Low sperm quality and increased testicular caspases in chronic stress mice induced by dexamethasone.

Abstract

Chronic stress (CS) from physical stressors and glucocorticoid administrations has been shown to induce germ cell apoptosis and low sperm quality. Among CS animal models, the effects of dexamethasone induced CS (DexCS) on testicular apoptosis and epididymal sperm parameters have not been fully demonstrated. This study aimed to investigate the changes of male reproductive system after CS induction by Dex. Adult male mice were divided into control and DexCS groups. Control mice were injected with sodium phosphate while DexCS mice were injected with DEX (4 mg/kg BW) for 21 consecutive days. The stress tests (sucrose preference, tail suspension, and forced swimming) were used to confirm CS behaviors. Sperm concentration, motility, morphology, viability, and acrosome status were assessed using computer-assisted semen analysis (CASA) and special staining. Histopathology of testis, epididymis, and penis was observed. Apoptotic protein expressions (Hsp70, caspases 3 and 9) in the testicular lysate were also determined. The results revealed that DexCS mice had significant increase of the immobility periods with decrease of total sucrose intake. DexCS significantly decreased sperm quality parameters particularly progressive motility. Testicular damages and decreased sperm mass in epididymis were obviously found in DexCS group. The expressions of testicular caspases 3 and 9, but not Hsp 70 were significantly increased in DexCS group compared to the control. It was concluded that DEX is a potential drug to induce chronic stress in mouse model, affecting male reproductive system via testicular histopathology and apoptotic pathway. Such effect may cause sperm physiology impairments like low progressive motile patterns.