Neonatal bisphenol A exposure induces meiotic arrest and apoptosis of spermatogenic cells
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Meina Xie1,2, Pengli Bu3,4, Fengjie Li1, Shijian Lan2, Hongjuan Wu5, Lu Yuan2, Ying Wang2
1Medicine Experiment Center, Weifang Medical University, Wei Fang 261053, P. R. China
2School of Bioscience and Technology, Weifang Medical University, Wei Fang 261053, P. R. China
3Department of Biological Sciences, St. John’s University, Queens, NY 11439, USA
4Department of Pharmaceutical Sciences, St. John’s University, Queens, NY 11439, USA
5School of Basic Medical Sciences, Weifang Medical University, Wei Fang 261053, P. R. China
Meina Xie, e-mail: firstname.lastname@example.org
Keywords: bisphenol A, spermatogenic cells, meiotic arrest, Boule, estrogen receptor α/β
Received: October 13, 2015 Accepted: January 18, 2015 Published: February 06, 2016
Bisphenol A (BPA) is a widely used industrial plasticizer, which is ubiquitously present in the environment and organisms. As an endocrine disruptor, BPA has caused significant concerns regarding its interference with reproductive function. However, little is known about the impact of BPA exposure on early testicular development. The aim of the present study was to investigate the influence of neonatal BPA exposure on the first wave of spermatogenesis. Newborn male mice were subcutaneously injected with BPA (0.01, 0.1 and 5 mg/kg body weight) daily from postnatal day (PND) 1 to 21. Histological analysis of testes at PND 22 revealed that BPA-treated testes contained mostly spermatogonia and spermatocytes with markedly less round spermatids, indicating signs of meiotic arrest. Terminal dUTP nick-end labeling (TUNEL) assay showed that BPA treatment significantly increased the number of apoptotic germ cells per tubule, which corroborated the observation of meiotic arrest. In addition, BPA caused abnormal proliferation of germ cells as revealed by Proliferating Cell Nuclear Antigen (PCNA) immunohistochemical staining. Mechanistically, BPA-treated testes displayed a complete lack of BOULE expression, which is a conserved key regulator for spermatogenesis. Moreover, BPA significantly increased the expression of estrogen receptor (ER) α and β in the developing testis. The present study demonstrated that neonatal BPA exposure disrupted meiosis progression during the first wave of spermatogenesis, which may be, at least in part, due to inhibition of BOULE expression and/or up-regulation of ERα/β expression in BPA-exposed developing testis.
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