Gene action in erythrocyte deficiency of glucose-6-phosphate dehydrogenase: tissue enzyme-levels.

Abstract

THE susceptibility to increased haemolysis following ingestion of such agents as primaquine, naphthaline, nitrofurans, other drugs and the fava bean is associated with intrinsic defects in erythrocyte metabolism. These defects include a lower concentration of reduced glutathione1, instability of reduced glutathione during incubation of the cells with acetylphenylhydrazine2, and a deficiency in glucose-6-phosphate dehydrogenase3. Recent studies have suggested that this erythrocyte enzymatic deficiency is genetically determined, and inherited as a sex-linked characteristic of intermediate dominance4–6.