Article
- The EMBO Journal (2002) 21, 22 - 30
- doi:10.1093/emboj/21.1.22
Subject Categories:
Plasmodium falciparum activates endogenous Cl- channels of human erythrocytes by membrane oxidation
Stephan M. Huber1, Anne-Catrin Uhlemann1, Nikita L. Gamper1, Christophe Duranton1, Peter G. Kremsner2 and Florian Lang1
- Department of Physiology, University of Tübingen, Gmelinstrasse 5, D-72076 Tübingen, Germany
- Department of Parasitology, Institute for Tropical Medicine, University of Tübingen, Wilhelmstrasse 27, D-72074 Tübingen, Germany
Correspondence to:
Stephan M. Huber, E-mail: stephan.huber@uni-tuebingen.de
Received 2 April 2001; Accepted 13 November 2001; Revised 12 November 2001
Abstract
Intraerythrocytic survival of the malaria parasite Plasmodium falciparum requires that host cells supply nutrients and dispose of waste products. This solute transport is accomplished by infection-induced new permeability pathways (NPP) in the erythrocyte membrane. Here, whole-cell patch–clamp and hemolysis experiments were performed to define properties of the NPP. Parasitized but not control erythrocytes constitutively expressed two types of anion conductances, differing in voltage dependence and sensitivity to inhibitors. In addition, infected but not control cells hemolyzed in isosmotic sorbitol solution. Both conduct ances and hemolysis of infected cells were inhibited by reducing agents. Conversely, oxidation induced identical conductances and hemolysis in non-infected erythrocytes. In conclusion, P.falciparum activates endogenous erythrocyte channels by applying oxidative stress to the host cell membrane.
Keywords:
- hemolysis,
- human red blood cells,
- malaria,
- new permeability pathway,
- patch-clamp
