No abstract

Testis torsion-induced aspermatogenesis is not necessarily due to permanent loss of blood flow nor to dysfunctional Leydig cells or Sertoli cells. This investigation was undertaken to gain further insight into the mechanism underlying torsion-induced germ cell loss. Male rats were subjected to 1-h or 2-h ischemia-inducing torsion, and testes were examined at either 1, 2, 4, 24, or 48 h after torsion, depending on the study. Testes were examined for evidence of 1) in situ apoptosis by the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate (dUTP)-biotin nick-end labeling (TUNEL) technique, 2) apoptosis by the DNA "laddering" technique, 3) leukocyte margination and diapedesis in testicular vessels by immunocytochemical and histological techniques, and 4) testicular lipid peroxidation by the thiobarbituric acid reactive substances assay. The first TUNEL evidence for torsion-induced apoptosis was at 4 h after repair of 1-h torsion. Induction of apoptosis was confirmed by the electrophoretic laddering of DNA fragments. It was hypothesized that apoptosis was induced by reactive oxygen species arising from reperfusing leukocytes. A significant increase in both leukocyte margination and diapedesis occurred 4 h after torsion repair as did a significant increase in intratesticular lipid peroxidation products. These events were contemporaneous with the first appearance of apoptosis and consistent with the hypothesis that post-torsion, germ cell-specific apoptosis is induced by reactive oxygen species.

To examine the precise localization of lysosomal cysteine proteinases, cathepsins B, H, and L in rat epididymal epithelial cells, immunohistochemistry and enzyme assay were applied to the epididymal tissue. Granular immunodeposits for cathepsins B and H were detected in epididymal epithelial cells, whereas faint or no immunoreactivity for cathepsin L was found. Moreover, immunoreactivity for cathepsin B appeared mainly in principal cells and was more intense in the head of the epididymis than in the tail, whereas that for cathepsin H appeared in both principal and dear cells and was more intense in the tail than the head. By enzyme assay, activities of cathepsins B and H showed a similar distri-

The effect of cis-diamminedichloroplatinum (cisplatin: CDDP) on mouse spermatozoa was evaluated quantitatively by means of equilibrium sedimentation in Percoll. CDDP was administered subcutaneously at doses of 1, 3, and 10 mg/kg/week for 5 weeks. After different periods (1, 3, and 10 weeks) without CDDP, the quality of epididymal sperm was evaluated by sperm count, motility, morphology of sperm, and the apparent density of sperm. At 10 mg/kg dose, about 80% mortality occurred during the administration period. There were no sperm even 10 weeks after discontinuing CDDP. With the 3 mg/ kg dose, sperm count, motility, and normal morphology of sperm declined after 1 and 5 weeks, but recovered to the control level after 10 weeks. The sperm distribution profiles in the Percoll gradient were quite different among the groups. The control sperm showed two separated peaks in the gradient, whereas the peak of sperm at 1 and 3 mg/kg were shifted forward to lighter apparent density. CDDP causes a reduction in sperm apparent density and impairs semen quality in mice.

This study suggests the efficacy of early intervention in patients with undescended testes.