One, 1-dichloro-2,2-bis(p-chlorophenyl) ethylene (p,p'-DDE), the major metabolite of 2,2-bis(4-chlorophenyl)-1,1,1-trichloroethane (DDT), is a known persistent organic pollutant (POPs) and male reproductive toxicant. However, the mechanism by which p,p'-DDE exposure causes male reproductive toxicity remains unknown. The objective of this study was to elucidate some mechanisms involved in this process, including the mitochondria apoptosis pathway and the role of phospholipid hydroperoxide glutathione peroxidase (PHGPx). Puberty male SD rats were given different doses of p,p'-DDE (0, 20, 60, 100 mg/kg body weight), after the treatment, the semen quality was evaluated. Western blotting was used to detect the PHGPx protein expression. Furthermore, real-time PCR was used to analyze the genetic expression of PHGPx, Bax, Cytochrom C (Cyt C), Apaf-1, and caspase-3 in the testis. Results indicated that after the exposure, sperm malformation rate showed a significant rise compared with the control group, and meanwhile, the sperm density and sperm motility parameters were reduced to some extent in different treated groups. The mitochondria apoptosis pathway was activated. And remarkably, the expression of PHGPx protein was greatly reduced by the exposure. We conclude that p,p'-DDE can damage spermatogenesis via PHGPx depletion and mitochondria apoptosis pathway.
Keywords: PHGPx; mitochondria apoptosis pathway; p,p'-DDE; reproductive toxicity; spermatogenesis.
© 2014 Wiley Periodicals, Inc.