• Korean Journal of Veterinary Research
• /
• v.43 no.3
• /
• pp.485-492
• /
• 2003

The pathological mechanism of impaired spermatogenesis after vasectomy has not been completely investigated. In this study, we examined pathological changes of the testis and the Fas-Fas ligand (FasL) mediated signaling pathway in apoptotic germ cell death after vasectomy in rats. Ten-weeks old Sprague-Dawley rats were underwent bilateral vasectomy and sacrificed after 1 day, 2 days, 3 days, 5 days, 1 week, 2 weeks, and 4 weeks of surgery and the testes were removed. Histopathological evaluation of spermatogenesis was performed by hematoxylin-eosin and periodic acid-Schiff-hematoxylin staining. To elucidate the pathophysiology of seminiferous tubule damage, terminal dUTP nick end labeling staining, electrophoresis assay of DNA fragmentation, and Western blotting analysis for Fas-FasL were performed. Relative weights of testes were decreased from 5 days after vasectomy. Germ cell degeneration were first found in the spermatogonia and spermatocytes at stages I-VI, and XII-XIV seminiferous tubules. Mean incidence of apoptotic germ cells after vasectomy progressively increased to peak in 5 days, and then gradually decreased to the control levels in 2 weeks after vasectomy. The expression of Fas-FasL reached maximum level at 5 days after vasectomy and then declined. In conclusion, impaired spermatogenesis after vasectomy associated with an increase in germ cell apoptasis, which is partly mediated by the activation of Fas-FasL.