Abstract
The hemolytic nature of experimental protein deprivation (PD) anemia has been established (1) by in vitro evidence of (a) the abnormal hemolytic behavior of the PD erythrocytes and an impairment of their reactivity to the protective effect of normal serum and certain of its fractions, and (b) the defective antihemolytic potency of PD serum towards both PD and normal erythrocytes; and (2) by in vivo evidence of the PD erythrocytes’ decreased survival potential.
The hypersensitivity of the PD erythrocytes to chemical and mechanical trauma is interesting, in view of the fact that the cell population is heterogeneous and during the late stage actually includes a slightly elevated percentage of young forms which, normally, should be less sensitive to such trauma. Hence the findings of decreased chemical, alkali and mechanical resistance and increased osmotic resistance in vitro, decreased in vivo survival potential, and impaired responsiveness to in vitro protection by normal serum, lecithin and cholesterol against hemolytic factors, all point to a cellular origin, namely a structural defect, as the cause of the hemolytic nature of experimental PD anemia.
It is probable that the defective composition of PD serum which is less effective than normal serum in protecting normal erythrocytes against chemical, alkali and mechanical trauma in vitro, also contributes to the hemolytic nature of experimental PD anemia in the rat.
