Chemical and physical in vitro alterations of the erythrocyte membrane: a model for its pathophysiological states?
Plasmodia induce conspicuous structural and functional changes in the erythrocyte membrane. Besides the insertion and apposition of 'xenoproteins', and alterations of lipid composition (fatty acid pattern) and dynamics (transbilayer mobility and disposition of phospholipids, or related probes), new permeation pathways (NPP) are formed, which are still ill-defined in terms of their molecular origin. A remarkable ion selectivity and a high and complete sensitivity of the NPP to inhibitors indicate a rather specific nature. On the other hand, numerous experimental perturbations of the erythrocyte membrane structure induce unspecific alterations of its barrier function. In view of the apparent similarities--in simple physicochemical terms--between the experimentally and the plasmodially induced structural perturbations, one would expect, in Plasmodium-invaded cells, unspecific alterations of permeability and phospholipid dynamics of the type observed after in vitro modification, in contrast to much of the experimental evidence. In order to highlight this puzzling discrepancy, this chapter outlines techniques of producing and analysing experimental barrier defects in erythrocytes, and summarizes the properties of the defects induced by electroporation and oxidative damage, in terms of solute permeability, transbilayer mobility of phospholipid probes and the disposition of native phospholipids. The possible absence of comparable unspecific defects in Plasmodium-modified cells may provide an interesting example for the evolutionary adaptation of the parasite.
Deuticke
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Institute of Physiology, Faculty of Medicine, Rheinisch-Westfälische Technische Hochschule, Aachen, Germany.
D000818:Animals; D016764:Cell Polarity; D004910:Erythrocyte Membrane / Q000737:chemistry / Q000469:parasitology* / Q000502:physiology; D006801:Humans; D008288:Malaria / Q000097:blood