Permselectivity changes in malaria (Plasmodium falciparum) infected human red blood cell membranes.

摘要: The development of the malaria parasite Plasmodium falciparum in human red blood cells induces parasite-dependent perturbations permselectivity properties host cell membrane. changes appear as parasites develop from ring to trophozoite stage and persist during schizogony. In present work we assessed permeability infected anionic substances by use radioactive fluorescent probes. Our data show that i) covalent binding probes, such diisothiocyano ditritiostilbene disulfonic acid [3H]H,DIDS, which are virtually impermeant normal cells, became markedly permeant trophozoites schizonts, evidenced high labeling intracellular hemoglobin; ii) permeation anion transport substrate NBD-taurine, measured efflux mode, was very rapid substantially enhanced parasitized erythrocytes, compared with noninfected cells; iii) this could not be blocked H,DIDS, is a specific inhibitor iv) probes temperature dependent (Ea:II +I kcathole); v) nonspecific inhibitors known interact membrane lipids. appearance new pathway associated structural modification matrix. erythrocytic cycle characterized defined developmental stages growth propagation. A key role played cell, .which largely responsible for supplying metabolites removing catabolites produced obligatory (Sherman, 1979). traffic material between external milieu likely mediatd mechanisms. To what extent constituents erythrocyte can subserve growing demands internal still unknown. Although previous studies indicated functional alterations membranes 1977, 1979; Schmidt-Ullrich Wallach, 1978; Howard et al., 1980; Howard, 1982), little about cause these alterations, let alone their physiological significance. Following through various intraerythrocytic growth, recently demonstrated marked abnormalities barrier P. fulciparum developed (Kutner 1982). study investigated nature following uninfected demonstrably chemically modified cells. We have also studield effect well profiles compounds.