Volume 54, Issue 5
  • ISSN: 0002-9637
  • E-ISSN: 1476-1645



Growth of the human malaria parasite, , within the red blood cell (RBC) requires external Ca and is associated with a markedly elevated intracellular Ca concentration, [Ca]. We used Ca flux studies and patch clamp recordings to examine the mechanisms responsible for this increased [Ca]. The Ca flux studies indicated that net Ca entry into parasitized RBCs (PRBCs) is 18 times faster than into unparasitized RBCs. This increased accumulation rate is too rapid to be explained by inhibition of the Ca extrusion pump, an ATPase that keeps the [Ca] of unparasitized RBCs exceedingly low. Acceleration of the preexisting Ca entry, mediated by a divalent cation carrier, also cannot explain Ca accumulation in PRBCs: there are fundamental differences in substrate preference and in the effects of external Ca on Ca efflux between unparasitized RBCs and PRBCs. Patch clamp of intact PRBC surface membranes revealed rare unitary channel openings not observed on unparasitized RBCs. With 80 mM CaCl in the patch pipette, this channel carried inward current, suggesting Ca entry at a rate comparable with the observed Ca flux. These data indicate that the malaria parasite induces a novel pathway in the host RBC membrane for Ca entry and suggest that this pathway is a Ca-permeable channel.


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