Cocaine induced apoptosis in rat testes

Purpose: Exposure of rats to chronic cocaine results in disruption of sperm atogenesis including reduction of germ cells. However, the cellular mechani sm responsible for the testicular damage in testes is still unknown. We hav e studied the role of apoptosis in cocaine induced testicular damage. Materials and Methods: Thirty-day-old male Sprague-Dawley rats were given c ocaine hydrochloride (15 mg./kg. body weight) subcutaneously daily for 90 d ays. Control animals received equal volumes of normal saline daily for 90 d ays. Testes were removed at 15, 30, 60, and 90 days of cocaine administrati on. In situ detection of germ cells with DNA strand breaks in paraffin-embe dded testicular section (5 mu m.) was achieved by the terminal deoxynucleot idyl transferase (TdT)-mediated dUTP in situ nick end-labeling (TUNEL) meth od. DNA fragmentation was also determined by gel electrophoresis. Results: Apoptotic cells were found in the spermatocytes and spermatogonia of germinal epithelium. Less than 7% of seminiferous tubule cross sections showed a high level of apoptosis (greater than or equal to 3 apoptotic cell s per tubule) in control animals compared with experimental group where 25% of the tubules showed a high level of apoptosis (p <0.05). The number of a poptotic cells was significantly increased by 15 days, peaked at 30 days an d persisted up to 90 days of cocaine exposure when compared with controls ( p <0.05). DNA isolated from the cocaine treated testes displayed a clear la dder pattern whereas the DNA from controls did not. Conclusions: The experimental results presented here suggest that cocaine e xposure leads to significant apoptosis in rat testes and the mechanism of c ocaine induced testicular injury may be related to the induction of apoptos is.