Effects of chloroquine on the feeding mechanism of the intraerythrocytic human malarial parasite Plasmodium falciparum.
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.
D000818:Animals; D002462:Cell Membrane / Q000187:drug effects / Q000648:ultrastructure; D002738:Chloroquine / Q000494:pharmacology*; D004705:Endocytosis / Q000187:drug effects; D004912:Erythrocytes / Q000469:parasitology*; D006801:Humans; D008561:Membrane Fusion / Q000187:drug effects; D008854:Microscopy, Electron; D010963:Plasmodium falciparum / Q000187:drug effects / Q000502:physiology / Q000648:ultrastructure*; D014617:Vacuoles / Q000187:drug effects / Q000648:ultrastructure
D002738:Chloroquine