Mechanisms of lipid peroxidation in erythrocytes of vitamin E-deficient rats and in phospholipid model systems

Erythrocytes from vitamin E-deficient and control rats were peroxidized by glucose oxidase-glucose or dialuric acid. Losses of polyunsaturated fatty acids from membrane phospholipids, and of dimethylacetals from plasmalogens, were quantitated by gas-liquid chromatography. Similar treatment of solubilized or micellar phospholipids or plasmalogens in vitro showed that in both erythrocytes and micellar systems, arachidonic acid and the 16-carbon plasmalogen are most susceptible to peroxidation by either reagent. The same narrow concentration range of dialuric acid found effective in peroxidizing erythrocytes from tocopherol-deficient rats was also found effective in peroxidizing micellar phospholipids in vitro.Partially peroxidized erythrocytes from tocopherol-deficient rats were subjected to treatment with phospholipase A or phospholipase C. Hemolysis by either phospholipase was accelerated in partially peroxidized cells as compared to controls, suggesting that peroxidation exposes both polar and nonpolar lipid sites in the erythrocyte membrane.