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 Blood, 1 November 2006, Vol. 108, No. 9, pp. 3187-3194.
Prepublished online as a Blood First Edition Paper on July 13, 2006; DOI 10.1182/blood-2006-02-001693.

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RED CELLS

Solute transport via the new permeability pathways in Plasmodium falciparum–infected human red blood cells is not consistent with a simple single-channel model

Henry M. Staines, Stephanie Ashmore, Hannah Felgate, Jessica Moore, Trevor Powell, and J. Clive Ellory

From the Centre for Infection, Division of Cellular and Molecular Medicine, St George's, University of London, London, United Kingdom; and the University Laboratory of Physiology, Oxford, United Kingdom.

After infection of a red blood cell (RBC), the malaria parasite, Plasmodium falciparum, increases the permeability of the host's plasma membrane by inducing new permeability pathways (NPPs). Single-channel patch-clamp experiments have shown the presence in infected RBCs of novel anion-selective channel types with low open-state probabilities at positive membrane potentials. These channels have been postulated to form the NPPs. Here, we have used a range of transport techniques to study whether electroneutral solutes use these channels or altered/separate pathways. Transport of the electroneutral solute sorbitol via the NPPs was found to increase by a small but significant amount after gross membrane depolarization. This is inconsistent with transport via a channel with a reduced open-state probability at positive membrane potentials. As has been demonstrated previously for parasite-induced anion currents, sorbitol transport in infected RBCs was found to be sensitive to the presence of bovine serum albumin (BSA). However, it remains to be shown whether the effect is due to serum/BSA altering a single channel type or activating a new pathway. In addition, the study highlights problems that can occur when using different transport techniques to study the NPPs.


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