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Try out PMC Labs and tell us what you think. Learn More. The recognition of vitamin C is associated with a history of an unrelenting search for the cause of the ancient haemorrhagic disease scurvy. Isolated invitamin C is essential for the development and maintenance of connective tissues. It plays an important role in bone formation, wound healing and the maintenance of healthy gums.

Vitamin C plays an important role in a of metabolic functions including the activation of the B vitamin, folic acid, the conversion of cholesterol to bile acids and the conversion of the amino acid, tryptophan, to the neurotransmitter, serotonin. It is an antioxidant that protects body from free radical damage. It is used as therapeutic agent in many diseases and disorders.

Vitamin C protects the immune system, reduces the severity of allergic reactions and helps to fight off infections. However the ificance and beneficial effect of vitamin C in respect to human disease such as cancer, atherosclerosis, diabetes, neurodegenerative disease and metal toxicity however remains equivocal.

Thus further continuous uninterrupted efforts may open new vistas to understand its ificance in disease management. Vitamins are essential nutrients that are required for various biochemical and physiological processes in the body. It is well known that most of the vitamins cannot be synthesized in the body and hence their supplementation in diet is essential. Vitamins are classified on the basis of their solubility as water soluble C and B complexes and fat soluble vitamins A, D, E, K.

It exists in reduced [ascorbate] and oxidized forms as dehydroascorbic acid which are easily inter-convertible and biologically active thus it acts as important antioxidant. Vitamin C is easily oxidized acid and destroyed by oxygen, alkali and high temperature. Most of the plant and animal species have the ability to synthesize vitamin C from glucose and galactose through uronic acid pathway but man and other primates cannot do so because of deficiency of enzyme gulonolactone oxidase [EC 1.

Deficiency of this enzyme is a result of a mutation which occurred approximately 40 million years ago [ 2 ]. The body requires vitamin C for normal physiological functions. It helps in the synthesis and metabolism of tyrosine, folic acid and tryptophan, hydroxylation of glycine, proline, lysine carnitine and catecholamine.

It facilitates the conversion of cholesterol into bile acids and hence lowers blood cholesterol levels. It also increases the absorption of iron in the gut by reducing ferric to ferrous state. As an antioxidant, it protects the body from various deleterious effects of free radicals, pollutants and toxins. The therapeutic effect of vitamin C was explored by Linus Pauling however his work on therapeutic role of vitamin C in his later years generated much controversy yet he was the first to introduce the concept of high doses of vitamin C for the treatment of various conditions from common cold to cancer [ 3 ].

Since then mega doses of vitamin C have been widely used in the treatment and prevention of a large of disorders like diabetes, atherosclerosis, common cold, cataracts, glaucoma, macular degeneration, stroke, heart diseases, cancer and so on. Deficiency of this vitamin is often associated with anemia, infections, bleeding gums, scurvy, poor wound healing, capillary haemorrhage, muscle degeneration, atherosclerotic plaques and neurotic disturbances.

For the correction of deficiency, vitamin C is often supplemented in large doses and unlike fat soluble vitamins, toxicity is rare. Recently the role of vitamin C in infection and immunity has also been investigated. In view of the vast biological, physiological functions and therapeutic role of vitamin C, this review is an attempt to summarise various evidences in this context.

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Vitamin C is found in citrus fruits, green peppers, red peppers, strawberries, tomatoes, broccoli, brussels sprouts, turnip, Indian gooseberry and other leafy vegetables. Bioavailability or the effective concentration of vitamin C essentially depends on its effective absorption from intestine and renal excretion. Vitamin C, consumed either with diet or dietary supplements, is absorbed by the epithelial cells of the small intestine by SVCT1 or, subsequently diffuses into the surrounding capillaries and then the circulatory system [ 5 — 7 ].

The difference between the amount of AA filtered and reabsorbed constitutes renal excretion [ 8 ]. Together, intestinal absorption and renal excretion controls the serum level of vitamin C and thus its bioavailability. At low concentrations, most vitamin C is absorbed in the small intestine and reabsorbed from the renal tubule [ 9 ]. However, at high concentrations, SVCT1 is down regulated [ 10 ] which limits the amount of AA absorbed from the intestine and kidney [ 11 ].

This imposes a physiological restriction on the maximal effective serum vitamin C concentration or its bioavailability that is attainable by oral consumption [ 12 ]. Vitamin C levels in circulating blood cells, such as platelets, are much higher than the plasma [ 13 ], as these cells express the SVCT2 transporter [ 14 ], which mediates intracellular ascorbate accumulation [ 15 ]. Reduced bioavailability of vitamin C is often seen in stress, alcohol intake, smoking, fever, viral illnesses, usage of antibiotics, pain killers, exposure to petroleum products or carbon monoxide, heavy metals toxicity and so on.

However, the precise mechanism behind low vitamin C level in the body is not well defined. In the event of high consumption, AA and its metabolites such as dehydroascorbic acid, 2,3-diketogulonic acid and oxalic acid are excreted via kidney in humans.

The side effects are generally not serious and can be easily reversed by reducing the intake of AA. Furthermore, there is no consistent and compelling data on serious health effects of vitamin C in humans [ 1819 ].

The biochemical functions of AA are largely dependent on the oxido-reduction properties of l -AA which is a co-factor for hydroxylation and activity of mono-oxygenase enzymes in the synthesis of collagen, carnitine and neurotransmitters [ 20 ]. AA accelerates hydroxylation reactions by maintaining the active centre of metal ions in a reduced state for optimal activity of enzymes hydroxylase and oxygenase. Thus, it is crucial in the maintenance of collagen which represents about one-third of the total body protein.

In an experimental study AA has been shown to have involvement in synthesis and release of type IV collagen into the culture medium [ 21 ]. Further, it has also been reported that AA 2-phosphate, a long-acting vitamin C derivative, stimulates both cell growth and the expression of mRNA for type III collagen in human osteoblast-like MG cells and in normal human osteoblasts, as well as in human bone marrow mesenchymal stem cells, but not the expression of type I collagen in these cells [ 22 ].

However, in another study Kishimoto et al. Collagen constitutes the principal protein of skin, bones, teeth, cartilage, tendons, blood vessels, heart valves, inter vertebral discs, cornea, eye lens. AA is essential to maintain the enzyme prolyl and lysyl hydroxylase in an active form. AA deficiency in reduced hydroxylation of proline and lysine, thus affecting collagen synthesis. Carnitine is required for the transport and transfer of long chain fatty acids into mitochondria for energy production. In addition, AA catalyzes other enzymatic reactions involving amidation necessary for maximal activity of hormones oxytocin, vasopressin, cholecystokinin and alpha-melanotropin [ 26 ].

Deficiency of AA affects this conversion and as a result cholesterol accumulates in the liver leading to hypercholesterolemia [ 2829 ], cholesterol gall stones formation etc [ 3031 ]. Apart from the well accepted role of vitamin C in the prevention of scurvy, the most widely known health beneficial effect of AA is in the prevention and relief of common cold. The role of oral vitamin C in the prevention and treatment of cold however remains controversial despite many controlled studies [ 33 ].

A of clinical trials with varying doses of AA showed that it does not have ificant prophylactic effect, but reduces the severity and duration of symptoms of cold during the period of infection. In both preventive and therapeutic trials, there was a consistent beneficial but generally modest therapeutic effect on the duration of cold symptoms. There was no clear indication of the relative benefits of different regimes of vitamin C doses.

However, in trials that tested vitamin C after cold symptoms occurred, there was some evidence of greater benefits with larger doses than with lower doses [ 3435 ]. Attenuation of immunity in common cold is well known. There has been a continuous debate about the role of AA in boosting immunity during rhinitis. AA has been shown to stimulate immune system by enhancing T-cell proliferation in response to infection. These cells are capable of lysing infected targets by producing large quantities of cytokines and by helping B cells to synthesize immunoglobulins to control inflammatory reactions.

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Further, it has been shown that AA blocks pathways that lead to apoptosis of T-cells and thus stimulate or maintain T-cell proliferation to attack the infection. This mechanism has been proposed for the enhanced immune response observed after administration of vitamin C during rhinitis [ 3637 ].

It is also fairly understood that wound healing requires synthesis and accumulation of collagen and subsequent cross-linking of the fibre to give new tensile strength to the damaged tissue. An early study demonstrated that maximum tensile strength of scar tissue in guinea pig was achieved after supplementation of vitamin C [ 38 ].

Of late, Jagetia et al. AA is known to enhance the availability and absorption of iron from non-heme iron sources [ 41 ]. The reduction of iron by AA has been suggested to increase dietary absorption of non-heme iron [ 4243 ]. Vitamin C rich fruits such as goose berry has been reported to increase the bioavailability of iron from staple cereals and pulses [ 44 ]. Recent observations are of the view that vitamin C inhibits the expression of hepcidin and by affecting erythropoietin receptor in HepG2 cells and the bioavailability of iron provides protection against anaemia due to iron deficiency [ 45 ].

Darius Lane et al. It is also well known that AA acts as a pro-oxidant in invitro in the presence of redox-active iron and might contribute to the formation of hydroxyl radical, which eventually may lead to lipid, DNA or protein oxidation [ 47 ]. Thus vitamin C supplementation in individuals with high iron and or bleomycin detectable iron in some preterm infants could be deleterious due to the production of oxidatively damaged molecules [ 48 — 51 ]. However, Proteggente et al.

Vitamin C has been used in the management of male infertility on empirical grounds, particularly in the presence of non-specific seminal infections [ 53 ]. However, the precise role of vitamin C in relation to male reproduction is not yet clear. Chinoy [ 56 ] stated that AA was essential for the structural and functional integrity of androgen-dependent reproductive organs.

Low concentration of vitamin C showed marked degenerative changes in the testes, epididymis and vas deferens of scorbutic guinea pigs [ 57 ]. Besides degeneration of the spermatogenic epithelium, steroidogenesis and plasma testosterone level also showed a decline [ 58 ].

On the other hand, excessive intake of vitamin C has been reported to cause reproductive failure in the males [ 59 ]. However, Sapra et al. In various studies AA content in seminal plasma of fertile and infertile men was found to be ificantly different [ 6263 ] and the percentage of sperm with normal morphology correlated ificantly with seminal AA in both the groups [ 63 — 65 ]. This is further corroborated by association of decreased AA with increase seminal plasma lipid peroxidation as observed in human trial [ 67 ].

Others have also observed oxidative stress induced deleterious effect on male fertility [ 6869 ]. Increased free radicals in the seminal plasma of infertile subjects by lowering the effective vitamin C levels may potentiate the deleterious effects that result in abnormal sperm parameters [ 7071 ].

Further studies report that supplementation of AA le to ificant reduction in ROS concentration [ 7273 ], sperm membrane lipid per-oxidation [ 73 ] and sperm DNA oxidation [ 74 ] and increased sperm quality [ 72 — 74 ]. The of a recent animal experimental study indicated that, vitamin C improves antioxidant enzymes activity and ificantly reduce MDA in testis compared with the test group [ 75 ]. Vitamin C supplementation as antioxidant in dose dependent manner in men may improve sperm quality [ 76 ].

There are several publications on the role of vitamin C in lipid metabolism and atherogenesis with diverse observations. The ificance of dietary inadequacy of vitamin C in the aetiology of dyslipidemia and atherosclerosis first became apparent from the clinical studies of Myasnikova in The study showed lowering of cholesterol level by administration of AA in the hypercholesterolemic patients [ 78 ].

Since then several authors have also persuaded similar studies. One reviewed the evidence for the role of vitamin C in bile acid synthesis [ 27 ] while others gave particular emphasis on the potential involvement of vitamin C in pathogenesis of atherosclerosis [ 7980 ]. There are reports indicating increase in total body cholesterol and hypercholesterolemia in acutely scorbutic guinea pigs.

However, some studies could not observe any effect of vitamin C in similar animal models [ 81 ]. Das et al. Most of the earlier studies were conducted using rabbit as an animal model for examining vitamin C deficiency. As such rabbit is not a suitable model for such studies as it can synthesize AA unlike higher primates and human beings.

It is difficult to elicit vitamin C deficiency in animal models. In view of the conflicting observations based on the acutely scorbutic animal model chosen by most of the workers, Ginter et al. This model in contrast to others, enabled the effect of AA deficiency on lipid metabolism and atherosclerosis to be followed in long term experiments.

In protracted hypovitaminosis C lasting for 10 weeks, there was a considerable accumulation of cholesterol in liver and also increased concentration in serum [ 83 — 85 ]. It was also reported that the deficiency of vitamin C le to enhanced accumulation of cholesterol in thoracic aorta along with pathomorphological changes in blood vessels [ 838687 ].

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Various human trials have also indicated vitamin C induced reduction in blood lipid levels in normal and hypercholesterolemic subjects [ 8889 ]. Similar observations have been given by others also [ 91 — 96 ]. Chronic AA deficiency in man can lead to impaired cholesterol metabolism resulting in atheromatous changes in the vascular system [ 87 ]. This is further supported by the observation that vitamin C lowers cholesterol [ 88 ] and reduces the risk of developing cardiovascular disease CHD [ 9798 ].

Numerous studies have also looked into the association between AA intake and blood lipids. A large prospective epidemiological study in Finnish men and women suggested that high intake of AA was associated with a reduced risk of death from CHD in women than in men [ 98 ]. Similarly, several other studies showed that high intake of AA in American men and women appeared to benefit only women [ 9799 ].

Yet, another cohort study suggested that cardiovascular mortality was reduced in both sexes by vitamin C [ ]. It is likely that cholesterol lowering effect of vitamin C is affected by several factors like initial cholesterol levels, age and sex of the subjects, dose and mode of the administration.

The influence of age may be important because SAA levels have been found to be lower in elderly as compared to adolescents [] and therefore elderly subjects could be more responsive to the administration of vitamin C. In UK, a study showed that the risk of stroke in those with highest intake of vitamin C was only half that of subjects with the lowest intake. No evidence is suggestive of lower rate of CHD in those with high vitamin C intake [ ]. A recent meta-analysis study on the role of AA and antioxidant vitamins also showed no evidence of ificant benefit in prevention of CHD [ ].

Thus, no conclusive evidence is available on the possible protective effect of AA supplementation on CHD. Increased attention is being paid to involvement of low density lipoprotein LDL in atherogenesis. There are reports indicating that lipid peroxidation and oxidative modification of LDL are implicated in development of atherosclerosis [ ]. Vitamin C provides protection against oxidative changes in LDL in different types of oxidative stress including metal induced oxidative stress [ ].

Addition of iron to plasma devoid of AA resulted in lipid peroxidation, whereas endogenous and exogenous AA was found to inhibit the lipid oxidation in iron-over loaded human plasma [ ].

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