Volume 19, Issue 3 (September 2015)                   Physiol Pharmacol 2015, 19(3): 208-215 | Back to browse issues page

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Nasimi P, Tabandeh M R, Vahdati A, Khatamsaz S. Busulfan induces oxidative stress- and Bcl-2 family gene-related apoptosis in epididymal sperm and testis of adult male mice. Physiol Pharmacol 2015; 19 (3) :208-215
URL: http://ppj.phypha.ir/article-1-1123-en.html
Abstract:   (5494 Views)

Introduction: Busulfan as a chemotherapeutic agent causes testicular germinal epithelium depletion and cytotoxicity in germ cells. The aim of this study was to assess antioxidant status, reactive oxygen species (ROS) generation and apoptosis-related genetic markers of adult male mouse sperm following busulfan treatment. Materials and Methods: Forty adult NMRI mice (30 ± 5 g) were divided into two groups. Control and busulfan treated group were administered with 100 &muL dimethyl sulfoxide and 3.2 mg/kg/day busulfan for 4 days, respectively. The superoxide dismutase and glutathione peroxidase assays were used for analyzing antioxidant status. Then, the levels of Bcl-2 family gene expression, lipid peroxidation and cytotoxicity were evaluated by Real-Time PCR, thiobarbituric and lactate dehydrogenase assays, respectively. Results: The results showed significant decrease on antioxidant status, increase on lipid peroxidation and lactate dehydrogenase in epididymal sperm and testis of busulfan treated mice in comparison with control (P< 0.05). Real Time PCR demonstrated significantly increased-Bax gene expression and decreased-Bcl-2 gene expression in epididymal sperm of treated group (P< 0.05). Conclusion: The high levels of lipid peroxidation and lactate dehydrogenase revealed increased-ROS and severe cytotoxicity in epididymal sperm and testis tissue following busulfan treatment at clinical dose. The oxidative stress and increased-ROS may induce Bcl-2 family gene expression-related apoptosis following busulfan therapy in normal cells.

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