الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Eryptosis, the suicidal death of erythrocytes, is characterized by cell shrinkage, membrane blebbing and cell membrane phospholipid scrambling with phosphatidylserine exposure at the cell surface. Phosphatidylserine-exposing erythrocytes are recognized by macrophages, which engulf and degrade the affected cells. Diseases associated with accelerated eryptosis include sepsis, malaria, sickle-cell anemia, b-thalassemia, glucose-6-phosphate dehydrogenase (G6PD)-deficiency, phosphate depletion, iron deficiency, spherocytosis and Wilsons disease. Eryptosis may be inhibited by erythropoietin, adenosine, catecholamines, nitric oxide and activation of G-kinase. Eryptosis is an important physiological mechanism allowing erythrocytes to escape hemolysis. On the other hand, accelerated eryptosis leads to anemia, due to excessive loss of circulating erythrocyte. Thus, a delicate balance between proeryptotic and antieryptotic mechanisms is required to maintain an adequate number of circulating erythrocytes and yet avoid noneryptotic death of injured erythrocytes.