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Superoxide, a key precursor of important reactive oxygen/nitrogen species (ROS/RNS), may release iron from its protein complex. By mediating the generation and/level of superoxide, vitamin E, the most important fat-soluble anti-oxidant and free radical scavenger, may exert its antioxidant function by limiting the formation of reactive hydroxyl radi-cals and peroxynitrite. The antioxidant function of vitamin E is augmented by GSH peroxidase and related metabolic sys-tems which respond adaptively and compensatively to oxidative stress. By mediating the levels of ROS/RNS, vitamin E may also modulate the activation and/or expression of redox-sensitive biological response modifiers, and thereby attenu-ate the cellular events leading to the onset and development of aging and other degenerative disorders. Earlier epidemiol-ogical data and retrospective studies show an association between increased intake of vitamin E and reduced risk of car-diovascular disease, cancer, and other disorders. However, subsequent prospective randomized placebo-controlled studies and interventional trials have provided inconsistent findings. Data available from recent large-scale interventional trials suggest that vitamin E supplements at high doses are not beneficial.