Chapter 3 Erythrocyte Aging

This chapter discusses erythrocyte aging and the factors responsible for it. The mammalian erythrocyte is a unique model for the study of aging at the cellular and molecular levels, partly because it is devoid of organelles and incapable of protein synthesis. Erythrocyte aging is accompanied by the inactivation of cellular enzymes (including enzymes of antioxidative defense) and of many membrane transporters. Some of the most important functional impairments are increased hemoglobin oxygen affinity and decreased cellular deformability of aged red blood cells. There are no gross alterations in the composition of membrane proteins, but products of proteolytic degradation of Band 3 accumulate and the ratio of Band 4.1a/b increases. The latter phenomenon may be a basis for the assessment of mean red cell age in a sample. Senescent erythrocytes bind immunoglobulin G, which may take part in their elimination from the circulation. Damage of cellular constituents by reactive oxygen species may significantly contribute to the aging processes. There are various hypotheses on the mechanism of selective recognition and removal of senescent red cells invoking decreased deformability, phosphatidylserine exposure on the cell surface, and the appearance of a senescent cell antigen on molecules of the Band 3 protein (anion exchange protein).