• ISSN 1674-8301
  • CN 32-1810/R
Volume 27 Issue 2
Mar.  2013
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Pengpeng Jin, Xiaoli Wang, Fei Chang, Yinyang Bai, Yingchun Li, Rong Zhou, Ling Chen. Low dose bisphenol A impairs spermatogenesis by suppressing reproductive hormone production and promoting germ cell apoptosis in adult rats[J]. The Journal of Biomedical Research, 2013, 27(2): 135-144. doi: 10.7555/JBR.27.20120076
Citation: Pengpeng Jin, Xiaoli Wang, Fei Chang, Yinyang Bai, Yingchun Li, Rong Zhou, Ling Chen. Low dose bisphenol A impairs spermatogenesis by suppressing reproductive hormone production and promoting germ cell apoptosis in adult rats[J]. The Journal of Biomedical Research, 2013, 27(2): 135-144. doi: 10.7555/JBR.27.20120076

Low dose bisphenol A impairs spermatogenesis by suppressing reproductive hormone production and promoting germ cell apoptosis in adult rats

doi: 10.7555/JBR.27.20120076
Funds:

This work was supported by grants for Major State Basic Research De-velopment Program of China (Program 973, 2009CB941701) to Ling Chen, 11KJB310003 and 2010NJMUZ26 to Yingchun Li

  • Received Date: 2012-07-10
  • Publish Date: 2013-03-28
  • Bisphenol A (BPA), an estrogenic chemical, has been shown to reduce sperm count; however, the underlying mechanisms remain unknown. Herein, we show that oral administration of BPA (2 μg/kg) for consecutive 14 days in adult rats (BPA rats) significantly reduced the sperm count and the number of germ cells compared to controls. The serum levels of testosterone and follicle-stimulating hormone (FSH), as well as the level of GnRH mRNA in BPA rats were lower than those of control rats. Testosterone treatment could partially rescue the reduction of germ cells in BPA rats. Notably, the number of apoptotic germ cells was significantly increased in BPA rats, which was insensitive to testosterone. Furthermore, the levels of Fas, FasL and caspase-3 mRNA in the testicle of BPA rats were increased in comparison with controls. These results indicate that exposure to a low dose of BPA impairs spermatogenesis through decreasing reproductive hormones and activating the Fas/FasL signaling pathway.
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    沈阳化工大学材料科学与工程学院 沈阳 110142

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Low dose bisphenol A impairs spermatogenesis by suppressing reproductive hormone production and promoting germ cell apoptosis in adult rats

doi: 10.7555/JBR.27.20120076
Funds:

This work was supported by grants for Major State Basic Research De-velopment Program of China (Program 973, 2009CB941701) to Ling Chen, 11KJB310003 and 2010NJMUZ26 to Yingchun Li

Abstract: Bisphenol A (BPA), an estrogenic chemical, has been shown to reduce sperm count; however, the underlying mechanisms remain unknown. Herein, we show that oral administration of BPA (2 μg/kg) for consecutive 14 days in adult rats (BPA rats) significantly reduced the sperm count and the number of germ cells compared to controls. The serum levels of testosterone and follicle-stimulating hormone (FSH), as well as the level of GnRH mRNA in BPA rats were lower than those of control rats. Testosterone treatment could partially rescue the reduction of germ cells in BPA rats. Notably, the number of apoptotic germ cells was significantly increased in BPA rats, which was insensitive to testosterone. Furthermore, the levels of Fas, FasL and caspase-3 mRNA in the testicle of BPA rats were increased in comparison with controls. These results indicate that exposure to a low dose of BPA impairs spermatogenesis through decreasing reproductive hormones and activating the Fas/FasL signaling pathway.

Pengpeng Jin, Xiaoli Wang, Fei Chang, Yinyang Bai, Yingchun Li, Rong Zhou, Ling Chen. Low dose bisphenol A impairs spermatogenesis by suppressing reproductive hormone production and promoting germ cell apoptosis in adult rats[J]. The Journal of Biomedical Research, 2013, 27(2): 135-144. doi: 10.7555/JBR.27.20120076
Citation: Pengpeng Jin, Xiaoli Wang, Fei Chang, Yinyang Bai, Yingchun Li, Rong Zhou, Ling Chen. Low dose bisphenol A impairs spermatogenesis by suppressing reproductive hormone production and promoting germ cell apoptosis in adult rats[J]. The Journal of Biomedical Research, 2013, 27(2): 135-144. doi: 10.7555/JBR.27.20120076

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