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|Title:||Vitamin C and genomic stability|
|Citation:||Halliwell, B. (2001). Vitamin C and genomic stability. Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis 475 (1-2) : 29-35. ScholarBank@NUS Repository. https://doi.org/10.1016/S0027-5107(01)00072-0|
|Abstract:||Vitamin C, a water-soluble glucose derivative, has considerable antioxidant activity in vitro, in part because of its ease of oxidation and because the semidehydroascorbate radical derived from it is of low reactivity. Vitamin C in vivo is an essential cofactor for a range of enzymes involved in diverse metabolic pathways, but much recent literature has focused on its antioxidant effects. Consumption of foods rich in Vitamin C (fruits and vegetables) is associated with decreased risk of cardiovascular disease, of many types of cancer and possibly of neurodegenerative disease, but the extent to which Vitamin C contributes to these effects is uncertain. Data using biomarkers of oxidative damage to DNA bases have given no compelling evidence to date that ascorbate supplements can decrease the levels of oxidative DNA damage in vivo, except perhaps in subjects with very low Vitamin C intakes. Similarly, there is no conclusive evidence from studies of strand breaks, micronuclei, or chromosomal aberrations for a protective effect of Vitamin C. There is limited evidence that supplements of Vitamin C might have beneficial effects in disorders of vascular function, and that diet-derived Vitamin C may decrease gastric cancer incidence in certain populations, but it is not clear whether it is the antioxidant or other properties of ascorbate that are responsible for these two actions. © 2001 Elsevier Science B.V.|
|Source Title:||Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis|
|Appears in Collections:||Staff Publications|
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