Following invasion by the
malaria parasite there appear in the parasitized erythrocyte new ("induced") permeation pathways that mediate the transport of a wide variety of small solutes. Although
anion-selective, these pathways have a significant
cation permeability and cause a substantial increase in the basal leak of
cations into and out of the infected cell. In this study of human erythrocytes infected in vitro with Plasmodium falciparum it was shown that the transport of
monovalent cations (Rb+ and
choline), but not that of a nonelectrolyte (
sorbitol) or a monovalent
anion (
lactate), via the
malaria-induced pathways is strongly dependent on the nature of the
anion in the suspending medium. Substitution of NO3- for Cl- resulted in a 4-6-fold increase in the unidirectional influx and efflux of Rb+, and a 2-3-fold increase in the influx of
choline via the induced pathways. By contrast, replacement of Cl- with NO3- caused a slight (although not significant) decrease in the
malaria-induced influx of
sorbitol and
lactate.
Hemolysis experiments with a range of K+
salts revealed that the net influx of K+ into infected cells showed the same novel
anion dependence as seen for the unidirectional flux of Rb+ and
choline, with
hemolysis occurring much faster in iso-osmotic KNO3 and
KSCN solutions than in KCl,
KBr, or KI solutions.
Hemolysis in the corresponding Na+
salt solutions was very much slower, consistent with the induced pathways being selective for K+ over Na+, and raising the possibility that the efflux of cell K+ via these pathways may play a role in host cell volume regulation. A number of models that would account for the
anion dependence of
malaria-induced
cation transport are considered.