What makes vitamin c an antioxidant

Vitamin C also forms the semidehydroascorbyl radical, a relatively long-lived radical, in regenerating vitamin E from its radical form, as well as in scavenging radicals. Both enzymatically and nonenzymatically, it can irreversibly decompose into diketogluconic acid or it can be converted to ascorbate in a glutathione-dependent reaction [ 3 , 13 , 14 ]. As being a reducing substance and an electron donor, during free radical scavenging, vitamin C donates high-energy electrons to neutralize free radicals, and it is oxidized to dehydroascorbic acid.

Dehydroascorbic acid may be converted back into ascorbic acid for reuse or may be metabolized, further releasing more electrons. Although vitamin C is absorbed from the gut via a sodium-dependent vitamin C transporter, most cells transport vitamin C in an oxidized form dehydroascorbic acid via glucose transporter 1. Dehydroascorbic acid is reduced to generate ascorbic acid inside the cell, protecting mitochondria from free radical-induced oxidative damage Figures 2 and 3.

Highly reactive free radicals e. Ascorbate can also scavenge nonradical reactive species, derived from peroxynitrite, such as hypochlorous acid, ozone, and nitrating agents. Vitamin C is a monosaccharide oxidation-reduction redox catalyst found in both animals and plants. The antioxidant effect of vitamin C is due to its ability to donate electrons from both the second and third carbon.

During primate evolution, one of the enzymes needed to make ascorbic acid has been lost by mutation, humans must obtain it from the diet [ 15 ]; most animals can synthesize this vitamin in their bodies and do not require it in their diets [ 16 ].

Vitamin C is needed in the conversion of the procollagen to collagen by oxidizing proline residues to hydroxyproline. In other cells, it is maintained in its reduced form by reaction with glutathione [ 17 ].

As shown in Figures 2 and 3 , ascorbic acid is a redox catalyst which can reduce, and thereby neutralize, ROS such as hydrogen peroxide H 2 O 2 Figures 2 and 3. Synthesis and degradation of l -ascorbic acid in plant tissues [ 18 ]. Ascorbic acid has direct antioxidant effects, and also it is a substrate for the redox enzyme ascorbate peroxidase, that is particularly important in stress resistance in plants.

Ascorbic acid is present at high levels in all parts of plants, especially in chloroplasts that reach concentrations of 20 mM there [ 19 ]. Dehydroascorbate DHA and ascorbate free radical AFR , as an intermediate, the ascorbate free radical AFR , that are reversible, one-electron oxidations are generated from ascorbate Figure 4. CAT turnover number is very high, but its affinity for H 2 O 2 is relatively low, and consequently a certain amount of H 2 O 2 remains in the cell.

Blue dotted lines indicate nonenzymatic reactions. H 2 O 2 can react with superoxide anion formed in oxidative metabolism generating the highly reactive hydroxyl radical. Foyer-Halliwell-Asada cycle [ 20 ]. The chemical and biological properties of l -ascorbic acid suggest that it can act as an antioxidant in vivo [ 21 ]. Vitamin C is a primary antioxidant in that it directly neutralizes radical species.

It is not very reactive with prevalent cellular oxidants such as hydrogen peroxide and probably reacts mostly with hydrogen peroxide breakdown products [ 22 ].

Vitamin C has the ability to protect against lipid peroxidation by acting as a scavenger of ROS and by one-electron reduction of lipid hydroperoxyl radicals via the vitamin E redox cycle [ 23 ] Figure 6. Schematic presentation of ROS-mediated lipid peroxidation chain reaction. Vitamin C serves dual role of a prooxidant and an antioxidant [ 23 ]. The reducing agents, antioxidants, can also act as prooxidants. Vitamin C is also known to act as a prooxidant in vitro. Antioxidant vitamin C reduces oxidizing substances, such as hydrogen peroxide; however, it also reduces metal ions that generate free radicals through the Fenton reaction [ 25 ].

Vitamin C is a reducing agent and antioxidant, and reacts with reactive oxygen species, such as the hydroxyl radical. Therefore, vitamin C-mediated Fenton reactions should be controlled in the human body due to efficient iron sequestration by metal-binding proteins such as ferritin and transferrin. It has been suggested that the prooxidant effect may not be relevant in vivo [ 26 ].

Vitamin C also removes hydrogen peroxide and other free radicals, thus adjusting the activity of glutathione peroxidase and catalase [ 46 ]. Alpha-tocopherol, ascorbic acid, and reduced glutathione are important chain breaking antioxidants responsible for scavenging the free radicals and suppression of peroxidation in aqueous and lipid region of the cell [ 10 , 28 , 31 ].

Regeneration of tocopherol radicals to tocopherols by ascorbic acid has been known since the s. The phenol group of tocopherol is located near the interface of a biological membrane water phase, and ascorbic acid can easily access the antioxidant active site of tocopherols and regenerate tocopherols from tocopherol radicals [ 31 ].

Catecholamine synthesis is an ascorbate-dependent function and ascorbate levels are known to be in the millimolar range in the adrenal gland. Ascorbate in chromaffin granules is then secreted concomitant with catecholamines from cultured chromaffin cells [ 47 ] and in vivo by human adrenal glands, the latter in response to adreno-corticotrophin stimulation [ 48 ]. Ascorbate is a neuromodulator; it releases into the extracellular fluid of the brain and regulates dopaminergic and glutamatergic transmission.

Ascorbate is released from glutamatergic neurons as part of the glutamate reuptake process, in which the high-affinity glutamate transporter exchanges ascorbate for glutamate [ 49 ]. This hetero-exchange process, which also may occur in glial cells, ensures a relatively high level of extracellular ascorbate in forebrain [ 49 , 50 ]. Hence it protects nerve cells against glutamate excitotoxicity. The cooperation of ascorbic acid and glutamate is important for neuron metabolism so ascorbic acid participates as a metabolic switch that modulates neural metabolism between resting and activation periods [ 1 ].

Furthermore,ascorbic acid release is regulated by glutamate from astrocyte in the CNS [ 51 ]. It seems ascorbic acid may act like a dopamine antagonist in some areas of brain [ 52 ]. Recently, it has been reported that treatment with vitamin C prevents compression-induced blood-brain barrier BBB disruption and both low and high vitamin C levels have an impact on the number and size of mitochondria [ 53 ], as BBB disruption and mitochondrial dysfunction are well-known risk factors for oxidative stress and Alzheimer disease pathogenesis [ 54 ].

Neuroprotective actions of vitamin C have been investigated in other studies. Most recently, Akbari et al. Naseer et al. Santos et al. Shokouhi et al. Finally, we suggest that vitamin C, as a readily available and safe agent, could be used for the treatment and prevention of the neurodegenerative diseases in CNS. Also, evaluation of motor function and measuring nerve conduction velocity could be performed to confirm the therapeutic benefits of vitamin C in future studies [ 57 ]. Ascorbic acid positively affects the synthesis of collagen, the most abundant extracellular protein.

It is a required component in the synthesis of hydroxyproline and hydroxylysine in collagen. Hydroxyproline serves to stabilize the collagen triple helix; its absence results in structurally unstable collagen which is not secreted from cells at a normal rate. Hydroxylysine is necessary for formation of the intermolecular cross-links in collagen.

In addition, specific carbohydrate residues are linked glycosidically to collagen through hydroxylysine, a process that may be important in the regulation of crosslink formation [ 58 , 59 ].

The immune system is strongly influenced by the intake of nutrients. Supplementation of vitamin C was found to improve components of the human immune system such as antimicrobial and natural killer cell activities, lymphocyte proliferation, chemotaxis, and delayed-type hypersensitivity. Several cells of the immune system can indeed accumulate vitamin C and need the vitamin to perform their task, especially phagocytes and t-cells [ 60 ].

Thus a vitamin C deficiency results in a reduced resistance against certain pathogens whilst a higher supply enhances several immune system parameters. Vitamin C concentrations in the plasma and leukocytes rapidly decline during infections and stress. Vitamin C also contributes to maintaining the redox integrity of cells and thereby protects them against reactive oxygen species generated during the respiratory burst and in the inflammatory response [ 60 , 61 ].

Vitamin C is an essential nutrient for human's and it might be said that it is the most important vitamin in the body. It takes part in many biochemical processes in organism. Chemically, the pharmacophore of vitamin C is the ascorbate that is capable of reacting with most of the physiologically important radicals and oxidants, so that it acts as a reducing agent and antioxidant.

However, its pro-oxidant activity is different antioxidant activity. It is to serve as a co-substrate for several hydroxyls and oxygenize enzymes, maintaining their active center metal ions in a reduced state. It can interfere with glutamatergic, dopaminergic, cholinergic and GABAergic transmission and related behaviors.

These neurotransmitter systems have a basic and crucial role in many processes in CNS. Ascorbic acid is essential for normal collagen formation by virtue of the fact that it is a required component in the synthesis of hydroxyproline and hydroxylysine in collagen. It also improves components of the human immune system such as antimicrobial and natural killer cell activities, lymphocyte proliferation, chemo taxis, and delayed-type hypersensitivity.

Together, ascorbate involves many biologic and metabolic processes so its mechanism remains to be clarified and perhaps it should be mentioned that this vitamin is not well known. Therefore, further investigation is necessary to evaluate the exact mechanism s underlying the effect of vitamin C in order to discover its further effects in the body.

Given the wide role of vitamin C in relation to the prevention and treatment of many diseases and disorders, it is recommended that future research studies be conducted on the increased half-life and bio-availability of vitamin C as a medicine.

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Electromagn Biol Med. Antioxidant systems and oxidative stress in the testes. Oxid Med Cell Longev. Localization of a GSH-dependent dehydroascorbate reductase in rat tissues and subcellular fractions. Arch Biochem Biophys. Vitamin C: its chemistry and biochemistry. Reactive oxygen species, aging, and antioxidative nutraceuticals. Comprehensive reviews in food science and food safety. Electron transfer across the chromaffin granule membrane. Use of EPR to demonstrate reduction of intravesicular ascorbate radical by the extravesicular mitochondrial NADH:ascorbate radical oxidoreductase.

J Biol Chem. Mechanism of the disproportionation of ascorbate radicals. J American Chem Soc. Whether these protective effects are directly attributable to vitamin C is not known. Intervention studies with vitamin C have shown no change in markers of oxidation or clinical benefit.

Dose concentration studies of vitamin C in healthy people showed a sigmoidal relationship between oral dose and plasma and tissue vitamin C concentrations. Hence, optimal dosing is critical to intervention studies using vitamin C. It is also an antioxidant. Vitamin C occurs naturally in some foods, especially fruits and vegetables.

Vitamin C supplements are also available. Vitamin C is water soluble, and the body does not store it. To maintain adequate levels of vitamin C, people need to consume food that contains it every day. ROS are substances such as free radicals that result from natural bodily processes, exposure to pollution, and other factors. They can lead to oxidative stress , which can, in turn, cause cell damage.

The body needs vitamin C to produce collagen. Low levels of vitamin C in the body can lead to scurvy. Symptoms of scurvy include swollen joints, bleeding gums and loose teeth, anemia , and tiredness.

People with a low intake of vitamin C may experience slower wound healing, as their bodies will be less able to produce collagen. During times of recovery, healthcare professionals may recommend supplements for people with low vitamin C levels.

Vitamin C may benefit cardiovascular health for several reasons. Studies have suggested that it may:. This could help protect against heart disease and hypertension , or high blood pressure. However, there is not enough evidence to suggest that taking supplements will help protect heart health. Vitamin C may help lower the risk of cataracts and slow the progression of age-related macular degeneration.

However, more research is needed. A study looked at 31 people aged around 60 years to see whether or not taking vitamin C supplements made a difference to their glucose levels after eating. This suggests that vitamin C could, one day, be a treatment for diabetes. Vitamin C enhances the absorption of iron , and some healthcare professionals recommend taking vitamin C supplements with iron tablets to improve absorption in people with iron deficiency anemia.

One study looked at people who took iron supplements for iron deficiency anemia. Some took vitamin C with their iron supplement, and others did not.