| Abstract: | Malarial parasites reproduce asexually inside the erythrocytes of their vertebrate host. Relatively little is known about the interaction between host cell and parasite metabolism. In the present study the effect of host cell cation composition and osmotic shrinkage on in vitro growth and propagation of Plasmodium falciparum in human erythrocytes was investigated. It is shown that throughout the parasite cell cycle, infected cells lose potassium and gain sodium. Compartment analysis of infected cells revealed that host cell cytosol is poor in potassium and rich in sodium while in the parasite this relationship is reversed, indicating that the parasite is able to regulate its ionic composition independently. Parasites proceeded normally through their cell cycle in the presence of the sodium-pump inhibitor ouabain, although host cells lost up to 75-80% of their normal potassium content. Potassium-depleted erythrocytes harboring trophozoites and schizonts also display normal rates of protein synthesis as measured by isoleucine incorporation. Parasite growth was inhibited when infected cells were osmotically shrunken in hypertonic media, but this was not due to parasite dehydration. It is suggested that increased viscosity of host cell cytosol and/or hemoglobin gelation, are responsible for the effect, probably through interference with parasite feeding. The relevance of these results to understanding of the cellular mechanism involved in the inhibiton of parasite growth in deoxygenated sickle-trait erythrocytes is discussed. |
