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Exposure to bisphenol A results in a decline in mouse spermatogenesis

Guo-Liang Zhang A E, Xi-Feng Zhang B E, Yan-Min Feng A, Lan Li A, Evanna Huynh C, Xiao-Feng Sun A, Zhong-Yi Sun D and Wei Shen A F

A Key Laboratory of Animal Reproduction and Germplasm Enhancement in Universities of Shandong, Qingdao Agricultural University, Qingdao 266109, China.
B College of Biological and Pharmaceutical Engineering, Wuhan Polytechnic University, Wuhan 430023, China.
C Department of Animal and Poultry Science, University of Guelph, Guelph, Ontario N1G2W1, Canada.
D Daping Hospital, Third Military Medical University, Chongqing 400038, China.
E Equal first authors.
F Corresponding author. Email: shenwei427@163.com

Reproduction, Fertility and Development - http://dx.doi.org/10.1071/RD12159
Submitted: 19 May 2012  Accepted: 19 July 2012   Published online: 4 September 2012


 
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Abstract

Bisphenol A (BPA), a chemical used in many consumer products, interferes with the endocrine system of mammals, including humans. The aim of the present study was to investigate the effect of BPA on spermatogenesis and semen quality. The objective of this study was to assess the effects of BPA on mouse spermatogenesis. CD1 mice were used in all experiments. Mice were treated with different doses of BPA (0, 20 and 40 μg kg–1 day–1from postnatal Day (PND) 3 to PND21, PND 35 or PND49. After 5 weeks BPA treatment, oestrogen receptor α expression was increased in mouse testis, whereas the meiotic progression of germ cells was slowed. Thus, both the quality and quantity of spermatozoa were decreased in 7-week-old mice. However, BPA had no effect on DNA methylation of imprinted genes such as Igf2, Igf2r, Peg3 and H19, in germ cells. In addition, exposure of male mice to BPA resulted in abnormal offspring that were smaller with a low-quality pelage when they were 35 days old. In conclusion, BPA hampers spermatogenesis and the subsequent development of offspring.

Additional keywords: DNA methylation, meiosis, oestrogen receptor.


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