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Titolo:
Passive Ca2+ transport and Ca2+-dependent K+ transport in Plasmodium falciparum-infected red cells
Autore:
Staines, HM; Chang, W; Ellory, JC; Tiffert, T; Kirk, K; Lew, VL;
Indirizzi:
Univ Oxford, Physiol Lab, Oxford OX1 3PT, England Univ Oxford Oxford England OX1 3PT Physiol Lab, Oxford OX1 3PT, England Australian Natl Univ, Fac Sci, Div Biochem & Mol Biol, Canberra, ACT 0200,Australia Australian Natl Univ Canberra ACT Australia 0200 erra, ACT 0200,Australia Univ Cambridge, Physiol Lab, Cambridge CB2 3EG, England Univ Cambridge Cambridge England CB2 3EG Lab, Cambridge CB2 3EG, England
Titolo Testata:
JOURNAL OF MEMBRANE BIOLOGY
fascicolo: 1, volume: 172, anno: 1999,
pagine: 13 - 24
SICI:
0022-2631(19991101)172:1<13:PCTACK>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
CYTOSOLIC FREE CALCIUM; PARASITE P-CHABAUDI; HUMAN-ERYTHROCYTES; BLOOD-CELLS; CA-2+ CONCENTRATION; PUMP; PERMEABILITY; METABOLISM; POTASSIUM; CHANNEL;
Keywords:
calcium transport; potassium transport; red cells; Plasmodium falciparum;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
60
Recensione:
Indirizzi per estratti:
Indirizzo: Staines, HM Univ Oxford, Physiol Lab, Parks Rd, Oxford OX1 3PT, England Univ Oxford Parks Rd Oxford England OX1 3PT OX1 3PT, England
Citazione:
H.M. 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

Abstract

Previous reports have indicated that Plasmodium falciparum-infected red cells (pRBC) have an increased Ca2+ permeability. The magnitude of the increase 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, we have reassessed both the functional status of the K-Ca channel and the Ca2+ permeability properties of pRBC. For pRBC suspended in media containingCa2+, K-Ca channel activation was elicited by treatment with the Ca2+ ionophore A23187. In the absence of ionophore the channel remained inactive. Incontrast 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 normal 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 media the Ca2+ influx increased to over 1 mmol (1013 cells . hr)(-1), almost an order of magnitude higher than that seen in uninfected erythrocytes under equivalent conditions. The pathway responsible for the enhanced influx of Ca2+ into glucose-deprived pRBC was expressed at approximately 30 hr post-invasion, and was inhibited by Ni2+. Possible roles for this pathway in pRBC are considered.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/09/20 alle ore 11:28:44