Oxidant injury of caucasian glucose-6-phosphate dehydrogenase—deficient red blood cells by phagocytosing leukocytes during infection

Robert L. Baehner; David G. Nathan; William B. Castle

doi:10.1172/JCI106747

^{Division of Hematology of the Department of Medicine, Children's Hospital Medical Center and the Medical Service, Veterans Administration Hospital, West Roxbury, Massachusetts}

^{Department of Pediatrics and Medicine, Harvard Medical School, Boston, Massachusetts 02115}

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^{Division of Hematology of the Department of Medicine, Children's Hospital Medical Center and the Medical Service, Veterans Administration Hospital, West Roxbury, Massachusetts}

^{Department of Pediatrics and Medicine, Harvard Medical School, Boston, Massachusetts 02115}

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^{Division of Hematology of the Department of Medicine, Children's Hospital Medical Center and the Medical Service, Veterans Administration Hospital, West Roxbury, Massachusetts}

^{Department of Pediatrics and Medicine, Harvard Medical School, Boston, Massachusetts 02115}

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Published in Volume 50, Issue 12 on December 1, 1971
J Clin Invest. 1971;50(12):2466–2473. https://doi.org/10.1172/JCI106747.
© 1971 The American Society for Clinical Investigation

Published December 1, 1971 - Version history

Patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency of red blood cells (RBC) may develop sudden hemolytic anemia during infection. Since phagocytizing polymorphonuclear leukocytes (PMN) are known to generate hydrogen peroxide, we explored the influence of this oxidant product of PMN on juxtaposed G6PD-deficient and normal RBC. The oxidant stress induced by phagocytosis depleted G6PD-deficient RBC of reduced glutathione (GSH) and this was associated with rapid removal of these cells from the circulation by the liver and spleen. No such effect was observed on normal RBC. Phagocytizing chronic granulomatous disease (CGD) PMN which lack hydrogen peroxide generation, failed to diminish GSH level in G6PD-deficient RBC. Thus, PMN can pose as a source of oxidant damage to G6PD-deficient RBC due to hydrogen peroxide generated during phagocytosis.