intakes of vitamin E will reduce the risk for certain diseases. Still, even a positive outcome of these trials may not necessarily lead to a change in recommended individual intakes for the whole population. These trials generally are targeting groups at high risk for particular diseases. If the results of these studies are positive, it is likely that initial recommendations for higher intakes will be limited in their application to high-risk populations. Because of the myriad of actions of high doses of vitamin E, recommendations of higher intakes for the general population undoubtedly will require extensive investigation of the long-term consequences of the multiple metabolic and cellular modifications.



Most dietary vitamin E is found in food that contains fat. It is clear that vitamin E absorption requires micelle formation and chylomicron secretion by the intestine (Muller et al, 1974), although the optimal amount of fat to enhance vitamin E absorption has not been reported. This is probably a more important issue for vitamin E supplement users than for nonsupplement users where all of the vitamin E is in a dietary fat-rich environment.

Nutrient-Nutrient Interactions
Antioxidant Interactions

When vitamin E intercepts a radical, a tocopheroxyl radical is formed (Burton and Ingold, 1981). This radical can be reduced by ascorbic acid or other reducing agents (Doba et al., 1985; Niki et al., 1982), thereby oxidizing the latter and returning vitamin E to its reduced state.

The ability of one antioxidant to regenerate another oxidized species is dependent on the redox potential of the antioxidant (Buettner, 1993). Biologically relevant electron donors that have been shown to regenerate α-tocopherol effectively from the α-tocopheroxyl radical include vitamin C (McCay, 1985), glutathione (Niki, 1987), and ubiquinols (Stoyanovsky et al., 1995). (For further information see “Nutrient-Nutrient Interactions” in Chapter 5.) Cellular redox cycling is coupled with the energy status of the organism. Thus, it can be expected that during prolonged energy deficit or inadequate production of nicotinamide adenine dinucleotide

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