ArticleThe Journal of general physiology2004
Organic osmolyte permeabilities of the malaria-induced anion conductances in human erythrocytes.
Article in The Journal of general physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 44 citations in OpenAlex.
- Down the membrane hole: Ion channels in protozoan parasites.PLoS pathogens · 2022Review
- Article
- Malaria parasite clag3 genes determine channel-mediated nutrient uptake by infected red blood cells.Cell · 2011Article
- Parameterization of high magnetic field gradient fractionation columns for applications with Plasmodium falciparum infected human erythrocytes.Malaria journal · 2010Article
- Malaria parasite mutants with altered erythrocyte permeability: a new drug resistance mechanism and important molecular tool.Future microbiology · 2010Review
- Physiological tonicity improves human chondrogenic marker expression through nuclear factor of activated T-cells 5 in vitro.Arthritis research & therapy · 2010Article
- The Plasmodium falciparum-induced anion channel of human erythrocytes is an ATP-release pathway.Pflugers Archiv : European journal of physiology · 2009Article
- Toward a unifying model of malaria-induced channel activity.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- A blasticidin S-resistant Plasmodium falciparum mutant with a defective plasmodial surface anion channel.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Article
- Specific inhibition of the plasmodial surface anion channel by dantrolene.Eukaryotic cell · 2006Article
- Permselectivity and pH-dependence of Plasmodium falciparum-induced anion currents in human erythrocytes.Pflugers Archiv : European journal of physiology · 2005Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infection of human erythrocytes with the malaria parasite Plasmodium falciparum induces new permeability pathways (NPPs) in the host cell membrane. Isotopic flux measurements demonstrated that the NPP are permeable to a wide variety of molecules, thus allowing uptake of nutrients and release of waste products. Recent patch-clamp recordings demonstrated the infection-induced up-regulation of an inwardly and an outwardly rectifying Cl(-) conductance. The present experiments have been performed to explore the sensitivity to cell volume and the organic osmolyte permeability of the two conductances. It is shown that the outward rectifier has a high relative lactate permeability (P(lactate)/P(Cl) = 0.4). Sucrose inhibited the outward-rectifier and abolished the infection-induced hemolysis in isosmotic sorbitol solution but had no or little effect on the inward-rectifier. Furosemide and NPPB blocked the outward-rectifying lactate current and the sorbitol hemolysis with IC(50)s in the range of 0.1 and 1 microM, respectively. In contrast, the IC(50)s of NPPB and furosemide for the inward-rectifying current were >10 microM. Osmotic cell-shrinkage inhibited the inwardly but not the outwardly rectifying conductance. In conclusion, the parasite-induced outwardly-rectifying anion conductance allows permeation of lactate and neutral carbohydrates, whereas the inward rectifier seems largely impermeable to organic solutes. All together, these data should help to resolve ongoing controversy regarding the number of unique channels that exist in P. falciparum-infected erythrocytes.
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