Abstract
Erythrocytes of vitamin E-deficient rats and normal rats were oxidized at 37 degrees C by molecular oxygen using a free radical initiator. The erythrocytes were oxidized by a free radical chain mechanism with kinetic chain length considerably larger than 1 and resulted in hemolysis. Vitamin E suppressed both oxidation and hemolysis, but the extent of hemolysis was determined primarily by the extent of oxidation independent of the presence or absence of vitamin E.
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