Akademik Veri Yönetim Sistemi
ANDROLOGIA, cilt.40, sa.1, ss.38-43, 2008 (SCI-Expanded)
In the present study, we aimed to evaluate the effects of dehydroepiandrosterone (DHEA) on apoptosis of testicular germ cells after repair of testicular torsion in rats. Twenty-four adult male Sprague-Dawley rats were randomly divided into four groups, with six rats in each group: sham operation, torsion/detorsion (T/D), T/D + vehicle, and T/D + DHEA. Three hours before detorsion, 50 mg kg(-1) DHEA was given intraperitoneally to T/D + DHEA group. In all groups, bilateral orchiectomies were performed and both testicles were histologically examined, with apoptosis detected using the in situ DNA fragmentation [terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL)] system, with morphological damage detected using a four-level grading scale in each specimen. The testes of the sham group showed a normal histology. In T/D and T/D + vehicle groups, apoptotic spermatogonia and spermatocyte number were significantly higher than in the sham group (P < 0.01 for all). The T/D + DHEA group showed a reduction in apoptotic spermatocyte and spermatogonia number in seminiferous epithelia compared with T/D group (P < 0.01 for both). Apoptotic cell number of contralateral testes did not reveal any significant differences among these groups (P > 0.05). Specimens from T/D and T/D + vehicle had a significantly greater histological injury than sham and T/D + DHEA groups in the ipsilateral testes (P < 0.01 for both). Therefore, the results suggest that DHEA may be a protective agent for preventing apoptosis caused by testicular torsion.