Oxidation of vitamin E in red cell membranes by fatty acids, hydroperoxides and selected oxidants

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Abstract
Our laboratory previously reported that vitamin E (tocopherol) in human blood platelets was oxidizedin vitro by various oxidants. This paper shows that diamide, superoxide, hydroperoxides and polyunsaturated fatty acids induced oxidation of tocopherols in red cell membranes. In contrast to platelets, red cell membrane tocopherol was oxidized by hydrogen peroxide and tertiary butyl hydroperoxide. Alpha tocopherolquinone was one of the products of oxidation. Among the fatty acids, thecis polyunsaturated acids were the most potent oxidizing agents with monounsaturated andtrans compounds relatively ineffective. The oxidation is not a detergent effect of the fatty acids since neither the detergents Brij and Lubrol, when present in concentrations under 0.5 mM, nor sodium arachidate (1.25 mM), could oxidize the membrane tocopherol. When red cell membrane samples were incubated with 0.5 mM arachidonate, 47±11% (S.D.) of the tocopherol lost was converted to tocopherolquinone. Unlike arachidonate, oxidants such as diamide, hydrogen peroxide and tertiary butylhydroperoxide are unable to oxidize all of the membrane tocopherol and produce less tocopherolquinone from oxidation (10–15%) under the experimental conditions of this study. Linoleic acid hydroperoxide is a much more potent oxidant and produces less quinone than arachidonate. The mechanisms of tocopherol oxidations induced by the various compounds seem to be different since the yields of quinone during oxidation vary with the nature of the oxidant. Tocopherol is consumed by oxidation as it protects the membrane from oxidant damage induced by compounds such as unsaturated fatty acids and hydroperoxides.