Disruption of spermatogenesis and differential regulation of testicular estrogen receptor expression in mice after polychlorinated biphenyl exposure
Date
2011-05-26Author
Zuo, Zhenghong
Cai, Jiali
Wang, Chonggang
王重刚
Wu, Tian
Lopes Moreno
Joao Manuel
Zhong, Yuanfu
Huang, Xin
Chen, Yixin
Collections
- 生命科学-已发表论文 [5901]
Abstract
he testicular toxicity of polychlorinated biphenyls (PCBs) has been extensively studied. However, the detailed mechanism is still obscure. In the present study, male C57 mice were treated with different doses of Aroclor 1254 (a commercial PCB mixture) once every 3 days by oral gavage. After exposure to Aroclor 1254 for 50 days, the sperm count decreased in a dose-dependent manner. Cell proliferation and apoptosis are key processes regulating development of the testis, and alterations in these processes may underlie testicular dysgenesis. Our results showed that the germ cell proliferation was inhibited and the apoptosis of the germ cell was induced in a dose-dependent manner after treatment with Aroclor 1254. Although there was no significant change in serum testosterone levels and androgen receptor expression levels after treatment with different dosages of Aroclor 1254, the estradiol levels decreased and the expression of estrogen receptor (ER) beta increased in a dose-dependent manner, whereas an elevation of the expression of ER alpha was only observed in the 50 mu g/kg group. The data as a whole suggested that inhibited proliferation and induced apoptosis in germ cells, and a differential regulation of ER, may be involved in the testicular toxicity of PCBs. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
Citation
Toxicology. 2011 Sep 5;287(1-3):21-8URI
http://dx.doi.org/doi:10.1016/j.tox.2011.05.010WOS:000294196600004
https://dspace.xmu.edu.cn/handle/2288/11927