The study of Bax protein expression in Dexamethasone induced apoptosis in spermatogenic cells in mice

Some studies have shown that glucocorticoids affect testis homeostasis by decreasing testosterone level. In this study the influence of dexametasone (Dex), a widely used glucocorticoid drug, was evaluated on expression of Bax protein in mice testicular germ cells and spermatogenesis process. In this experimental study thirty five adult male mice randomly divided into 5 groups. Test groups (T1-T4) received 2, 4, 7 and 10 mg/kg Dex per day for 7 days, respectively. Control group received only saline daily for 7 days. Then the mice were sacrificed and their testes were incubated in formalin for immunohistochemistry and histology studies. T1 and T2 groups, which received 7 and 10 mg/kg Dex, showed significant decrease in the number of germ cells and somatic cells of testes, and also in the maturity of spermatogenesis (p<0.05). Immunohistochemical studies showed that Dex with doses of 7 and 10 mg/kg significantly increased Bax expression at all stages of spermatogenesis cycle except stage IX. It seems that glucocorticoid drugs such as Dex induce apoptosis in testicular germ cells by affecting proapoptotic proteins and causing defect in spermatogenesis process.