ABSTRACT
Reactive oxygen species are produced enzymatically in the course of normal metabolism. Near the bottom of the multilayered defense system, vitamin E appears to act nonenzymatically, and rather nonspecifically, as a terminal stopgap responding to all manner of prior system lapses and failures resulting in free radical leakage into the lipid phase. In some instances, however, the beneficial effects in certain clinically important situations have been reported to be sufficient to consider the use of supplemental vitamin E for protective purposes. This in turn has led to interest in the possible antioxidant activity of certain drugs and in the design of drugs related structurally to vitamin E. A double blind study of vitamin E in premature infants failed to document protection against retrolental fibroplasia and reported a significant increase in retinal hemorrhages. Herbert et al. noted in preliminary information gathered on a large scale work-site study that 27% of the subjects were already taking a vitamin supplement including vitamin E.
