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Summary. No evidence was found to support the claimed role of lipid peroxidation in the pathogenesis and haemolysis in paroxysmal nocturnal haemoglobinuria (PNH) including iron‐induced episodes of gross haemoglobinuria. Therapy with the antioxidant vitamin E failed to influence the course of two patients with PNH. Three separate techniques for inducing lipid peroxidation failed to lower AChE of normal and PNH red cells and to induce susceptibility to in vitro PNH haemolytic tests in normal cells whether iron was added to the test system or not. Under peroxidatic stress, PNH cells did not generate abnormally high amounts of lipid peroxides as measured by malonaldehyde formation. Similar results were obtained with human red cells with induced high concentrations of protoporphyrin IX. Such studies do not, however, vitiate the concept that lipid peroxidation may play an important role in biologic ageing and cell destruction.

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Erythrocytes from several animal species with widely differing catalase levels were exposed to H2O2and the susceptibility of Hb to oxidation measured. In the absence of glucose the rapidity of MHb formation was inversely related to the catalase activity and directly related to the concentration of H2O2attained. Added catalase or hemolysates of catalase-rich erythrocytes counteracted the effect of H2O2, while azide rendered Hb of even catalase-rich cells susceptible to rapid oxidation. Added glucose largely prevented the formation of MHb on exposure to H2O2; this protective effect was less marked in azide-treated cells than in control cells. These results suggest that catalase complements the protective action of glucose and thereby regulates MHb formation and accumulation in erythrocytes.