Degradation of membrane phospholipids and thiols in peroxide hemolysis: studies in vitamin E deficiency. Blood

sibly normal red cell senescence involve oxidative damage to the red cell.14 Suggestions that H2O2 is responsible for this damage both in senescent erythrocytes5 and in hemolytic reactions following administration of oxidant drugs68 have appeared but have been disputed.2’9 Recently drugs such as primaquine, pamaquine and hydroquinone, which cause oxidative hemolysis especially in G6PD-deficient patients, have been demonstrated to generate H202 in vitro.10’ If, in fact, H2O2 is the damaging material in oxidative he-molysis, the mechanism of its toxicity has not as yet been elucidated. A clear relationship between exposure to H2O2 and hemolysis occurs with deficiency of the lipid-soluble vitamin, tocopherol, (Vitamin E). Deficiency of this vitamin in human beings is almost entirely associated with G.I. mal-absorption syndromes. Large numbers of patients with steatorrhea of diverse etiology have low levels of tocopherol in their sera and harbor H202-sensitive red cells,12 presumably due to malabsorption of the lipid-soluble vitamin. Where studied, a moderate diminution in 51Cr-labeled red cell survival (half