Oxidant injury of caucasian glucose-6-phosphate dehydrogenase—deficient red blood cells by phagocytosing leukocytes during infection
AUTOR(ES)
Baehner, Robert L.
RESUMO
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.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=292196Documentos Relacionados
- METABOLIC CHANGES IN NORMAL AND GLUCOSE-6-PHOSPHATE DEHYDROGENASE-DEFICIENT ERYTHROCYTES INDUCED BY ACETYLPHENYLHYDRAZINE*
- Developmental implications of multiple tissue studies in glucose-6-phosphate dehydrogenase-deficient heterozygotes.
- THE EFFECT OF PHENYLHYDRAZINE ON THE ADENOSINE TRIPHOSPHATE CONTENT OF NORMAL AND GLUCOSE-6-PHOSPHATE DEHYDROGENASE-DEFICIENT HUMAN BLOOD*
- Ribose metabolism and nucleic acid synthesis in normal and glucose-6-phosphate dehydrogenase-deficient human erythrocytes infected with Plasmodium falciparum.
- EFFECTS OF PRIMAQUINE ON THE RED BLOOD CELL MEMBRANE. II. K+ PERMEABILITY IN GLUCOSE-6-PHOSPHATE DEHYDROGENASE DEFICIENT ERYTHROCYTES*