Kamchonwongpaisan S, Bunyaratvej A, Wanachiwanawin W, Yuthavong Y
Department of Pathology, Faculty of Medicine, Ramathibodi Hospital, Bangkok, Thailand.
Parasitology. 1989 Oct;99 Pt 2:171-4. doi: 10.1017/s0031182000058601.
The susceptibility to oxidant-mediated killing of Plasmodium falciparum infecting normal and glucose-6-phosphate dehydrogenase (G6PD)-deficient erythrocytes was assessed by exposure to hydrogen peroxide generated by the glucose-glucose oxidase system. The parasites infecting G6PD-deficient erythrocytes had markedly greater susceptibility to hydrogen peroxide under a variety of conditions than those infecting normal erythrocytes. In both cases, the killing effect was mediated mainly through the host cells since treatment of the erythrocytes with hydrogen peroxide did not change their relatively susceptibility. The parasites were most susceptible during maturation, especially in G6PD-deficient erythrocytes, although a reduction in parasite invasion was also observed. The role of oxidant-mediated killing in the protection of G6PD-deficient hosts from P. falciparum infection is discussed.
通过暴露于葡萄糖-葡萄糖氧化酶系统产生的过氧化氢,评估了感染正常红细胞和葡萄糖-6-磷酸脱氢酶(G6PD)缺乏红细胞的恶性疟原虫对氧化剂介导杀伤的敏感性。在各种条件下,感染G6PD缺乏红细胞的疟原虫比感染正常红细胞的疟原虫对过氧化氢的敏感性明显更高。在这两种情况下,杀伤作用主要通过宿主细胞介导,因为用过氧化氢处理红细胞并没有改变它们的相对敏感性。疟原虫在成熟过程中最易受影响,尤其是在G6PD缺乏的红细胞中,尽管也观察到疟原虫入侵减少。讨论了氧化剂介导的杀伤在保护G6PD缺乏宿主免受恶性疟原虫感染中的作用。