Vitamin C, also known as ascorbic acid and L-ascorbic acid, is a vitamin found in food and used as a dietary supplement. The disease scurvy is prevented and treated with vitamin C containing foods or dietary supplements. Evidence does not support use in the general population for the prevention of the common cold. There is, however, some evidence that regular use may shorten the length of colds. It is unclear if vitamin C supplementation affects the risk of cancer, heart disease, or dementia. It may be taken by mouth or by injection. Vitamin C is generally well tolerated. Large doses may cause gastrointestinal discomfort, headache, trouble sleeping, and flushing of the skin. Normal doses are safe during pregnancy. Drugs.com |url=https://www.drugs.com/pregnancy/ascorbic-acid.html |website=www.drugs.com |accessdate=30 December 2016 |deadurl=no |archiveurl=https://web.archive.org/web/20161231075819/https://www.drugs.com/pregnancy/ascorbic-acid.html |archivedate=December 31, 2016 |df=mdy-all}} Vitamin C is an essential nutrient involved in the repair of tissue. Foods containing vitamin C include citrus fruits, broccoli, Brussels sprouts, raw bell peppers, and strawberries. Prolonged storage or cooking may reduce vitamin C content in foods. Summary needed --> Vitamin C was discovered in 1912, isolated in 1928, and first made in 1933. It is on the World Health Organization's List of Essential Medicines, the most effective and safe medicines needed in a health system. Vitamin C is available as a generic medication and over the counter. In 2015, the wholesale cost in the developing world was about 0.003 to 0.007 USD per tablet. In some countries, ascorbic acid may be added to foods such as breakfast cereal.
Biological significanceVitamin C is an essential nutrient for certain animals including humans. Vitamin C describes several vitamers that have vitamin C activity in animals, including ascorbic acid and its salts, and some oxidized forms of the molecule like dehydroascorbic acid. Ascorbate and ascorbic acid – represented by the collective term, vitamin C – are both naturally present in the body when either of these is introduced into cells, since the forms interconvert according to pH. Vitamin C is a cofactor in at least eight enzymatic reactions, including several collagen synthesis reactions that, when dysfunctional, cause the most severe symptoms of scurvy. In animals, these reactions are especially important in wound-healing and in preventing bleeding from capillaries. The biological role of vitamin C is to act as a reducing agent, donating electrons to various enzymatic and non-enzymatic reactions. The one- and two-electron oxidized forms of vitamin C, semidehydroascorbic acid and dehydroascorbic acid, respectively, can be reduced in the body by glutathione and NADPH-dependent enzymatic mechanisms. The presence of glutathione in cells and extracellular fluids helps maintain ascorbate in a reduced state. In humans, adequate vitamin C intake results from consumption of raw plant foods or fortified foods, providing antioxidant functions from its ability to donate electrons, and so lessen oxidative stress. Vitamin C is an enzyme cofactor for the biosynthesis of many biochemicals required for normal metabolism. It is a substrate for ascorbate peroxidase in plants. This enzyme utilizes ascorbate to neutralize toxic hydrogen peroxide (H2O2) by converting it to water (H2O). Vitamin C is required for a range of essential metabolic reactions in all animals and plants. Although it is made internally by almost all vertebrates, there are exceptions which do not synthesize it, including humans, tarsiers, and monkeys. All vertabrate species that do not make vitamin C require it in the diet.
DeficiencyScurvy is an avitaminosis resulting from lack of vitamin C, since without this vitamin, collagen made by the body is too unstable to perform its function. Scurvy leads to the formation of brown spots on the skin, spongy gums, and bleeding from all mucous membranes. The spots are most abundant on the thighs and legs, and a person with the ailment looks pale, feels depressed, and is partially immobilized. In advanced scurvy there are open, suppurating wounds and loss of teeth and, eventually, death. The human body can store only a certain amount of vitamin C, and so the body stores are depleted if fresh supplies are not consumed. The time frame for onset of symptoms of scurvy in unstressed adults on a completely vitamin C free diet, however, may range from one month to more than six months, depending on previous loading of vitamin C. Notable human dietary studies of experimentally induced scurvy have been conducted on conscientious objectors during WWII in Britain and on Iowa state prisoners in the late 1960s to the 1980s. These studies both found that all obvious symptoms of scurvy previously induced by an experimental scorbutic diet with extremely low vitamin C content could be completely reversed by additional vitamin C supplementation of only 10 mg a day. In these experiments, there was no clinical difference noted between men given 70 mg vitamin C per day (which produced blood level of vitamin C of about 0.55 mg/dl, about 1/3 of tissue saturation levels) and those given 10 mg per day. Men in the prison study developed the first signs of scurvy about 4 weeks after starting the vitamin C-free diet, whereas in the British study, six to eight months were required, possibly due to the pre-loading of this group with a 70 mg/day supplement for six weeks before the scorbutic diet was fed. Men in both studies on a diet devoid, or nearly devoid, of vitamin C had blood levels of vitamin C too low to be accurately measured when they developed signs of scurvy, and in the Iowa study, at this time were estimated (by labeled vitamin C dilution) to have a body pool of less than 300 mg, with daily turnover of only 2.5 mg/day, implying an instantaneous half-life of 83 days by this time (elimination constant of 4 months).
UsesVitamin C has a definitive role in treating scurvy, which is a disease caused by vitamin C deficiency. Beyond that, a role for vitamin C as prevention or treatment for various diseases is disputed, with reviews reporting conflicting results. A 2012 Cochrane review reported no effect of vitamin C supplementation on overall mortality. It is on the World Health Organization's List of Essential Medicines as one of the most effective and safe medicines needed in a health system.
ScurvyThe disease scurvy is caused by vitamin C deficiency and can be prevented and treated with vitamin C containing foods or dietary supplements. It takes at least a month of little to no vitamin C before symptoms occur. Early symptoms are malaise and lethargy, progressing to shortness of breath, bone pain, bleeding gums, susceptibility to bruising, poor wound healing, and finally fever, convulsions and eventual death. Until quite late in the disease the damage is reversible, as with vitamin C repletion, healthy collagen replaces the defective collagen. Treatment can be orally or by intramuscular or intravenous injection. Scurvy was known to Hippocrates in the classical era. The disease was shown to be prevented by citrus fruit in an early controlled trial by a Royal Navy surgeon, James Lind, in 1747, and from 1796 lemon juice was issued to all Royal Navy crewmen.
Common coldadvocated taking vitamin C for the common cold in a 1970 book.]] The effect of vitamin C on the common cold has been extensively researched. The earliest publication of a controlled clinical trial appears to be from 1945. Researchers continued to work on this question, but research interest and public interest spiked after Linus Pauling, two-time awardee of the Nobel Prize (Chemistry Prize, 1954, Peace Prize 1962), started publishing research on the topic and also published a book "Vitamin C and the Common Cold" in 1970. A revised and expanded edition "Vitamin C, the Common Cold and the Flu" was published in 1976. The most recent meta-analysis, a Cochrane Review published in 2013, with inclusion criteria limited to trials that called for at least 200 mg/day, concluded that vitamin C taken on a regular basis was not effective in prevention of the common cold. Limiting inclusion to trials that called for at least 1000 mg/day made no difference. However, taking vitamin C on a regular basis did reduce average duration by 8% in adults and 14% in children, and also reduced severity of colds. A subset of trials reported that supplementation reduced the incidence of colds by half in marathon runners, skiers, or soldiers in subarctic conditions. Another subset of trials looked at therapeutic use, meaning that vitamin C was not started unless the people started to feel the beginnings of a cold. In these, vitamin C did not impact duration or severity. An earlier review stated that vitamin C did not prevent colds, did reduce duration, did not reduce severity. The authors of the Cochrane review concluded that "...given the consistent effect of vitamin C on the duration and severity of colds in the regular supplementation studies, and the low cost and safety, it may be worthwhile for common cold patients to test on an individual basis whether therapeutic vitamin C is beneficial for them."
CancerA 2014 review concluded: "Currently, the use of high-dose intravenous vitamin C an anticancer agent cannot be recommended outside of a clinical trial." A 2013 Cochrane review found no evidence that vitamin C supplementation reduces the risk of lung cancer in healthy or high risk (smokers and asbestos-exposed) people. A 2014 meta-analysis found that vitamin C intake might protect against lung cancer risk. A second meta-analysis found no effect on the risk of prostate cancer. Two meta-analyses evaluated the effect of vitamin C supplementation on the risk of colorectal cancer. One found a weak association between vitamin C consumption and reduced risk, and the other found no effect of supplementation. A 2011 meta-analysis failed to find support for the prevention of breast cancer with vitamin C supplementation, but a second study concluded that vitamin C may be associated with increased survival in those already diagnosed.
Cardiovascular diseaseA 2013 meta-analysis found no evidence that vitamin C supplementation reduces the risk of myocardial infarction, stroke, cardiovascular mortality, or all-cause mortality. However, a second analysis found an inverse relationship between circulating vitamin C levels or dietary vitamin C and the risk of stroke. A meta-analysis of 44 clinical trials has shown a significant positive effect of vitamin C on endothelial function when taken at doses greater than 500 mg per day. The endothelium is a layer of cells that line the interior surface of blood vessels. Endothelial dysfunction is implicated in many aspects of vascular diseases. The researchers noted that the effect of vitamin C supplementation appeared to be dependent on health status, with stronger effects in those at higher cardiovascular disease risk.
Rheumatoid arthritisA 2010 review found no role for vitamin C supplementation in the treatment of rheumatoid arthritis.
DementiaStudies examining the effects of vitamin C intake on the risk of Alzheimer's disease have reached conflicting conclusions. Maintaining a healthy dietary intake is probably more important than supplementation for achieving any potential benefit.
CataractVitamin C supplementation does not prevent or slow the progression of age-related cataract.
Side effectsMore than two to three grams may cause indigestion, particularly when taken on an empty stomach. However, taking vitamin C in the form of sodium ascorbate and calcium ascorbate may minimize this effect. Other symptoms reported for large dose include nausea, abdominal cramps and diarrhea. These effects are attributed to the osmotic effect of unabsorbed vitamin C passing through the intestine. In theory, high vitamin C intake may cause excessive absorption of iron. A summary of reviews of supplementation in healthy subjects did not report this problem, but left as untested the possibility that individuals with hereditary hemochromatosis might by adversely affected. There is a longstanding belief among the mainstream medical community that vitamin C increases risk of kidney stones. Reports of kidney stone formation associated with excess ascorbic acid intake appear to be limited to individuals with renal disease. Reviews state that data from epidemiological studies do not support an association between excess ascorbic acid intake and kidney stone formation in apparently healthy individuals, although one large, multi-year trial did report a nearly two-fold increase in kidney stones in men who regularly consumed a vitamin C supplement. Vitamin C is a water-soluble vitamin, with dietary excesses not absorbed, and excesses in the blood rapidly excreted in the urine, so it exhibits remarkably low acute toxicity.
Recommended levelsRecommendations for vitamin C intake by adults have been set by various national agencies:
- 40 milligrams per day: India National Institute of Nutrition, Hyderabad
- 45 milligrams per day or 300 milligrams per week: the World Health Organization
- 80 milligrams per day: the European Commission Council on nutrition labeling
- 90 mg/day (males) and 75 mg/day (females): Health Canada 2007
- 90 mg/day (males) and 75 mg/day (females): United States National Academy of Sciences.
- 100 milligrams per day: Japan National Institute of Health and Nutrition. Dietary Reference Intakes for Japanese 2010: Water-Soluble Vitamins Journal of Nutritional Science and Vitaminology 2013(59):S67-S82.
- 110 mg/day (males) and 95 mg/day (females): European Food Safety Authority
Food labelingFor U.S. food and dietary supplement labeling purposes the amount in a serving is expressed as a percent of Daily Value (%DV). For vitamin C labeling purposes 100% of the Daily Value was 60 mg, but as of May 27, 2016 it was revised to 90 mg to bring it into agreement with the RDA. A table of the old and new adult Daily Values is provided at Reference Daily Intake. Food and supplement companies have until January 1, 2020 to comply with the change. "Changes to the Nutrition Facts Panel - Compliance Date" European Union regulations require that labels declare energy, protein, fat, saturated fat, carbohydrates, sugars, and salt. Voluntary nutrients may be shown if present in significant amounts. Instead of Daily Values, amounts are shown as percent of Reference Intakes (RIs). For vitamin C, 100% RI was set at 80 mg in 2011. REGULATION (EU) No 1169/2011 OF THE EUROPEAN PARLIAMENT AND OF THE COUNCIL Official Journal of the European Union. page 304/61. (2009).
Sourcess are a particularly rich source of vitamin C]] The richest natural sources are fruits and vegetables. Vitamin C is the most widely taken nutritional supplement and is available in a variety of forms, including tablets, drink mixes, and in capsules. Vitamin C is absorbed by the intestines using a sodium-ion dependent channel. It is transported through the intestine via both glucose-sensitive and glucose-insensitive mechanisms. The presence of large quantities of sugar either in the intestines or in the blood can slow absorption.
Plant sourcesWhile plants are generally a good source of vitamin C, the amount in foods of plant origin depends on the precise variety of the plant, soil condition, climate where it grew, length of time since it was picked, storage conditions, and method of preparation. The following table is approximate and shows the relative abundance in different raw plant sources. As some plants were analyzed fresh while others were dried (thus, artifactually increasing concentration of individual constituents like vitamin C), the data are subject to potential variation and difficulties for comparison. The amount is given in milligrams per 100 grams of fruit or vegetable:
Animal sourcesAnimal-sourced foods do not provide much vitamin C, and what there is, is destroyed by the heat of cooking. For example, raw chicken liver contains 17.9 mg/100 g, but fried, the content is reduced to 2.7 mg/100 g. Chicken eggs contain no vitamin C, raw or cooked. USDA Food Composition Databases United States Department of Agriculture, Agricultural Research Service. Release 28 (2015). Vitamin C is present in human breast milk at 5.0 mg/100 g and 6.1 mg/100 g in one tested sample of infant formula, but cow's milk contains only 1.0 gm/ 100 g.
Food preparationVitamin C chemically decomposes under certain conditions, many of which may occur during the cooking of food. Vitamin C concentrations in various food substances decrease with time in proportion to the temperature at which they are stored and cooking can reduce the Vitamin C content of vegetables by around 60% possibly partly due to increased enzymatic destruction as it may be more significant at sub-boiling temperatures. Longer cooking times also add to this effect, as will copper food vessels, which catalyse the decomposition. Another cause of vitamin C being lost from food is leaching, where the water-soluble vitamin dissolves into the cooking water, which is later poured away and not consumed. However, vitamin C does not leach in all vegetables at the same rate; research shows broccoli seems to retain more than any other. Research has also shown that freshly cut fruits do not lose significant nutrients when stored in the refrigerator for a few days.
SupplementsVitamin C dietary supplements are available as tablets, capsules, drink mix packets, in multi-vitamin/mineral formulations, in antioxidant formulations, and as crystalline powder. Vitamin C is also added to some fruit juices and juice drinks. Tablet and capsule content ranges from 25 mg to 1500 mg per serving. The most commonly used supplement compounds are ascorbic acid, sodium ascorbate and calcium ascorbate. Vitamin C molecules can also be bound to the fatty acid palmitate, creating ascorbyl palmitate, or else incorporated into liposomes.
Food fortificationIn 2014, the Canadian Food Inspection Agency evaluated the effect of fortification of foods with ascorbate in the guidance document, Foods to Which Vitamins, Mineral Nutrients and Amino Acids May or Must be Added. Voluntary and mandatory fortification was described for various classes of foods. Among foods classified for mandatory fortification were fruit-flavored drinks, mixes, and concentrates, foods for a low-energy diet, meal replacement products, and evaporated milk.
Testing for levelsSimple tests use dichlorophenolindophenol, a redox indicator, to measure the levels of vitamin C in the urine and in serum or blood plasma. However these reflect recent dietary intake rather than the level of vitamin C in body stores. Reverse phase high performance liquid chromatography is used for determining the storage levels of vitamin C within lymphocytes and tissue. It has been observed that while serum or blood plasma levels follow the circadian rhythm or short term dietary changes, those within tissues themselves are more stable and give a better view of the availability of ascorbate within the organism. However, very few hospital laboratories are adequately equipped and trained to carry out such detailed analyses, and require samples to be analyzed in specialized laboratories.
Biosynthesis. Black is carbon, red is oxygen, and white is hydrogen]] The vast majority of animals and plants are able to synthesize vitamin C, through a sequence of enzyme-driven steps, which convert monosaccharides to vitamin C. In plants, this is accomplished through the conversion of mannose or galactose to ascorbic acid. In some animals, glucose needed to produce ascorbate in the liver (in mammals and perching birds) is extracted from glycogen; ascorbate synthesis is a glycogenolysis-dependent process. Among the mammals that have lost the ability to synthesize vitamin C are simians and tarsiers, which together make up one of two major primate suborders, Haplorrhini. This group includes humans. The other more primitive primates ( Strepsirrhini) have the ability to make vitamin C. Synthesis does not occur in a number of species (perhaps all species) in the small rodent family Caviidae that includes guinea pigs and capybaras, but occurs in other rodents (rats and mice do not need vitamin C in their diet, for example). In reptiles and birds the biosynthesis is carried out in the kidneys. A number of species of passerine birds also do not synthesize, but not all of them, and those that do not are not clearly related; there is a theory that the ability was lost separately a number of times in birds. In particular, the ability to synthesize vitamin C is presumed to have been lost and then later re-acquired in at least two cases. The ability to synthesize vitamin C has also been lost in about 96% of fish (the teleosts). Most tested families of bats (Order Chiroptera), including major insect and fruit-eating bat families, cannot synthesize vitamin C. A trace of gulonolactone oxidase (GULO) was detected in only 1 of 34 bat species tested, across the range of 6 families of bats tested. There are at least two species of bats, frugivorous bat ( Rousettus leschenaultii) and insectivorous bat ( Hipposideros armiger), that retain (or regained) their ability of vitamin C production. These animals all lack the L-gulonolactone oxidase (GULO) enzyme, which is required in the last step of vitamin C synthesis. The genomes of these species contain GULO as pseudogenes, which serve as insight into the evolutionary past of the species. Some of these species (including humans) are able to make do with the lower levels available from their diets by recycling oxidised vitamin C. Most simians consume the vitamin in amounts 10 to 20 times higher than that recommended by governments for humans. This discrepancy constitutes much of the basis of the controversy on current recommended dietary allowances. It is countered by arguments that humans are very good at conserving dietary vitamin C, and are able to maintain blood levels of vitamin C comparable with simians on a far smaller dietary intake, perhaps by recycling oxidised vitamin C.
Routes]] In vertebrates that can synthesize ascorbic acid, the biosynthesis pathway starts with glucose, either taking place in the liver for mammals and some birds, or the kidneys for amphibians, reptiles and some birds.Figure 2 in The Natural History of Ascorbic Acid in the Evolution of the Mammals and Primates and Its Significance for Present Day Man Stone I. Orthomolecular Psychiatry 1972;1:82-89. The pathway is the same. Several enzymes catalyze steps from D-glucose to D-glucuronate. Next, the enzyme glucuronate reductase converts D-glucuronate to L-gluconate. Then the enzyme gulonolactonase converts L- gluconate to L-gulonolactone. The final enzymatic conversion is by the enzyme L-gulonolactone oxidase (GLO), to 2-keto-gulonolactone. From this compound, the last step is a spontaneous, i.e., non-enzymatic conversion to ascorbic acid (vitamin C). GLO is the enzyme that is absent in animal species unable to synthesize vitamin C. s]] All plants synthesize ascorbic acid. Ascorbic acid functions as a cofactor for enzymes involved in photosynthesis, synthesis of plant hormones, as an antioxidant and also regenerator of other antioxidants. Plants use multiple pathways to synthesize vitamin C. The major pathway starts with glucose, fructose or mannose (all simple sugars) and proceeds to L- galactose, L-galaconolactone and ascorbic acid. This process follows a diurnal rhythm, so that enzyme expression peaks in the morning to support biosynthesis later on when mid-day sunlight intensity demands high ascorbic acid concentrations. Minor pathways may be specific to certain parts of plants; these can be either identical to the vertebrate pathway (including the GLO enzyme), or start with inositol and get to ascorbic acid via L-galactonic acid to L-galactonolactone.
EvolutionAscorbic acid is a common enzymatic cofactor in mammals used in the synthesis of collagen, as well as a powerful reducing agent capable of rapidly scavenging a number of reactive oxygen species (ROS). Given that ascorbate has these important functions, it is surprising that the ability to synthesize this molecule has not always been conserved. In fact, anthropoid primates, Cavia porcellus (guinea pigs), teleost fishes, most bats, and some Passeriform birds have all independently lost the ability to internally synthesize Vitamin C in either the kidney or the liver. In all of the cases where genomic analysis was done on an ascorbic acid auxotroph, the origin of the change was found to be a result of loss-of-function mutations in the gene that codes for L-Gulono-γ-lactone oxidase, the enzyme that catalyzes the last step of the ascorbic acid pathway outlined above. In the case of the simians, it is thought that the loss of the ability to make vitamin C may have occurred much farther back in evolutionary history than the emergence of humans or even apes, since it evidently occurred soon after the appearance of the first primates, yet sometime after the split of early primates into the two major suborders Haplorrhini (which cannot make vitamin C) and its sister suborder of non-tarsier prosimians, the Strepsirrhini ("wet-nosed" primates), which retained the ability to make vitamin C. According to molecular clock dating, these two suborder primate branches parted ways about 63 to 60 million years ago. Approximately three to five million years later (58 million years ago), only a short time afterward from an evolutionary perspective, the infraorder Tarsiiformes, whose only remaining family is that of the tarsier ( Tarsiidae), branched off from the other haplorrhines. Since tarsiers also cannot make vitamin C, this implies the mutation had already occurred, and thus must have occurred between these two marker points (63 to 58 million years ago). One explanation for the repeated loss of the ability to synthesize vitamin C is that it was the result of semi-random genetic drift. If a function that a gene provides is redundant to an organism, it could become effectively disposable to that organism. Given that a certain allele does not affect fitness, a pseudogenic version could fix in the population by random genetic drift, because there is no longer any disadvantage conveyed by a non-synonymous mutation. At the very least, natural selection might have been lessened, paving the way for genetic drift to control the fate of the gene. In the case of the L-Gulono-γ-lactone oxidase coding region, its function in organisms with a diet high in Vitamin C might have been redundant, which might subsequently allow the trait to be lost by genetic drift. Some scientists have suggested that loss of the vitamin C biosynthesis pathway may have played a role in rapid evolutionary changes, leading to hominids and the emergence of human beings. According to this theory, the loss of ascorbic acid's anti-oxidizing properties would have led to an increase in free radicals in the body. Free radicals are known to increase the frequency of genetic mutations, which would subsequently increase the speed of evolution. It has also been noted that the loss of the ability to synthesize ascorbate strikingly parallels the inability to break down uric acid, also a characteristic of primates. Uric acid and ascorbate are both strong reducing agents. This has led to the suggestion that, in higher primates, uric acid has taken over some of the functions of ascorbate.
Absorption, transport, and excretionFrom the U.S. National Institutes of Health: "Approximately 70%–90% of vitamin C is absorbed at moderate intakes of 30–180 mg/day. However, at doses above 1000 mg/day, absorption falls to less than 50%. Absorbed, unmetabolized ascorbic acid is excreted in the urine." Ascorbic acid is absorbed in the body by both active transport and simple diffusion. Sodium-Dependent Active Transport—Sodium-Ascorbate Co-Transporters (SVCTs) and Hexose transporters (GLUTs)—are the two transporters required for active absorption. SVCT1 and SVCT2 import the reduced form of ascorbate across plasma membranes. GLUT1 and GLUT3 are glucose transporters, and transfer only the dehydroascorbic acid form of Vitamin C. Although dehydroascorbic acid is absorbed in higher rate than ascorbate, the amount of dehydroascorbic acid found in plasma and tissues under normal conditions is low, as cells rapidly reduce dehydroascorbic acid to ascorbate. Thus, SVCTs appear to be the predominant system for vitamin C transport in the body. SVCT2 is involved in vitamin C transport in almost every tissue, the notable exception being red blood cells, which lose SVCT proteins during maturation. "SVCT2 knockout" animals genetically engineered to lack this functional gene, die shortly after birth, suggesting that SVCT2-mediated vitamin C transport is necessary for life. Excretion is via urine, having passed through kidneys. With low dietary intake, vitamin C is reabsorbed by the kidneys; above a certain threshold, triggered by plasma concentrations of about 1.4 mg/dL or higher, re-absorption declines and excess amounts passes freely into the urine and are excreted. Concentrations less than this threshold amount are actively retained by the kidneys, and the excretion half-life for the remainder of the vitamin C store in the body thus increases greatly, with the half-life lengthening as the body stores are depleted. This half-life rises until it is as long as 83 days by the onset of the first symptoms of scurvy.
Enzymatic cofactorAscorbic acid performs numerous physiological functions in the human body. These functions include the synthesis of collagen, carnitine, and neurotransmitters; the synthesis and catabolism of tyrosine; and the metabolism of microsome. During biosynthesis ascorbate acts as a reducing agent, donating electrons and preventing oxidation to keep iron and copper atoms in their reduced states. Vitamin C acts as an electron donor for eight enzymes:
- Three enzymes ( prolyl-3-hydroxylase, prolyl-4-hydroxylase, and lysyl hydroxylase) that are required for the hydroxylation of proline and lysine in the synthesis of collagen. These reactions add hydroxyl groups to the amino acids proline or lysine in the collagen molecule via prolyl hydroxylase and lysyl hydroxylase, both requiring vitamin C as a cofactor. Hydroxylation allows the collagen molecule to assume its triple helix structure, and thus vitamin C is essential to the development and maintenance of scar tissue, blood vessels, and cartilage.
- Two enzymes ( ε-N-trimethyl-L-lysine hydroxylase and γ-butyrobetaine hydroxylase) that are necessary for synthesis of carnitine. Carnitine is essential for the transport of fatty acids into mitochondria for ATP generation.
- The remaining three enzymes have the following functions in common, alongside their other functions:
- * dopamine beta hydroxylase participates in the biosynthesis of norepinephrine from dopamine.
- * Peptidylglycine alpha-amidating monooxygenase amidates peptide hormones by removing the glyoxylate residue from their c-terminal glycine residues. This increases peptide hormone stability and activity.
- * 4-hydroxyphenylpyruvate dioxygenase modulates tyrosine metabolism.