Endosulfan inhibiting the meiosis process via depressing expressions of regulatory factors and causing cell cycle arrest in spermatogenic cells

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• 作者：Fang-Zi Guo ; Lian-Shuang Zhang ; Jia-Liu Wei…
• 关键词：Endosulfan ; Meiosis start ; Meiosis process ; Cell cycle arrest ; Spermatogenic cell ; Rat
• 刊名：Environmental Science and Pollution Research
• 出版年：2016
• 出版时间：October 2016
• 年：2016
• 卷：23
• 期：20
• 页码：20506-20516
• 全文大小：2,042 KB
• 刊物类别：Earth and Environmental Science
• 刊物主题：Environment
  Environment
  Atmospheric Protection, Air Quality Control and Air Pollution
  Waste Water Technology, Water Pollution Control, Water Management and Aquatic Pollution
  Industrial Pollution Prevention
  
• 出版者：Springer Berlin / Heidelberg
• ISSN：1614-7499
• 卷排序：23

文摘

Endosulfan is a persistent organic pollutant and widely used in agriculture as a pesticide. It is present in air, water, and soil worldwide; therefore, it is a health risk affecting especially the reproductive system. The aim of this study was to evaluate the toxicity of endosulfan in the reproductive system. To investigate the effect of endosulfan on meiosis process, 32 rats were divided into four groups, treated with 0, 1, 5, and 10 mg/kg/day endosulfan, respectively, and sacrificed after the 21 days of treatments. Results show that endosulfan caused the reductions in sperm concentration and motility rate, which resulted into an increased in sperm abnormality rate; further, endosulfan induced downregulation of spermatogenesis- and oogenesis-specific basic helix-loop-helix transcription factor (Sohlh1) which controls the switch on meiosis in mammals, as well cyclin A1, cyclin-dependent kinases 1 (CDK1), and cyclin-dependent kinases 2 (CDK2). In vitro, endosulfan induced G2/M phase arrest in the spermatogenic cell cycle and caused proliferation inhibition. Moreover, endosulfan induced oxidative stress and DNA damage in vivo and vitro. The results suggested that endosulfan could inhibit the start of meiosis by downregulating the expression of Sohlh1 and induce G2/M phase arrest of cell cycle by decreasing the expression of cyclin A1, CDK1, and CDK2 via oxidative damage, which inhibits the meiosis process, and therefore decrease the amount of sperm.