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Functional state of the plasma membrane Ca 2+ pump in Plasmodium falciparum ‐infected human red blood cells
Author(s) -
Tiffert Teresa,
Staines Henry M.,
Ellory J. Clive,
Lew Virgilio L.
Publication year - 2000
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.2000.00125.x
Subject(s) - plasmodium falciparum , ionophore , red blood cell , biophysics , red cell , biology , membrane potential , chemistry , microbiology and biotechnology , membrane , biochemistry , malaria , immunology , medicine
1 The active Ca 2+ transport properties of malaria‐infected, intact red blood cells are unknown. We report here the first direct measurements of Ca 2+ pump activity in human red cells infected with Plasmodium falciparum , at the mature, late trophozoite stage. 2 Ca 2+ pump activity was measured by the Co 2+ ‐exposure method adapted for use in low‐K + media, optimal for parasitised cells. This required a preliminary study in normal, uninfected red cells of the effects of cell volume, membrane potential and external Na + /K + concentrations on Ca 2+ pump performance. 3 Pump‐mediated Ca 2+ 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 effect was prevented by clotrimazole, an inhibitor of the Ca 2+ ‐sensitive K + (K Ca ) channel, suggesting that it was due to minor cell dehydration. 4 The Ca 2+ ‐saturated Ca 2+ extrusion rate through the Ca 2+ 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 (co‐culture). Thus, Ca 2+ pump function is largely conserved in parasitised cells up to the mature, late trophozoite stage. 5 A high proportion of the ionophore‐induced Ca 2+ load in parasitised red cells is taken up by cytoplasmic Ca 2+ buffers within the parasite. Following pump‐mediated Ca 2+ removal from the host, there remained a large residual Ca 2+ pool within the parasite which slowly leaked to the host cell, from which it was pumped out.