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The previous studies have showed that endosulfan induced male reproductive toxicity and oxidative stress is related to its toxicity.However, the effect of endosulfan on meiosis process and its mechanism are still unknown.The present study was designed to investigate the effect of endosulfan on meiosis process in vivo and cell cycle in spermatogenic cell in vitro.In vivo study, 32 rats were divided into 4 groups, treated with 0, 1, 5 and 10 mg/kg endosulfan per day, respectively, and sacrificed after the 21 successive treatments.Results showed that endosulfan caused the reductions in concentration, motility rate of sperm and index of testes, resulted in the increases in abnormality rate of sperm, ROS level and expression of 8-OHdG.Endosulfan also induced down-regulation of Sohlh1, which is a factor of controling the switch on meiosis in mammals, and depressed the expressions of Cyclin A 1, CDK1 and CDK2, which are the regulating factors of meiosis process in testicular tissue.Moreover, in vitro study, after treatment with various concentrations of MT (0, 15, 20 and 25 μg/mL) for 18 h, the GC-1 spg cells were treated with endosulfan (24 μg/mL) for 24 h.Results in vitro showed that 24 μg/mL endosulfan led to a reduction in cell viability,resulted in increases in MDA level and the degree of DNA damage, While 20 μg/mL MT significantly relieved the changes of both cell viability and degree of DNA caused by endosulfan;endosulfan caused cell cycle arrest and proliferation inhibition, and damaged the mitochondrial structures in GC-1 spg cells.The results suggested that endosulfan could lead to the decrease of sperm amount by inhibiting the start of meiosis process and spermatophore development through down-regulating the expression of Sohlh1 on one hand, and by depressing the meiosis process of spermatogenic cell via decreasing the expression of Cyclin A1, CDK1 and CDK2 on the other hand, which resulted in cell cycle arrest at G2/M phase.Besides, endosulfan could reduce sperm quality by directly damaging the DNA in testicular tissue and mitochondrial structures in spermatogenic cell resulted from oxidative stress.The finding provides new evidence to explain the mechanism of endosulfan-induced male reproductive toxicity.