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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。
Objective To investigate the correlation between gene promoter methylation and early course of hepatotoxicity induced by perfluorooctane sulfonate (PFOS). Methods Female Sprague-Dawley rats were intragastrically administrated with PFOS (0.1, 0.6 and 2.0 mg / kg) 2 to 21 days after conception. Liver samples were collected 21 d after birth and sequenced with sodium bisulphite (BSP) combined with plasmid cloning and sequencing to detect methylation status of nicotinamide adenine dinucleotide: quinone oxidoreductase 1 (NQO1) and carnitine palmitoyl transferase 1A (CPT1A) gene promoter region . Results Compared with the control group (0%), the methylation status of NQO1 gene in liver of high-dose PFOS group rats increased, and the number of -573, -523 and -507 increased by 10% There was no change in the group (all 0%). There was no significant change in the methylation status of CPT1A gene promoter region. Conclusions The NQO1 gene promoter methylation level in the livers of offspring exposed to PFOS before birth is increased.