(NADH), nicotinamide adenine dinucleotide phosphate (NADPH) or glutathione [GSSG] reductase due to dietary deficiencies of niacin (component of NADP or NADPH) or riboflavin (cofactor for GSSG reductase), the ability of the organism to produce sufficient reducing equivalents for recycling oxidized products will be compromised. Conversely, intakes of plant phenolic compounds and flavonoids may add to the total antioxidant pool (de Vries et al., 1998; Manach et al., 1998). The extent, involvement, and contribution of these newer compounds which may be acting as antioxidants to the redox cycling reactions in vitro and in vivo remain to be determined.
The regeneration of α-tocopherol from the α-tocopheroxyl radical may be faster than the further oxidation of the α-tocopheroxyl radical. The extent to which vitamin E is recycled in humans and which antioxidant species are preferentially used for recycling are not known. In human platelet homogenates, distinct chemical and enzymatic pathways for the regeneration of oxidized tocopherol, afforded by vitamin C and glutathione, have been identified (Chan et al., 1991). A metabolic study in humans designed to demonstrate the occurrence of vitamin E recycling by vitamin C had limitations since the body pools of vitamin C and E cannot be totally depleted (Jacob et al., 1996). Although the data were inconclusive, the authors did comment that there is “a trend towards sparing of tissue tocopherol by vitamin C” and that more study was warranted. This is an important area of investigation because the tocopheroxyl radical has been shown in vitro to increase lipid peroxidation in the absence of water-soluble antioxidants, and it has been proposed that this mechanism may be an important factor in potentiating in vivo atherogenesis (Stocker, 1999; Upston et al., 1999). However, there are still no data to determine whether this mechanism is operative in vivo.
Vitamin E requirements have been reported to increase when intakes of polyunsaturated fatty acids (PUFAs) are increased (Dam, 1962; Horwitt, 1962). Based on these data it was suggested that a ratio of at least 0.4 mg (1 µmol) α-tocopherol per gram of PUFA should be consumed by adults (Bieri and Evarts, 1973; Horwitt, 1974; Witting and Lee, 1975). However, the method of determining the vitamin E requirement generated by PUFA intakes is not universally accepted because the amount of vitamin E required to stabilize PUFAs in tissues is influenced to a greater extent by their degree of