Hm. Staines et al., Passive Ca2+ transport and Ca2+-dependent K+ transport in Plasmodium falciparum-infected red cells, J MEMBR BIO, 172(1), 1999, pp. 13-24
Previous reports have indicated that Plasmodium falciparum-infected red cel
ls (pRBC) have an increased Ca2+ permeability. The magnitude of the increas
e is greater than that normally required to activate the Ca2+-dependent Kchannel (K-Ca channel) of the red cell membrane. However, there is evidence
that this channel remains inactive in pRBC. To clarify this discrepancy, w
e have reassessed both the functional status of the K-Ca channel and the Ca
2+ permeability properties of pRBC. For pRBC suspended in media containing
Ca2+, K-Ca channel activation was elicited by treatment with the Ca2+ ionop
hore A23187. In the absence of ionophore the channel remained inactive. In
contrast to previous claims, the unidirectional influx of Ca2+ into pRBC in
which the Ca2+ pump was inhibited by vanadate was found to be within the n
ormal range (30-55 mu mol (10(13) cells . hr)(-1)), provided the cells were
suspended in glucose-containing media. However, for pRBC in glucose-free m
edia the Ca2+ influx increased to over 1 mmol (1013 cells . hr)(-1), almost
an order of magnitude higher than that seen in uninfected erythrocytes und
er equivalent conditions. The pathway responsible for the enhanced influx o
f Ca2+ into glucose-deprived pRBC was expressed at approximately 30 hr post
-invasion, and was inhibited by Ni2+. Possible roles for this pathway in pR
BC are considered.