Vitamin C functions physiologically as a water-soluble antioxidant by virtue of its very strong reducing power (high redox potential) and facile regeneration via ubiquitous reductants such as glutathione, nicotinamide adenine dinucleotide, and nicotinamide adenine dinucleotide phosphate. The primary method used to estimate the requirement relates to the vitamin C intake needed to maintain near-maximal neutrophil ascorbate concentration with minimal urinary excretion. Because smokers suffer increased oxidative stress and metabolic turnover of vitamin C, their requirement is increased. Although there is ample evidence that vitamin C administration can result in decreases in markers of oxidative stress, a Recommended Dietary Allowance (RDA) derived from a direct antioxidant function of vitamin C could not be calculated because of the lack of a quantitative relationship between this antioxidant function and a health-related endpoint. Since vitamin C reduces markers of oxidative stress, it meets the definition of a dietary antioxidant.
Vitamin E functions as a chain-breaking antioxidant that prevents the propagation of lipid peroxidation. To estimate the requirement, data were examined on the intake of vitamin E that would prevent hydrogen peroxide-induced lysis of erythrocytes. Under these circumstances, vitamin E is acting as an ex vivo antioxidant, maintaining a normal physiological function in humans. Although it is not yet possible to relate vitamin E intake to a lowering of chronic disease risk, it still meets the definition of a dietary antioxidant.
Selenium functions through selenoproteins, several of which are oxidant defense enzymes. The criterion used to estimate the requirement for selenium relates to the intake needed to maximize the activity of the plasma selenoprotein glutathione peroxidase, an oxidant defense enzyme. It is not clear if the diseases associated with selenium deficiencies, Keshan disease or Kashin-Beck disease, are due to oxidative stress. The selenium in several selenoproteins has a biochemical role in oxidant defense, thus maintaining normal physiological function, and as such plays a role as a dietary antioxidant.
β-Carotene and other carotenoids function as sources of vitamin A and, due to this provitamin A activity, can prevent vitamin A deficiency. Because no other specific nutrient functions have been identified at this time, no requirements have been established for any of the carotenoids. β-Carotene and the other carotenoids display in vitro antioxidant activity, but the evidence that they act as in vivo