Functional state of the plasma membrane Ca2+ pump in Plasmodium falciparum-infected human red blood cells

1. The active Ca2+ transport properties of malaria-infected, intact red blo od cells are unknown. We report here the first direct measurements of Ca2pump activity in human red cells infected with Plasmodium falciparum, at th e mature, late trophozoite stage. 2. Ca2+ pump activity was measured by the Co2+-exposure method adapted for use in low-K+ media, optimal for parasitised cells. This required a prelimi nary study in normal, uninfected red cells of the effects of cell volume, m embrane potential and external Na+/K+ concentrations on Ca2+ pump performan ce. 3. Pump-mediated Ca2+ extrusion in normal red cells was only slightly lower in low-K+ media relative to high-K+ media despite the large differences in membrane potential predicted by the Lew-Bookchin red cell model. The effec t was prevented by clotrimazole, an inhibitor of the Ca2+-sensitive K+ (K-C a) channel, suggesting that it was due to minor cell dehydration. 4. The Ca2+-saturated Ca2+ extrusion rate through the Ca2+ pump (V-max) of parasitised red cells was marginally inhibited (2-27%) relative to that of both uninfected red cells from the malaria-infected culture (cohorts), and uninfected red cells from the same donor kept under identical conditions (c o-culture). Thus, Ca2+ pump function is largely conserved in parasitised ce lls up to the mature, late trophozoite stage. 5. A high load in parasitised red cells is taken up by A high proportion of the ionaphore-induced Ca2+ load in parasitised red cells is taken up by cy toplasmic Ca2+ buffers within the parasite. Following pump-mediated Ca2+ re moval from the host, there remained a large residual Ca2+ pool within the p arasite which slowly leaked to the host cell, from which it was pumped out.