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用5-羟基-6-去甲基伯氨喹治疗的葡萄糖-6-磷酸脱氢酶缺乏红细胞的变形性变化和海因茨小体形成

Change of deformability and Heinz body formation in G6PD-deficient erythrocytes treated with 5-hydroxy-6-desmethylprimaquine.

作者信息

Thompson S F, Fraser I M, Strother A, Bull B S

机构信息

Department of Physiology, School of Medicine, Loma Linda University, California 92350.

出版信息

Blood Cells. 1989;15(2):443-52; discussion 453-4.

PMID:2765673
Abstract

Glucose-6-phosphate deficient human erythrocytes were incubated with low concentrations of 5-hydroxy-6-desmethylprimaquine, a metabolite of primaquine in animals, for up to 18 hours under sterile conditions. These erythrocytes became less deformable than untreated erythrocytes. This decrease in deformability was closely associated with the extent and time course of formation of Heinz bodies in the G6PD-deficient erythrocytes. These results support the hypothesis that the in vivo formation of low concentrations of 5H6DPQ by metabolism of primaquine could be the cause of Heinz body formation and the hemolytic anemia seen when primaquine is administered to G6PD-deficient individuals.

摘要

将葡萄糖-6-磷酸缺乏的人类红细胞与低浓度的5-羟基-6-去甲基伯氨喹(伯氨喹在动物体内的一种代谢产物)在无菌条件下孵育长达18小时。这些红细胞的变形能力比未处理的红细胞更差。这种变形能力的降低与葡萄糖-6-磷酸脱氢酶缺乏的红细胞中亨氏小体形成的程度和时间进程密切相关。这些结果支持了这样一种假说,即伯氨喹代谢在体内形成低浓度的5H6DPQ可能是导致亨氏小体形成以及给葡萄糖-6-磷酸脱氢酶缺乏的个体服用伯氨喹时出现溶血性贫血的原因。

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