Deletion of cells by apoptosis during castration-induced involution of the rat prostate

Summary

Extensive loss of epithelial cells as a result of enhanced apoptosis was found to play a major role in castration-induced involution of the rat ventral prostate, the ultrastructural features of the phenomenon being essentially the same as those described in other tissues under both physiological and pathological conditions. Affected cells condensed and fragmented to produce membrane-bounded apoptotic bodies with morphologically intact organelles. These were either extruded into acinar lumina, where they underwent a change resembling coagulative necrosis, or were ingested by viable cells, to be rapidly degraded within phagolysosomes. The majority of the bodies were disposed of by macrophage-like cells found scattered along the basal part of the acinar lining, but some were taken up by epithelial cells. Whilst the participation of autophagy in the genesis of diffuse atrophy of remaining viable epithelial cells was confirmed, it should be stressed that the distinction between autophagic vacuoles and apoptotic bodies within heterophagosomes in epithelial cells is sometimes difficult to make.

A low basal rate of ultrastructurally typical apoptosis was observed in the prostates of normal rats, and this was moderately augmented by estradiol administration. Exogenous testosterone prevented both atrophy of epithelial cells and enhancement of apoptosis after orchidectomy. However the dose used did not completely suppress apoptosis. The results indicate that apoptosis can be triggered and inhibited in a differentiated adult tissue by hormones normally present in the blood, and suggest that the control of cell deletion might play just as important a role in the homeostasis of cell populations as does the control of mitosis.