Background and Objectives: Apoptosis (programmed cell death) is an important regulatory event in spermatogenesis. Abnormally accelerated apoptosis in germ cells, may lead to an imbalance between cell proliferation and death, resulting in impairment in spermatogenic. Some studies have shown that glucocorticoids affect testialar homeostasis by decreasing of testosterone level. In the present study, the influence of dexametasone (Dex), a widely used glucocorticoid agent, on expression of FasL (Fas-Ligand) protein (a proapoptotic protein) in mouse testicular germ cells is investigated. Materials and Methods: Twenty-four adult male (6- 8 weeks) mice were randomly divided into 3 groups. The first and second test groups received 2 and 7 mg/kg Dex per day, respectively, for 7 days. The control group received only saline daily for 7 days. One day after the final injection, the mice were sacrificed and the test groups were placed in formalin solution for immunohistochemistry studies. Positive immunoreactivity was calculated by H-score method. Results: The results revealed that expression of FasL in seminiferous epithelium is spermatogenic stage dependent, and the stage VII was the most susceptible to Dex. FasL expression was observed only at stages VII-VIII of spermatogenic cycle in 2 mg/kg Dex treated group (P<0.05). H-score was significantly increased in all stages of 7 mg/kg Dex treated group (P<0.05). The number of spermatocytes decreased significanhy in this group. Conclusions: It appears that glucocorticoid agents such as Dex, induces apoptosis by affecting proapoptotic proteins.
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