ABSTRACT
During the asexual intraerythrocytic stage of malaria and babesia parasites, membrane transport pathways are induced in the host erythrocyte that have substrate selectivities dependent upon the parasite species. In the present paper we review some recent findings which show that, in addition to the wide range of solutes described previously, two positively charged substrates, choline and L-carnitine (but not the basic amino acid L-lysine), and the anionic substrate 2-oxoglutarate (aketoglutarate) have enhanced transport into Plasmodium falciparum-infected human erythrocytes. In contrast to the parasite-induced influx of L-carnitine, acetylL-carnitine remains almost excluded from the parasitized human red cell. Normal human red cells seem to lack constitutive transport systems for both L-carnitine and the acetylated derivative, whereas a saturable endogenous transport system for choline influx has been well characterized. The cinchona alkaloids (quinine and quinidine) selectively inhibit both the P. falciparum-induced choline influx and the constitutive choline transport systems, but have no inhibitory effects on the parasiteinduced influx of 2-oxoglutarate (or of L-glutamine). These data indicate that heterogeneous and functionally separate transport systems for anionic and cationic substrates (and possibly amino acids) are induced during the maturation of P. falciparum trophozoites.
