感染期间，吞噬白细胞对高加索人葡萄糖-6-磷酸脱氢酶缺乏的红细胞造成氧化损伤。
Oxidant injury of caucasian glucose-6-phosphate dehydrogenase-deficient red blood cells by phagocytosing leukocytes during infection.
作者信息
Baehner R L, Nathan D G, Castle W B
出版信息
J Clin Invest. 1971 Dec;50(12):2466-73. doi: 10.1172/JCI106747.
Abstract
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.
摘要
红细胞葡萄糖-6-磷酸脱氢酶（G6PD）缺乏的患者在感染期间可能会突然发生溶血性贫血。由于已知吞噬多形核白细胞（PMN）会产生过氧化氢，我们探讨了PMN的这种氧化产物对并列的G6PD缺乏和正常红细胞的影响。吞噬作用诱导的氧化应激使G6PD缺乏的红细胞内的还原型谷胱甘肽（GSH）耗竭，这与肝脏和脾脏迅速从循环中清除这些细胞有关。在正常红细胞上未观察到这种效应。缺乏过氧化氢生成能力的慢性肉芽肿病（CGD）PMN进行吞噬时，未能降低G6PD缺乏红细胞中的GSH水平。因此，由于吞噬过程中产生的过氧化氢，PMN可成为G6PD缺乏红细胞氧化损伤的来源。
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