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氯喹对人红细胞内疟原虫恶性疟原虫进食机制的影响。

Effects of chloroquine on the feeding mechanism of the intraerythrocytic human malarial parasite Plasmodium falciparum.

作者信息

Yayon A, Timberg R, Friedman S, Ginsburg H

出版信息

J Protozool. 1984 Aug;31(3):367-72. doi: 10.1111/j.1550-7408.1984.tb02981.x.

Abstract

Ultrastructural investigations of P. falciparum cultivated in vitro in human erythrocytes revealed new features of the feeding mechanism of the parasite. Mature trophozoites and schizonts take up a portion of the host cytosol by endocytosis which is restricted to cytostomes and which involves the invagination of both parasitophorous and parasite membranes. The resulting endocytic vesicles, surrounded by two concentric membranes, migrate towards the central food vacuole membrane. The external membrane of the endocytic vesicles apposes that of the food vacuole, leading to the internalization of vesicles bounded by a single membrane into the vacuole space where they are rapidly degraded. We conclude from this sequence of events that endocytic vesicles fuse with the food vacuole. Treatment of infected cells with therapeutic concentrations of chloroquine inhibited the last step of the feeding process, i.e. vacuolar degradation. This was manifested by the accumulation within the vacuolar space of intact vesicles bounded by single membranes. The implications of these findings for the antimalarial activity of chloroquine are discussed.

摘要

对在人体红细胞中体外培养的恶性疟原虫进行的超微结构研究揭示了该寄生虫摄食机制的新特征。成熟滋养体和裂殖体通过胞吞作用摄取宿主细胞溶质的一部分,这种胞吞作用局限于胞口,涉及寄生泡膜和寄生虫膜的内陷。产生的被两个同心膜包围的胞吞小泡向中央食物泡膜迁移。胞吞小泡的外膜与食物泡的外膜并置,导致由单层膜界定的小泡内化到泡腔空间,在那里它们迅速被降解。从这一系列事件中我们得出结论,胞吞小泡与食物泡融合。用治疗浓度的氯喹处理感染细胞可抑制摄食过程的最后一步,即泡腔降解。这表现为在泡腔空间内积累由单层膜界定的完整小泡。讨论了这些发现对氯喹抗疟活性的影响。

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