Journal
TOXICOLOGY
Volume 253, Issue 1-3, Pages 53-61Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.tox.2008.08.013
Keywords
Apoptosis; Bax family members; Caspase; Mitochondria; ROS; p,p '-DDE
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Funding
- National Natural Science Foundation of China [30671734]
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p,p'-Dichlorodiphenoxydichloroethylene (p,p'-DDE), the major metabolite of dichlorodiphenoxytrichloroethane (DDT), is a known persistent organic Pollutant and male reproductive toxicant. However, the mechanism underlying male reproductive toxicity of p.p'-DDE remains limited. In the present study, Sertoli cells were used to investigate the molecular mechanism involved in p,p'-DDE's male reproductive toxicity. Results showed that p,p'-DDE exposure at over 30 mu M showed induction of apoptotic cell death. p.p'-DDE could induce mitochondria-mediated apoptotic changes including elevation in reactive oxygen species (ROS) generation, decrease in mitochondrial membrane potential (Delta Psi(m)), and release of cytochrome c into the cytosol, which Could be blocked by antioxidant agent N-acetyl-L-cysteine (NAC). In addition, elevated ratios of Bax/Bcl-w and Bak/Bcl-w and cleavages of procaspase-3 and -9 were induced by p,p'-DDE treatment. All of the results suggested that ROS generation may play a critical role in the initiation of p,p'-DDE-induced apoptosis by mediation of the disruption of the release of cytochrome c into the cytosol and further the activation of caspase cascade. (c) 2008 Elsevier Ireland Ltd. All rights reserved.
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