中文摘要：

[目的]了解砷暴露对人体生物样品p53、p16启动子区甲基化的影响，探讨p53、p16动子区DNA甲基化改变及在砷致病中的作用。[方法]于贵州省燃煤污染型地方性砷中毒病区，选择42名常驻居民为暴露组，另于距病区约12km的非砷暴露村，选择40例居民作为对照组。在知情同意的原则下，采集受试对象尿液、血液和发样，使用电感耦合等离子体质谱（ICP-MS）法检测受试对象尿砷和发砷，采用亚硫酸盐修饰后测序法（BSP）法检测p53、p16启动子区CpG位点甲基化情况。[结果]暴露组尿砷为（40．59±27．12）州队发砷为（0．32±0．36）oe,／g，p53平均甲基化率为（8．32±1.51）％，暴露组-71、＋42、＋109位CpG位点甲基化率分别为（11．44±3．64）％，（2．58±1．29）％和（4．98±1．33）％，均高于对照组（均P〈0．05）；暴露组和对照组p16平均甲基化率和各CpG位点甲基化率差异均无统计学意义（均P〉0．05）。[结论]p53基因启动子区CpG位点的甲基化-9砷暴露有关，砷暴露所致的DNA甲基化可能存在位点的特异性。

英文摘要：

[ Objective ] To test the effects of arsenic exposure on DNA methylation of promoter of p53 and p16 genes in human biological samples. [ Method ] Arsenic-exposed residents from a burning-coal-type endemic arsenic poisoning area in Guizhou Province （n=42） and another control residents who lived 12 km away from the endemic area （n=40） were recruited in the study. Blood, urine, and hair samples were collected from all the subjects giving informed consent. The levels of urinary and hair arsenic were measured by inductively coupled plasma mass spectrometry, and DNA methylation at CpG site of p53 and p16 were determined by bisulfite sequencing. [ Results ] Compared with the control group, the arsenic-exposed residents exhibited higher levels of urinary [（40.59± 27.12） μg/g] and hair arsenic [（0.32 ± 0.36） μg/g], p53 methylation [（8.32 ± 1.51）%], and the methylation at CpG sites of -71 [（11.44 ±3.64）%], ＋42 [（2.58 ± 1.29）%], and ＋109 [（4.98 ± 1.33）%] （all Ps 〈0.05）. There was no difference inpl6 methylation between the exposed and non-exposed residents （all Ps 〉 0.05）. [ Conclusion ] Arsenic exposure is associdted with CpG site methylation inp53 promoter and may induce CpG site-specific DNA methylation.