Journal
ANDROLOGIA
Volume 42, Issue 4, Pages 247-253Publisher
WILEY
DOI: 10.1111/j.1439-0272.2009.00985.x
Keywords
Apoptosis; dexamethasone; spermatogenesis
Categories
Funding
- research council of the Ahwaz Jundi-Shapour University of Medical Sciences [u-86044]
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P>Exposure to glucocorticoids (GCs) leads to numerous changes in various biological systems including the reproductive system. This work evaluated effects of dexamethasone (Dex), a widely used GC, on mouse testicular germ cells. Experimental groups (E1-E3) received one of the following treatments daily for 7 days: 4, 7 and 10 mg kg-1 Dex respectively. Control groups were treated with equivalent volumes of saline. Testicular histopathology, morphometric analysis and deoxy-UTP-digoxigenin nick end labeling (TUNEL) assessment were performed for evaluation of the toxic effects of Dex and detection of the apoptotic cells. The results showed that Dex induces histopathological alterations such as epithelial vacuolisation, atrophy and reduction in testicular spermatozoid. Morphometrical data showed that Dex significantly reduced tubular diameter and epithelial height (P < 0.05). Johnsen's scoring also showed poor spermatogenesis in E2 and E3 groups (P < 0.05). Apoptotic index of germ cells was significantly increased in E2 (18.9% versus 1.76%, P < 0.01) and E3 (24.6 versus 1.76%, P < 0.001) groups. It is concluded that Dex acts as testicular toxicant and that further studies are needed to establish its mechanism of action upon spermatogenesis.
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