Send to

Choose Destination
See comment in PubMed Commons below
Toxicology. 2008 Nov 20;253(1-3):53-61. doi: 10.1016/j.tox.2008.08.013. Epub 2008 Sep 4.

p,p'-DDE induces mitochondria-mediated apoptosis of cultured rat Sertoli cells.

Author information

  • 1MOE Key Laboratory of Environment and Health, Department of Occupational and Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, 13 Hangkong Road, Wuhan 430030, PR China.


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 microM 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 (DeltaPsi(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 DeltaPsi(m), the release of cytochrome c into the cytosol and further the activation of caspase cascade.

[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Write to the Help Desk