Inhibitory effect of a fava bean component on the in vitro development of Plasmodium falciparum in normal and glucose-6-phosphate dehydrogenase deficient erythrocytes.
Inhibitory effect of a fava bean component on the in vitro development of Plasmodium falciparum in normal and glucose-6-phosphate dehydrogenase deficient erythrocytes.
复制标题
蚕豆成分对正常和葡萄糖-6-磷酸脱氢酶缺陷红细胞中恶性疟原虫体外发育的抑制作用。
作者：
J. Golenser;J. Miller;D. Spira;T. Navok;M. Chevion
我们通过研究疟疾寄生虫（恶性疟原虫）、具有不同程度G-6-PD缺乏的人红细胞和异乌拉米（IU）（一种已知会引起G-6-PD缺乏的红细胞的氧化应激和溶血的蚕豆提取物）之间的体外相互作用，检验了与蚕豆摄入相关的G-6-PD缺乏赋予对疟疾抗性的假设。未经处理的G-6-PD缺陷和正常红细胞同样支持恶性疟原虫的体外生长。然而，在用IU预处理后，G-6-PD缺陷型红细胞在体外不支持寄生虫生长，而在正常红细胞中生长仍然很高。寄生虫的生长与IU处理的红细胞的G-6-PD活性成正比。相反，当寄生的红细胞暴露于IU时，即使在正常红细胞中的寄生虫也被破坏。环状的敏感性远低于晚期滋养体和滋养体。结果表明，有两种模式，IU影响恶性疟原虫的发展，并在体外证明，G-6-PD缺乏症赋予抗疟疾蚕豆相关的氧化应激条件下。
We examined the hypothesis that G-6-PD deficiency associated with fava bean ingestion confers resistance to malaria by studying the in vitro interactions between malaria parasites (Plasmodium falciparum), human erythrocytes with varying degrees of G-6-PD deficiency, and isouramil (IU), a fava bean extract that is known to cause oxidant stress and hemolysis of G-6-PD-deficient erythrocytes. Untreated G-6-PD-deficient and normal erythrocytes supported the in vitro growth of P. falciparum equally well. However, after pretreatment with IU, G-6-PD-deficient erythrocytes did not support parasite growth in vitro, whereas growth remained high in normal erythrocytes. Parasite growth was proportional to the G-6-PD activity of the IU-treated erythrocytes. In contrast, when parasitized erythrocytes were exposed to IU, parasites even in normal erythrocytes were destroyed. Ring forms were much less sensitive than late trophozoites and schizonts. The results suggest that there are two modes by which IU affects the development of P. falciparum and demonstrate in vitro that G-6-PD deficiency confers resistance against malaria under conditions of fava-bean-associated oxidant stress.