ALTERED MEMBRANE PHOSPHOLIPID ORGANIZATION AND ERYTHROPHAGOCYTOSIS INE-BETA-THALASSEMIA

The underlying cause behind the accelerated destruction of erythrocyte s in the bone marrow and in the peripheral circulation, accompanying t he beta-thalassemic syndromes is still not clearly understood. The pre sent investigation demonstrates that increased phagocytosis of erythro cytes in E beta-thalassemia is inhibited by the presence of phosphatid ylserine (PS) vesicles, suggesting a PS-'PS-receptor' type of interact ion in premature recognition of these erythrocytes by macrophages. Inc reased exposure of both aminophospholipids phosphatidylethanolamine (P E) and PS was demonstrated by fluorescamine labeling and annexin bindi ng, respectively. The slower rate of translocation of PS across the bi layer suggested that this contributed towards the increased exposure o f PS in E beta-thalassemic erythrocytes.