| 저자(한글) |
Zhang, Linyuan,Ding, Sijin,Qiao, Peihuan,Dong, Li,Yu, Miao,Wang, Chong,Zhang, Ming,Zhang, Lixia,Li, Yimin,Tang, Ning,Chang, Bing |
| 초록 |
Abstract It is well known that inappropriate exposure to exogenous hormones during fetal or neonatal life, such as testosterone (T) and estradiol (E 2 ), leads to adverse reproductive outcomes. In our previous study, the reproductive dysfunction of male rats was characterized by an E 2 increase and T decrease after in utero and lactation exposures to n #8208;butylparaben ( n #8208;BP). In this study, we investigated the synthesis and metabolism pathways of steroid hormones, hormone receptors and the epigenetic modification of male offspring on postnatal day (PND) 21 and PND90 to explore the possible mechanisms of endocrine and reproductive disorders. The expression of steroidogenic acute regulatory protein (StAR), cytochrome cholesterol side #8208;chain cleavage enzyme (P450scc), estrogen sulfotransferase (SULT1E1) and androgen receptor (AR) in the testes was significantly decreased at the transcript and protein levels; in addition, aromatase (CYP19) and estrogen receptor alpha; (ER alpha;) expression was significantly increased and the methylation rate of the ER alpha; promoter was significantly decreased. These results suggest that increased CYP19 expression and decreased SULT1E1 expression are responsible for the E 2 increase. This effect promotes the expression of ER alpha;, which plays a pivotal role in regulating reproductive and endocrine disorders of male rats exposed to n #8208;BP. Furthermore, the epigenetic hypomethylation of ER alpha; is involved in this regulation processes. Our study is the first to report on the possible mechanism of male rat reproductive disorders induced by the xenoestrogenic chemical n #8208;BP. Copyright ⓒ 2016 John Wiley Sons, Ltd. |
