Oxidative Hemolysis and Erythrocyte Metabolism in Hereditary Acatalasia*

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Abstract
The role of peroxides in erythrocyte aging and in drug-induced hemolysis and the effects of H2O2 on the thiol and glucose metabolism of erythrocytes were investigated in studies performed in several members of a Swiss family with hereditary acatalasia. These findings indicate that H2O2 is not involved in oxidative hemolysis induced by acetylphenylhydrazine and its congeners, although it is generated on standing by primaquine. In acatalasia, the oxidative challenge of H2O2 whether spontaneously generated or drug-induced, is dissipated by glutathlone peroxldation. Therefore, H2O2 both stimulates and is offset by hexosemonophosphate shunt activation. In the normal erythrocyte, this mechanism and catalasic decomposition combine to prevent oxidative injury; when both mechanisms are overcome, H2O2 induces irreversible oxidative damage.