抄録
The life span of human red blood cells (RBCs) is approximately for 120 days, and finally destroyed in reticuloendothelial systems. In pathological conditions, RBCs fall into premature death, i.e. hemolysis. Recent studies have unveiled that senescent RBCs as well as RBCs of hemolytic anemia subjects shared the common feature of exposure of phosphatidylserine (PS) in the outer leaflet of the RBC membrane. In addition, dying RBCs showed morphological and biochemical alterations resembling to apoptosis of nucleated cells such as cell shrinkage and protein degradation. In this review, mechanisms and physiological significance of PS externalization triggered by oxidative stress are discussed.
