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沈杰, 夏玮, 万延建, 许冰, 李媛媛, 徐顺清. 全氟辛烷磺酸促大鼠肝脏NQO1甲基化作用[J]. 中国公共卫生, 2012, 28(12): 1597-1599. DOI: 10.11847/zgggws-2012-28-12-16
引用本文: 沈杰, 夏玮, 万延建, 许冰, 李媛媛, 徐顺清. 全氟辛烷磺酸促大鼠肝脏NQO1甲基化作用[J]. 中国公共卫生, 2012, 28(12): 1597-1599. DOI: 10.11847/zgggws-2012-28-12-16
SHEN Jie, XIA Wei, WAN Yan-jian, . Prenatal exposure to PFOS alters individual genes NQO1 promoter methy-lation levels of liver in postnatal SD rats[J]. Chinese Journal of Public Health, 2012, 28(12): 1597-1599. DOI: 10.11847/zgggws-2012-28-12-16
Citation: SHEN Jie, XIA Wei, WAN Yan-jian, . Prenatal exposure to PFOS alters individual genes NQO1 promoter methy-lation levels of liver in postnatal SD rats[J]. Chinese Journal of Public Health, 2012, 28(12): 1597-1599. DOI: 10.11847/zgggws-2012-28-12-16

全氟辛烷磺酸促大鼠肝脏NQO1甲基化作用

Prenatal exposure to PFOS alters individual genes NQO1 promoter methy-lation levels of liver in postnatal SD rats

  • 摘要: 目的 探讨基因启动子甲基化水平与全氟辛烷磺酸(PFOS)诱导的肝毒性早期过程相关性。方法 在雌性SD大鼠受孕后2~21 d采用PFOS(0.1、0.6、2.0 mg/kg)灌胃染毒;在子鼠出生后21 d收集肝脏组织样本,用亚硫酸氢钠测序聚合酶链式反应法(BSP)结合质粒克隆后测序,检测烟酰胺腺嘌呤二核苷酸:醌氧化还原酶1(NQO1)和肉毒碱棕榈酰转移酶1A(CPT1A)基因启动子区域甲基化状态。结果 与对照组(0%)比较,高剂量PFOS组子鼠肝脏NQO1基因甲基化状态有所上升,-573、-523、-507 3个位点分别升高了10%,而中低剂量组无变化(均为0%);CPT1A基因启动子区域甲基化状态无明显变化。结论 出生前暴露于PFOS的子鼠肝脏中NQO1基因启动子甲基化水平升高。

     

    Abstract: Objective To examine the possibility of early epigenetic alteration in perfluorooctane sulphonate(PFOS)-exposed rat liver.Methods Pregnant Sprague-Dawley(SD)rats were exposed to PFOS at doses of 0.1,0.6, and 2.0 mg/kg/d and 0.05% Tween 80 as control by gavage from gestation day 2 to 21.The dams were allowed to give birth and liver samples from weaned(postnatal day 21)offspring rats were analyzed for individual genes such as NAD(P)H:quinone oxidoreductase(NQO1)and carnitine palmitoyltransferase 1A(CPT1A)promoter methylation level.Results In PFOS exposed weaned rats,compared to the control,methylation of critical CpG sites in NQO1 promoter was found up to 10% methylated in the livers of treated rats.Conclusion Early induced hypermethylation in critical cytosines within the NQO1 gene promoter region may be a significant biomarker of hepatic PFOS burden,though their direct role in PFOS induced-hepatotoxicity,including its potential carcinogenic action,needs further research.

     

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