Open AccessLong-term exposure to a ‘safe’ dose of bisphenol A reduced protein acetylation in adult rat testes
Author(s) -
Zhuo Chen,
Xuezhi Zuo,
Dan He,
Shibin Ding,
Fangyi Xu,
Huiqin Yang,
Xin Jin,
Ying Fan,
Ying Li,
Chong Tian,
Chenjiang Ying
Publication year - 2017
Publication title -
scientific reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.24
H-Index - 213
ISSN - 2045-2322
DOI - 10.1038/srep40337
Subject(s) - acetylation , epigenetics , histone , histone deacetylase , western blot , bisphenol a , offspring , endocrinology , medicine , benzhydryl compounds , endocrine disruptor , estrogen receptor , lysine , biology , chemistry , endocrine system , biochemistry , genetics , pregnancy , gene , hormone , organic chemistry , amino acid , cancer , breast cancer , epoxy
Bisphenol A (BPA), a typical environmental endocrine-disrupting chemical, induces epigenetic inheritance. Whether histone acetylation plays a role in these effects of BPA is largely unknown. Here, we investigated histone acetylation in male rats after long-term exposure to a ‘safe’ dose of BPA. Twenty adult male rats received either BPA (50 μg/kg·bw/day) or a vehicle diet for 35 weeks. Decreased protein lysine-acetylation levels at approximately ~17 kDa and ~25 kDa, as well as decreased histone acetylation of H3K9, H3K27 and H4K12, were detected by Western blot analysis of testes from the treated rats compared with controls. Additionally, increased protein expression of deacetylase Sirt1 and reduced binding of Sirt1, together with increased binding of estrogen receptor β (ERβ) to caveolin-1 (Cav-1), a structural protein component of caveolar membranes, were detected in treated rats compared with controls. Moreover, decreased acetylation of Cav-1 was observed in the treated rats for the first time. Our study showed that long-term exposure to a ‘safe’ dose of BPA reduces histone acetylation in the male reproductive system, which may be related to the phenotypic paternal-to-offspring transmission observed in our previous study. The evidence also suggested that these epigenetic effects may be meditated by Sirt1 via competition with ERβ for binding to Cav-1.