Cryptorchidism induces mouse testicular germ cell apoptosis and changes in bcl-2 and bax protein expression.

Up to half of the germ cells die during their development. The mechanism involved in their death is still unclear. We investigated the possibility that the testicular germ cell loss may be due to a change in the testicular temperature and apoptosis through the interplay of bcl-2 and bax proteins. To investigate the effect of temperature on apoptosis and the role of bcl-2 and bax proteins in apoptosis in adult mouse testis, we used the experimental unilateral cryptorchidism model. We found that the weight of the affected testis decreases in 6 to 15 days after operation (p < 0.05). H&E staining showed vacuolization of the seminiferous epithelium and the appearance of multinucleated giant cells with loss of germ cells. The terminal deoxynucleotidyl transferase-mediated dUTP nick-end-labeling method (TUNEL) showed positive staining germ cells scattered in normal testicles that increased significantly 6 to 15 days after experimental cryptorchidism (p < 0.05). Positive cells were mainly primary spermatocytes and round spermatids. DNA ladder was seen in 1.5% agarose gel electrophoresis in 6 to 15 days-operated testicles. Biotin-avidin DCS system indirect immunofluorescence technique indicated that the bcl-2 protein was chiefly distributed in the cytoplasm of germ cells in normal testicles, whereas the bax protein was chiefly expressed in the cytoplasm of germ cells in 6 to 15 days-operated testicles. Western blot analysis showed that the bcl-2 protein down-regulated and the bax protein up-regulated apoptosis. Our data indicated that cryptorchidism-induced testicular cell degeneration was mediated by apoptosis probably as the result of increased temperature in the testicle; bcl-2 and bax proteins played important roles in male germ cell apoptosis.