Vitamin E is a generic term for all tocopherol (TocH) and tocotrienol (Toc-3H) homologues. The antioxidant effect of vitamin E has been ascribed to the oxidation of its phenolic hydroxyl group by lipid peroxyl radicals (LOO·), producing corresponding tocopheroxyl radicals (Toc·) or tocotrienoxy radicals (Toc-3·) (reaction 1). The mechanism involved has been studied extensively by several investigators (1-5).It is well known that lipophilic vitamin E is localized in biomembranes and functions as an efficient inhibitor of lipid peroxidation in membranes (6-10). We recently reported the second-order rate constants (ks) for the reactions of a-, b-, g-, d-TocH, and tocol with the 2,6-dit-butyl-4-(4-methoxyphenyl)phenoxyl radical (ArO·), which can be regarded as a model for lipid peroxyl radicals (LOO·), in membranes (reaction 2) using stoppedflow spectrophotometry (10).In this experiment, we used samples of egg yolk phosphatidylcholine (EYPC) vesicles as a membrane model in a 70% methanol solution with low turbidity, which is suitable for measuring by spectrophotometry. In the present work, we measured ks values in EYPC membranes for the reactions of a-, b-, g-, and d-Toc-3Hs with the ArO· radical.