DNA hypermethylation of acetoacetyl-CoA synthetase contributes to inhibited cholesterol supply and steroidogenesis in fetal rat adrenals under prenatal nicotine exposure
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- 作者：Dong-Mei Wua ; Zheng Hea ; Ting Chena ; Yang Liua ; Liang-Peng Maa ; Jie Pinga ; b ; pingjie@whu.edu.cn" class="auth_mail" title="E-mail the corresponding author
- 关键词：AACS ; acetoacetyl-CoA synthetase ; ACAT2 ; acetyl-CoA acetyltransferase 2 ; BSP ; bisulfite sequencing PCR ; CE ; cholesteryl esters ; CORT ; corticosterone ; DHEAS ; dehydroepiandrosterone sulfate ; GAPDH ; glyceraldehyde phosphate dehydrogenase ; GD ; gestational day ; HE ; hematoxylin and eosin ; HMGCR ; 3-hydroxy-3-methylglutaryl-CoA reductase ; HMGCS1 ; 3-hydroxy-3-methylglutaryl-CoA synthase 1 ; HPA ; hypothalamus-pituitary-adrenal ; IUGR ; intrauterine growth retardation ; P450c17 ; cytochrome P450 17alpha-hydroxy
- 刊名：Toxicology
- 出版年：2016
- 出版时间：18 January 2016
- 年：2016
- 卷：340
- 期：Complete
- 页码：43-52
- 全文大小：3434 K
文摘
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Prenatal nicotine exposure inhibits steroid hormone production in fetal rat adrenals.
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Prenatal nicotine exposure inhibits cholesterol uptake in fetal rat adrenals.
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Prenatal nicotine exposure inhibits the expression of AACS.
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Prenatal nicotine exposure induces aberrant DNA methylation of AACS promoter.