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Chemosphere


Title:Carbon disulfide induces rat testicular injury via mitochondrial apoptotic pathway
Author(s):Guo Y; Wang W; Dong Y; Zhang Z; Zhou Y; Chen G;
Address:"Key Laboratory of Environment and Health, Ministry of Education & Ministry of Environmental Protection, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, 13 Hangkong Road, Wuhan 430030, Hubei, PR China. Key Laboratory of Environment and Health, Ministry of Education & Ministry of Environmental Protection, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, 13 Hangkong Road, Wuhan 430030, Hubei, PR China; Department of Environmental Health, School of Public Health, Shanghai Jiaotong University, Shanghai 200025, PR China. Key Laboratory of Environment and Health, Ministry of Education & Ministry of Environmental Protection, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, 13 Hangkong Road, Wuhan 430030, Hubei, PR China. Electronic address: guoychen@163.com"
Journal Title:Chemosphere
Year:2014
Volume:20140226
Issue:
Page Number:367 - 375
DOI: 10.1016/j.chemosphere.2014.01.081
ISSN/ISBN:1879-1298 (Electronic) 0045-6535 (Linking)
Abstract:"Carbon disulfide (CS2), one of the most important volatile organic chemicals, was shown to have serious impairment to male reproductive system. But the underline mechanism is still unclear. In the present study, we aim to investigate the male germ cell apoptosis induced by CS2 exposure alone and by co-administration with cyclosporin A (CsA), which is the inhibitor of membrane permeability transition pore (MPTP). It was shown that CS2 exposure impaired ultrastructure of germ cells, increased the numbers of apoptotic germ cells, accumulated intracellular level of calcium, elevated ROS level, and increased activities of complexes of respiratory chain. Meanwhile, exposure to CS2 dramatically decreased the mitochondrial transmembrane potential (DeltaPsim) and levels of ATP and MPTP opening. Exposure to CS2 can also cause a significantly dose-dependent increase in the expression levels of Bax, Cytc, Caspase-9, and Caspase-3, but decreased the expression level of Bcl-2. Moreover, co-administration of CsA with CS2 can reverse or alleviate the above apoptotic damage effects of CS2 on testicular germ cells. Taken together, our findings suggested that CS2 can cause damage to testicular germ cells via mitochondrial apoptotic pathway, and MPTP play a crucial role in this process"
Keywords:"Animals Apoptosis/*drug effects Calcium/metabolism Carbon Disulfide/administration & dosage/*toxicity Caspase 3/metabolism Caspase 9/metabolism Cells, Cultured Cyclosporine/administration & dosage/toxicity Enzyme Inhibitors/administration & dosage/toxicit;"
Notes:"MedlineGuo, Yinsheng Wang, Wei Dong, Yu Zhang, Zhen Zhou, Yijun Chen, Guoyuan eng Research Support, Non-U.S. Gov't England 2014/03/04 Chemosphere. 2014 Aug; 108:367-75. doi: 10.1016/j.chemosphere.2014.01.081. Epub 2014 Feb 26"

 
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