field of research, but vitamin C, which gives its effect as a vitamin by oxidizing polypeptides, appears to have most of the antioxidant action in the human body. However, less data is available for other dietary antioxidants, such as vitamin E, or polyphenols. Likewise, the pathogenesis of a disease involving hyperuricemia may involve the direct and indirect pro-oxidant properties of uric acid.
That is, paradoxically, agents that are usually considered antioxidants can act as conditional pro-oxidants and actually increase oxidative stress. In addition to ascorbate, medically important conditional pro-oxidants include uric acid and sulfhydryl amino acids such as homocysteine. Typically, this involves several series-transition metals such as copper or iron as a catalyst. The potential role of the pro-oxidant role of uric acid in (eg) atherosclerosis and ischemic stroke is considered above. Another example is the role of postosis homocysteine ​​â € <â €
Some antioxidant supplements can increase the disease and increase mortality in humans under certain conditions. Hypothetically, free radicals induce an endogenous response that protects against exogenous radicals (and possibly other toxic compounds). Free radicals can increase life span. This increase can be prevented by antioxidants, providing direct evidence that toxic radicals may in effect provide the effect of prolonging life and promoting health.
Enzyme System
Like chemical antioxidants, cells are protected against oxidative stress by antioxidant enzyme interaction tissue. Here, superoxides released by processes such as oxidative phosphorylation are first converted to hydrogen peroxide and then subtracted again into water. This detoxification pathway is the result of several enzymes, with superoxide dismutase catalyzing the first step and then catalyzing and various peroxidases removing hydrogen peroxide. As with antioxidant metabolites, the contribution of these enzymes to antioxidant defenses can be difficult to separate from one another, but the generation of transgenic mice lacking an antioxidant enzyme alone can be informative.
Superoxide dismutase, catalase, and peroxiredoxin
Superoxide dismutase (SOD) is a class of closely related enzymes that catalyze the breakdown of superoxide anions into oxygen and hydrogen peroxide. SOD enzymes are present in almost all aerobic and extracellular fluid cells. Superoxide dismutase enzymes contain metal ion cofactors which, depending on the isozymes, may be copper, zinc, manganese or iron. In humans, SOD copper/zinc is present in the cytosol, while manganese SOD is present in the mitochondria. There is also a third form of SOD in extracellular fluid, which contains copper and zinc at its active site. The mitochondrial issozymes appear to be the most biologically important of these three, since the mice lacking this enzyme die soon after birth. In contrast, mice lacking copper/zinc SOD (Sod1) may be alive but have many pathologies and reduced lifespan (see article on superoxide), whereas mice without extracellular SOD have minimal defects (sensitive to hyperoxia). In plants, isozyme SOD is present in the cytosol and mitochondria, with iron SOD found in chloroplasts that do not exist from vertebrates and yeasts.
The catalyst is an enzyme that catalyzes the conversion of hydrogen peroxide into water and oxygen, using iron or manganese cofactors. This protein is localized to peroxisomes in most eukaryotic cells. Catalase is an unusual enzyme because, although hydrogen peroxide is the only substrate, it follows the ping-pong mechanism. Here, the cofactor is oxidized by one molecule of hydrogen peroxide and then regenerated by transferring the oxygen attached to the second molecule of the substrate. Although very important in the removal of hydrogen peroxide, humans with a catalase-genetic deficiency - "acatalasemia" - or genetically engineered mice for less catalase completely, suffer some adverse effects.
Peroxiredoxin is a peroxidase that catalyzes the reduction of hydrogen peroxide, organic hydroperoxides, and peroxinitrite. They are divided into three classes: typical 2-cysteine ​​peroxiredoxins; atoxic 2-cysteine ​​peroxyloxin; and peroxhedoxin 1-cysteine. These enzymes share the same basic catalytic mechanism, in which the active-redox cysteine ​​(peroxidic cysteine) in the active site is oxidized to sulfenic acid by the peroxide substrate. The oxidation of these cysteine ​​residues in peroxiredoxin inactivates these enzymes, but this can be reversed by the action of sulfiredoxin. Peroxiredoxin appears to be important in antioxidant metabolism, because rats lacking peroxiredoxin 1 or 2 have shorter life spans and hemolytic anemia, while plants use peroxiredoxins to remove the hydrogen peroxide produced in chloroplasts.
Thioredoxin and glutathione systems
The thioredoxin system contains 12-kDa thaceedoxin protein and its companion thioredoxin reductase. Proteins associated with thioredoxin are present in all sequential organisms. Plants, such as Arabidopsis thaliana, have a very large diversity of isoforms. The thioredoxin active site consists of two neighboring cysteines, as part of a highly sustainable CXXC motif, which can form a cycle between the active form of dithiol (reduced) and oxidized disulfide form. In active circumstances, thioredoxin acts as an efficient reducing agent, scavenging reactive oxygen species and retaining other proteins in a reduced state. After oxidation, the active thioredoxin is regenerated by the action of thioredoxin reductase, using NADPH as an electron donor.
Glutathione systems include glutathione, glutathione reductase, glutathione peroxidases, and glutathione S -transferases. This system is found in animals, plants and microorganisms. Glutathione peroxidase is an enzyme containing four selenium that catalyzes the breakdown of organic hydrogen peroxide and hydroperoxide. There are at least four different isozyme glutathione peroxidases in animals. Glutathione peroxidase 1 is the most abundant and highly efficient hydrogen peroxide scavenger, while glutathione peroxidase 4 is most active with lipid hydroperoxide. Surprisingly, glutathione peroxidase 1 can be discarded, because enzyme-deficient mice have a normal life span, but they are hypersensitive to induced oxidative stress. In addition, glutathione S -transferases showed high activity with lipid peroxide. These enzymes are at a very high level in the liver and also function in detoxification metabolism.
Oxidative stress in disease
Oxidative stress is thought to contribute to the development of various diseases including Alzheimer's disease, Parkinson's disease, diabetes-induced pathology, rheumatoid arthritis, and neurodegeneration in motor neurone disease. In many cases, it is unclear whether the oxidant triggers the disease, or if they are produced as a secondary consequence of the disease and from general tissue damage; One case in which this relationship is well understood is the role of oxidative stress in cardiovascular disease. Here, the oxidation of low density lipoprotein (LDL) appears to trigger the process of atherogenesis, which results in atherosclerosis, and ultimately cardiovascular disease.
Oxidative damage to DNA can cause cancer. Some antioxidant enzymes such as superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione S-transferase etc. protect the DNA from oxidative stress. It has been proposed that polymorphism in these enzymes is linked to DNA damage and then individual risks of cancer susceptibility.
Low-calorie diets extend median and maximum life in many animals. This effect may involve reduction of oxidative stress. Although there is some evidence to support the role of oxidative stress in aging in model organisms such as Drosophila melanogaster and Caenorhabditis elegans, the evidence in mammals is less clear. Indeed, a 2009 review of trials in mice concluded that almost all antioxidant system manipulations had no effect on aging.
Use in technology
Food preservatives
Antioxidants are used as food additives to help prevent food damage. Exposure to oxygen and sunlight are two major factors in food oxidation, so food is preserved by storing in the dark and sealing it in a container or even coating it in wax, like a cucumber. However, since oxygen is also important for plant respiration, storing plant material under anaerobic conditions produces unpleasant taste and unattractive colors. As a result, fresh fruit and vegetable packaging contains ~ 8% oxygen atmosphere. Antioxidants are a very important preservative class because, unlike bacterial or fungal decay, oxidation reactions still occur relatively quickly in frozen or refrigerated foods. These preservatives include natural antioxidants such as ascorbic acid (AA, E300) and tocopherol (E306), as well as synthetic antioxidants such as propyl gallate (PG, E310), tertiary butylhydroquinone (TBHQ), butylated hydroxytoluene (BHA, E320) and butylated hydroxytoluene , E321).
The molecules most commonly attacked by oxidation are unsaturated fats; oxidation causes them to become rancid. Because oxidized lipids often change color and usually have unpleasant flavors such as metallic or sulfur flavor, it is important to avoid oxidation in foods rich in fat. Thus, these foods are seldom preserved by drying; instead, they are preserved by smoking, marinating or fermenting. Even fewer fatty foods such as fruits are sprayed with sulfur antioxidants before air drying. Oxidation is often catalyzed by metals, which is why fat like butter should not be wrapped with aluminum foil or stored in a metal container. Some fatty foods such as olive oil are partially protected from oxidation by natural antioxidant content, but remain sensitive to photooxidation. Antioxidant preservatives are also added to fat-based cosmetics such as lipsticks and moisturizers to prevent rancidity.
Industrial use
Antioxidants are often added to industrial products. Common uses are as stabilizers in fuels and lubricants to prevent oxidation, and in gasoline to prevent polymerization leading to the formation of machine-contamination residues. By 2014, the global market for natural and synthetic antioxidants is US $ 2.25 billion with estimated growth to $ 3.25 billion by 2020.
They are widely used to prevent oxidative degradation of polymers such as rubber, plastics and adhesives that cause loss of strength and flexibility in these materials. Polymers containing double bonds in their main chains, such as natural rubber and polybutadiene, are particularly susceptible to oxidation and ozonolysis. They can be protected by antiozonants. The solid polymer product begins to crack on open surfaces when the material is degraded and the chain breaks. Cracked modes vary between oxygen and ozone attacks, the first causing a "crazy paving" effect, while ozone attacks produce deeper cracks aligned with the right angle to the tensile strain in the product. Oxidation and UV degradation are also often associated, especially since UV radiation creates free radicals by bond damage. Free radicals then react with oxygen to produce peroxy radicals that cause further damage, often in chain reactions. Other polymers susceptible to oxidation include polypropylene and polyethylene. The former is more sensitive because of the presence of secondary carbon atoms in each repeating unit. Attacks occur at this point because the free radicals formed are more stable than those formed on primary carbon atoms. Oxidation of polyethylene tends to occur in weak chains in chains, such as branch points in low density polyethylene.
Level in food
Vitamin antioxidants are found in vegetables, fruits, eggs, beans and nuts. Vitamins A, C, and E can be destroyed with long-term storage or old cooking. The effects of cooking and food processing are complex, as this process can also increase the bioavailability of antioxidants, such as some carotenoids in vegetables. Processed foods contain fewer antioxidant vitamins than fresh and un-cooked foods, as preparations put food into heat and oxygen.
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 intestine and made via the mevalonate pathway. Another example is glutathione, which is made of amino acids. Because glutathione in the intestine is broken down into free cysteine, glycine and glutamic acid before being absorbed, even a large oral intake has little effect on glutathione concentrations in the body. Although large amounts of sulfur-containing amino acids such as acetylcysteine ​​can improve glutathione, there is no evidence that consuming high-grade glutathione precursors is beneficial for healthy adults.
Measurement and cancellation ORAC
Measurement of antioxidant content in food is not a direct process, because antioxidants are collectively a diverse group of compounds with different reactivity for various species of reactive oxygen. In food science, the oxygen radical absorption capacity (ORAC) has once become the industry standard for the full antioxidant power of food, juice and food additives. However, the US Department of Agriculture withdraws this rank in 2012 because it is biologically invalid, stating that there is no existing in vivo physiological evidence available to support the theory or role of free radicals for digested phytochemicals, especially for polyphenols. As a result, the ORAC method, derived only from in vitro experiments , is no longer considered relevant to human or biological diets.
Alternative in vitro measurement of antioxidant content in foods including Folin-Ciocalteu reagents, and trolox is equivalent to antioxidant capacity.
History
As part of their adaptation of marine life, terrestrial plants begin to produce non-marine antioxidants such as ascorbic acid (vitamin C), polyphenols and tocopherol. The evolution of angiosperms between 50 and 200 million years ago resulted in the development of many antioxidant pigments - particularly during the Jurassic period - as a chemical defense against reactive oxygen species which is a byproduct of photosynthesis. Initially, the term antioxidant specifically refers to chemicals that prevent oxygen consumption. In the late 19th and early 20th centuries, extensive research concentrated on the use of antioxidants in important industrial processes, such as prevention of metal corrosion, vulcanization of rubber, and polymerization of fuels in the impurity of internal combustion engines.
Initial research on the role of antioxidants in biology is focused on its use in preventing the oxidation of unsaturated fats, which is the cause of rancidity. Antioxidant activity can be measured simply by placing the fat in a sealed container with oxygen and measuring the level of oxygen consumption. However, it is the identification of vitamins A, C, and E as antioxidants that revolutionize the field and lead to the embodiment of the importance of antioxidants in the biochemistry of living organisms. An antioxidant action mechanism that may be first explored when it is known that a substance with anti-oxidative activity is probably one that is itself readily oxidized. Research on how vitamin E prevents lipid peroxidation processes leads to the identification of antioxidants as reducing agents that prevent oxidation reactions, often by scavenging reactive oxygen species before they can damage cells.
See also
- Forensic engineering
- Mitohormesis - Hormesis
- Nootropic
- Degradation polymers
References
Further reading
External links
- Media related to Antioxidants in Wikimedia Commons
Source of the article : Wikipedia
0 Comments