Uptake of L-tryptophan by erythrocytes infected with malaria parasites (Plasmodium falciparum).
The initial rates of uptake of L-tryptophan into normal human red blood cells and into cells infected by the malarial parasite Plasmodium falciparum in vitro, were investigated. We find that transport in non-infected cells, which is mediated by the specific saturable T system and the apparently non-saturable L system (Rosenberg, Young and Ellory (1980) Biochim. Biophys. Acta 598, 375-384) is considerably enhanced by blood preservation and culture conditions. This increase is mostly due to an increase in the maximal velocity of the saturable component and of the rate constant of the linear component. Uptake is further enhanced in non-infected cells by factors released from infected cells into the culture medium and, even more so, in infected cells at the advanced stage of intraerythrocytic parasite development. At these stages the susceptibility of the transport system to the non-specific inhibitor phloretin and to the competitive inhibitor phenylalanine, is virtually lost. The effect of the parasite on L-tryptophan uptake by the host cell membrane is exerted only on the maximal velocity of the T system, which is carrying most of the substrate under physiological conditions. The possible implications of these findings to the life of the intraerythrocytic parasite are briefly discussed.
D001692:Biological Transport / Q000187:drug effects; D002738:Chloroquine / Q000494:pharmacology; D004912:Erythrocytes / Q000187:drug effects / Q000378:metabolism*; D006801:Humans; D007700:Kinetics; D008288:Malaria / Q000097:blood; D010649:Phenylalanine / Q000494:pharmacology; D010693:Phloretin / Q000494:pharmacology; D010963:Plasmodium falciparum / Q000502:physiology*; D012016:Reference Values; D014364:Tryptophan / Q000097:blood*
D010649:Phenylalanine; D002738:Chloroquine; D014364:Tryptophan; D010693:Phloretin