Neonatal bisphenol A exposure induces meiotic arrest and apoptosis of spermatogenic cells
Spermatocyte
Endocrine disruptor
Seminiferous tubule
DOI:
10.18632/oncotarget.7218
Publication Date:
2016-02-06T11:18:32Z
AUTHORS (7)
ABSTRACT
// Meina Xie 1, 2 , Pengli Bu 3, 4 Fengjie Li 1 Shijian Lan Hongjuan Wu 5 Lu Yuan Ying Wang Medicine Experiment Center, Weifang Medical University, Wei Fang 261053, P. R. China School of Bioscience and Technology, 3 Department Biological Sciences, St. John's Queens, NY 11439, USA Pharmaceutical Basic Correspondence to: Xie, e-mail: wfmcxiemeina@163.com Keywords: bisphenol A, spermatogenic cells, meiotic arrest, Boule, estrogen receptor α/β Received: October 13, 2015 Accepted: January 18, Published: February 06, 2016 ABSTRACT Bisphenol A (BPA) is a widely used industrial plasticizer, which ubiquitously present in the environment organisms. As an endocrine disruptor, BPA has caused significant concerns regarding its interference with reproductive function. However, little known about impact exposure on early testicular development. The aim study was to investigate influence neonatal first wave spermatogenesis. Newborn male mice were subcutaneously injected (0.01, 0.1 mg/kg body weight) daily from postnatal day (PND) 21. Histological analysis testes at PND 22 revealed that BPA-treated contained mostly spermatogonia spermatocytes markedly less round spermatids, indicating signs arrest. Terminal dUTP nick-end labeling (TUNEL) assay showed treatment significantly increased number apoptotic germ cells per tubule, corroborated observation In addition, abnormal proliferation as by Proliferating Cell Nuclear Antigen (PCNA) immunohistochemical staining. Mechanistically, displayed complete lack BOULE expression, conserved key regulator for Moreover, expression (ER) α β developing testis. demonstrated disrupted meiosis progression during spermatogenesis, may be, least part, due inhibition and/or up-regulation ERα/β BPA-exposed
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