What Is The Purpose Of Vitamin C – Vitamin C (ascorbic acid L) is a strong reducing agent, which means that it readily donates electrons to recipient molecules (Figure 1). Related to this potential to reduce oxidation (redox), the two main functions of vitamin C are as an antioxidant and as an enzyme cofactor (1).

Vitamin C is the primary water-soluble, non-enzymatic antioxidant in plasma and tissues. Even in small amounts, vitamin C can protect essential molecules in the body, such as proteins, lipids (fats), carbohydrates, and nucleic acids (DNA and RNA), from damage by free radicals and reactive oxygen species (ROS) produced . during normal metabolism, by active immune cells, and by exposure to toxins and pollutants (e.g., some chemotherapy drugs and cigarette smoke). Vitamin C also participates in redox recycling of other important antioxidants; for example, vitamin C is known to regenerate vitamin E from its oxidized form (see the article on Vitamin E).

What Is The Purpose Of Vitamin C

The role of vitamin C as a cofactor is also related to its redox potential. By maintaining enzyme-bound metals in their reduced forms, vitamin C assists mixed function oxidases in the synthesis of several critical biomolecules (1). These enzymes are either monooxygenases or dioxygenases (see Table 1). Symptoms of vitamin C deficiency, such as poor wound healing and lethargy, likely result from impairment of these vitamin C-dependent enzymatic reactions leading to insufficient synthesis of collagen, carnitine, and catecholamines (see Deficiency). Furthermore, vitamin C is required as a cofactor for several dioxygenases involved in the regulation of gene expression and maintenance of genome integrity. Indeed, research has recently revealed the essential role played by enzymes, such as the TET dioxygenases and Jumonji domain-containing histone demethylases, in the fate of cells and tissues (see Table 1). These enzymes contribute to the epigenetic regulation of gene expression by catalyzing reactions involving the demethylation of DNA and histones.

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*Monoxygenases catalyze the hydroxylation of a single substrate, while dioxygenases catalyze a reaction that couples the hydroxylation of a specific substrate to the conversion (decarboxylation) of α-ketoglutarate to succinate.

The ability of vitamin C to influence the methylation status of DNA and histones in mammalian cells supports a role for the vitamin in health and disease beyond what was previously understood, particularly by protecting genome integrity (3, 4).

Vitamin C affects several components of the human immune system in vitro; for example, vitamin C has been shown to stimulate the production (5-9) and function (10, 11) of leukocytes (white blood cells), especially neutrophils, lymphocytes, and phagocytes. Specific measures of functions stimulated by vitamin C include cellular motility (10), chemotaxis (10, 11), and phagocytosis (11). Neutrophils, mononuclear phagocytes, and lymphocytes accumulate vitamin C to high concentrations, which can protect these cell types from oxidative damage (12-14). In response to invading microorganisms, phagocytic leukocytes release nonspecific toxins, such as superoxide radicals, hypochlorous acid (“bleach”), and peroxynitrite; these reactive oxygen species kill pathogens and, in the process, can damage the leukocytes themselves (15). Vitamin C, through its antioxidant functions, has been shown to protect leukocytes from self-inflicted oxidative damage (14). Phagocytic leukocytes also produce and release cytokines, including interferons, which have antiviral activity (16). Vitamin C has been shown to increase interferon production in vitro (17). Additional studies have indicated that vitamin C enhances the chemotactic and microbial killing abilities of neutrophils and stimulates the proliferation and differentiation of B- and T-lymphocytes (reviewed in 18).

The general public thinks that vitamin C boosts immune function, but human studies published to date are conflicting. Different results are likely due to study design issues, which are often related to a lack of understanding of the pharmacokinetics and requirements of vitamin C (19, 20).

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Finally, vitamin C increases the bioavailability of iron from foods by improving the intestinal absorption of non-heme iron (see article on Iron) (21).

Depletion-repletion pharmacokinetic experiments showed that plasma vitamin C concentration is tightly controlled by three primary mechanisms: intestinal absorption, tissue transport, and renal reabsorption (22). In response to increasing oral doses of vitamin C, plasma vitamin C concentration rises sharply in an intake between 30 and 100 mg/day. Plasma ascorbate concentrations reach steady state at concentrations between 60 and 80 micromoles/L (μmol/L). This is typically seen in doses between 200 and 400 mg/day in healthy young adults, with some individual variation (23, 24).

One hundred percent absorption efficiency is seen when vitamin C is ingested in doses up to 200 mg at a time. Higher doses (>500 mg) result in slightly less vitamin C being absorbed as the dose increases. Once plasma vitamin C concentrations reach saturation, excess vitamin C is largely excreted in the urine. Notably, intravenous vitamin C administration bypasses absorptive control in the intestine so that very high concentrations of vitamin C in the plasma can be achieved; within a few hours, renal excretion restores vitamin C to baseline plasma concentrations (see Cancer Treatment) (25).

Although plasma vitamin C concentration reflects recent dietary intake, leukocyte (white blood cell) vitamin C is thought to be an indicator of body stores. However, leukocyte vitamin C concentration does not accurately reflect vitamin C in many tissues and may specifically underestimate vitamin C uptake into skeletal muscle (26). Yet plasma concentrations of vitamin C ≥50 μmol/L are sufficient to saturate muscle tissue with vitamin C.

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There is also some limited evidence to suggest that individuals carrying specific polymorphisms in genes involved in vitamin C transport and detoxification mechanisms may have lower plasma vitamin C concentrations, even with high vitamin C intake ( see also vascular complications of diabetes mellitus) (reviewed in 27) .

Due to pharmacokinetics and tight control of plasma vitamin C, vitamin C supplementation will have variable effects in vitamin C-supplied (plasma concentration near saturation) versus suboptimal (plasma concentrations <50 μmol/L), slightly deficient (plasma concentrations ). <23 μmol/L), or severe deficiency (plasma concentrations <11 μmol/L) individuals (28). Scientific studies investigating the effectiveness of vitamin C in preventing or treating disease need to assess baseline vitamin C status before initiating an intervention or statistical analysis (22, 29-31).

For a more detailed discussion of the bioavailability of different forms of vitamin C, see the article,  Bioavailability of Different Forms of Vitamin C.

Severe vitamin C deficiency has been known for many centuries as the potentially fatal disease, scurvy. By the late 1700s, the British navy was aware that scurvy could be cured by eating oranges or lemons, although vitamin C would not be isolated until the early 1930s. Symptoms of scurvy include subcutaneous bleeding, poor wound closure, easy bruising, loss of hair and teeth, and joint pain and swelling. Such symptoms appear to be related to the weakening of blood vessels, connective tissue, and bone, which all contain collagen. Early symptoms of fatigue such as scurvy can result from reduced levels of carnitine, which is needed to obtain energy from fat, or from reduced synthesis of the catecholamine norepinephrine (see Function). Scurvy is rare in developed countries because it can be prevented with as little as 10 mg of vitamin C daily (32). However, outbreaks have occurred in children and the elderly on very restricted diets (33, 34).

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The recommended dietary allowance (RDA) for vitamin C is based on the amount of vitamin C taken to maintain neutrophil vitamin C concentration with minimal urinary excretion of vitamin C and is intended to provide sufficient antioxidant protection ( Table 2) (35). The recommended intake for smokers is 35 mg per day higher than for non-smokers, because smokers are under increased oxidative stress from the toxins in cigarette smoke and generally have lower blood concentrations of vitamin C (36).

The amount of vitamin C needed to help prevent chronic disease is higher than the amount needed to prevent scurvy. Information on vitamin C and prevention of chronic disease is based on prospective observational cohort studies and randomized controlled trials (29, 37). Prospective cohort studies can examine the incidence of a particular disease in relation to vitamin C intake or body status in a cohort of participants who are followed over time. In contrast, trials are intervention studies that can establish a causal relationship between exposure and outcome, e.g., by evaluating the effect of vitamin C supplementation on the incidence of chronic disease in participants randomly assigned to receive either vitamin C or placebo for one specific. length of time

Endothelial dysfunction is considered to be an early stage in the development of atherosclerosis. Changes in the structure and function of the vascular endothelium that lines the inner surface of all blood vessels are associated with the loss of normal nitric oxide-dependent vasodilatation. Endothelial dysfunction leads to widespread vasoconstriction and coagulation abnormalities. Measurement of brachial artery flow-mediated dilation (FMD) is often used as a functional marker of endothelial function; FMD values ​​are inversely correlated with the risk of future cardiovascular events (38). A 2014 meta-analysis of 44 randomized controlled trials in subjects with and without chronic diseases summarized the effect of supplemental vitamin C on endothelial function by measuring FMD (19 studies), assessing arm blood flow (20 studies), or by wave analysis heartbeat 5 trials) (39). Short-term supplementation with vitamin C was found to reduce endothelial dysfunction in subjects with heart failure, atherosclerosis, or diabetes mellitus, but had no effect in those with hypertension. Vitamin

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