Membrane properties of senescent and carrier human erythrocytes.

Abstract

Studies about human red cell senescence have shown that the viability and post-transfusion survival of red cells is related to the structure of their plasma membrane.1 In an attempt to analyze the survival potential in the circulation of red cells manipulated for loading with drugs or biosubstances, we addressed our investigation to the identification of new parameters useful to describe membrane characteristics of red cells with a decreased life expectancy. In this study we have analyzed membrane properties of young, middle-aged, and senescent red cells, and compared them with those of red cells manipulated for loading, in order to discern the membrane structural lesions leading to a decreased survival potential. Removal from the circulation of senescent red cells seems to be triggered by the binding of autologous antibodies2 recognizing band 3 (B3) protein3–5, α-galactosyl groups, probably belonging to glycolipids6, and other epitopes not yet defined.5 Although the role played by autoantibodies in the removal of senescent cells has not been completely elucidated, their presence on the surface of senescent erythrocytes focused on plasma membrane studies about cell aging and raised questions about the mechanisms leading to the expression on the cell surface of the senescence antigens. Among the processes modifying the structure of membrane components and described to occur during red cell senescence, oxidation seems to play an important role.7–11 Therefore we have analyzed the oxidative state of membrane proteins in young, middle-aged and senescent normal red cells and tried to relate it with the functional activity of B3 protein12, considering that the involvement of B3 in the expression of the senescence antigen has been recognized by different authors.3–5,11 The same investigation was carried out on red cells submitted to hypotonic dialysis and resealed. The aim of this investigation was to identify steps of cell loading processes producing cell suffering and decrease of the survival potential, in order to prevent or minimize the cellular damage with appropriate protocols.