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Chemical and physical in vitro alterations of the erythrocyte membrane: a model for its pathophysiological states?
1Institute of Physiology, Faculty of Medicine, Rheinisch-Westfälische Technische Hochschule, Aachen, Germany.
Abstract:
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.
Insights
Plasmodium parasites alter red blood cell membranes, creating specific pathways (NPP) that differ from non-specific defects caused by experimental damage. This highlights parasite adaptation in erythrocyte membrane function.
Area of Science:
- Membrane Biology
- Parasitology
- Cellular Physiology
Background:
- Plasmodia significantly alter erythrocyte membranes, introducing xenoproteins and modifying lipid composition.
- New permeation pathways (NPP) form in infected cells, exhibiting ion selectivity and inhibitor sensitivity.
- Experimental membrane perturbations often cause non-specific barrier defects.
Purpose of the Study:
- To investigate the discrepancy between specific NPP in Plasmodium-infected cells and non-specific defects from experimental damage.
- To analyze experimental barrier defects in erythrocytes induced by electroporation and oxidative damage.
- To compare these experimental defects with those in Plasmodium-modified cells.
Main Methods:
- Induction and analysis of experimental barrier defects in erythrocytes.
- Assessment of solute permeability and phospholipid dynamics.
- Evaluation of transbilayer mobility of phospholipid probes.
Main Results:
- Experimental defects (electroporation, oxidative damage) cause non-specific alterations in erythrocyte permeability and phospholipid dynamics.
- Plasmodium-induced NPP display specific ion selectivity and inhibitor sensitivity, unlike experimental defects.
- A puzzling discrepancy exists between the specific nature of Plasmodium-induced defects and the non-specific nature of experimentally induced ones.
Conclusions:
- Plasmodium-modified erythrocytes exhibit specific barrier defects, contrasting with non-specific defects from experimental perturbations.
- The absence of comparable non-specific defects in Plasmodium-infected cells suggests evolutionary adaptation by the parasite.
- Understanding these differences provides insight into host-parasite interactions and membrane adaptation.
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