Factors that accelerate or retard red blood cell senescence.

This article explores information concerning alterations in the time of age-related red blood cell (rbc) death (rbc senescence) in experimental animals and humans. Those factors that accelerate or retard the mean time for senescent death [the mean potential rbc life-span, (T)] are discussed; specifically excluded are conditions in which rbc survival is shortened due to an increase in the rate of age-independent [random hemolysis, (k)]rbc death. The factors prolonging senescence are reduction in metabolic rate through hibernation, reduced environmental temperature, hypophysectomy and thyroidectomy, and splenectomy. In general, these processes prolong rbc senescence by about 10%-15% in the models studied to date. The failure of splenectomy to prolong rbc senescence to any physiologically meaningful extent casts serious doubt on the concept that splenic processes are a major factor in the senescence process. Rbcs made under conditions of increased erythropoiesis and/or increased metabolic rate show acceleration of senescence. Thus, rbcs of animals treated with thyroxine show a 15% acceleration of senescence. "Stress reticulocytes" and normal full-term human newborn rbc may show up to 25% reduction in (T). The maximum acceleration seen to date is 50%-90%, as seen in the rbcs of the fetal and newborn rat. rbc senescence is not accelerated in rats with splenomegaly and increased rates of random hemolysis, again casting strong doubts on the spleen's ability to alter rbc senescence by progressively modifying the rbc during successive passages through that organ. It is postulated that rbc senescence is mainly a function of the red cell's initial endowment, particularly in the dynamic ability of that cell (and its membrane) to adapt to cumulative stresses that exist during its circulation through the body.