Germ Cell Apoptosis and Endothelial Nitric Oxide Synthase (eNos) Expression Following Ischemia-Reperfusion Injury to Testis

• Published in: Archives of andrology 1998, Vol.41 (1), p.57-65
• Main Authors: Zini, A., Abitbol, J., Girardi, S. K., Schulsinger, D., Goldstein, M., Schlegel, P. N.
• Format: Article
• Language: English
• Subjects: Animals; Apoptosis; Biological and medical sciences; DNA Fragmentation; germ cells; Gynecology. Andrology. Obstetrics; ischemia; Male; Male genital diseases; Medical sciences; nitric oxide synthase; Nitric Oxide Synthase - metabolism; Nitric Oxide Synthase Type III; Non tumoral diseases; Organ Size; Rats; Rats, Sprague-Dawley; Reperfusion Injury - enzymology; Reperfusion Injury - pathology; Spermatozoa - enzymology; Spermatozoa - pathology; Staining and Labeling - methods; testis
• ISSN: 0148-5016; 1521-0375
• DOI: 10.3109/01485019808988547

There is evidence to suggest that reactive oxygen species (ROS) are involved in ischemia-reperfusion injury to the testis. Nitric oxide (NO), a ubiquitous free radical produced by the nitric oxide synthases (NOS), has been implicated in physiologic and pathologic interactions with ROS. We examined the effect of testicular ischemia on germ cell apoptosis and endothelial NOS (eNOS) expression. Adult rats were subjected to unilateral 720° testicular torsion for 1 or 3 hours and 24 hours later, testes were harvested for immunohistochemical studies. Apoptosis was detected by in situ 3′ end-labeling of DNA with digoxigenin-ddUTP and eNOS protein was detected using an eNOS monoclonal antibody. Testes subjected to 3 hours of torsion had a threefold increase in apoptotic germ cells per cross-sectionai area compared to sham testes (P