Free radical protection: why vitamin E, not vitamin C, beta-carotene or glutathione?
There is increasing evidence that as a result of infection or the action of toxic chemicals or radiation, the body may be continuously exposed to the damaging action of free radicals. While previous results have suggested that zinc may be involved in limiting the formation of these highly reactive species, natural organic antioxidants such as vitamin E may also play an important role in reducing their effect. Recent results showing quantitative and qualitative differences in the free radical reactivity of vitamin E, vitamin C, beta-carotene and glutathione are reported. The possibility that in vivo these compounds may sometimes act synergistically is discussed in the light of recent information on hydrogen atom and electron transfer reactions and the long-established findings that vitamin C can augment the antioxidant action of vitamin E whereas iron salts can have a deleterious effect.
D000818:Animals; D000975:Antioxidants; D001205:Ascorbic Acid / Q000494:pharmacology; D002338:Carotenoids / Q000494:pharmacology; D004579:Electron Transport; D005231:Fatty Acids, Unsaturated / Q000378:metabolism; D005609:Free Radicals; D005978:Glutathione / Q000494:pharmacology; D006801:Humans; D006859:Hydrogen; D066298:In Vitro Techniques; D007501:Iron / Q000494:pharmacology; D008054:Lipid Peroxides / Q000378:metabolism; D010545:Peroxides; D014810:Vitamin E / Q000378:metabolism / Q000494:pharmacology*; D019207:beta Carotene
D000975:Antioxidants; D005231:Fatty Acids, Unsaturated; D005609:Free Radicals; D008054:Lipid Peroxides; D010545:Peroxides; D019207:beta Carotene; D014810:Vitamin E; D002338:Carotenoids; D006859:Hydrogen; D007501:Iron; D005978:Glutathione; D001205:Ascorbic Acid