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目的探讨砷所致的氧化损伤与其所引起的基因启动子区高甲基化的关联。方法于2013年12月,在贵州省燃煤污染型地方性砷中毒病区招募74名常驻居民为研究对象,检测尿砷、发砷及尿中8-羟基脱氧鸟苷(8-OH-d G)的水平以及p53、p16启动子区CpG位点甲基化的情况。结果在控制年龄、性别、吸烟、饮酒后,尿砷与尿中8-OH-d G水平间呈正相关(P<0.05)。p16基因启动子区+248位和+317位CpG位点甲基化率与尿砷水平呈正相关(P<0.05),+248、+261、+314、+317、+320、+391位CpG位点甲基化率与尿中8-OH-d G水平呈正相关(P<0.05)。p53基因启动子区-9位、-127位CpG位点甲基化率与尿中8-羟基脱氧鸟苷水平呈正相关关系(P<0.05),+80位CpG位点甲基化率与尿砷水平呈正相关(P<0.05)。结论砷介导的氧化应激与砷所致基因异常甲基化间存在一定关联,其相关机制需进一步探索。
OBJECTIVE: To investigate the association between arsenic-induced oxidative damage and hypermethylation of the gene promoter region. Methods In December 2013, 74 resident residents were enrolled in the coal-burning endemic arsenism in Guizhou Province. Urinary arsenic, arsenic and urinary 8-OH- d G) and the methylation of CpG sites in p53 and p16 promoter regions. Results There was a positive correlation between urinary arsenic and 8-OH-d G in urine after controlling for age, sex, smoking and drinking (P <0.05). The methylation rates of +248 and +317 CpG sites in the promoter region of p16 gene were positively correlated with urinary arsenic levels (P <0.05), + 248, +261, +314, +317, +320 and +391 CpG There was a positive correlation between methylation rate and urinary 8-OH-d G level (P <0.05). There was a positive correlation between the methylation rate of -127 CpG sites and the level of 8-hydroxydeoxyguanosine in urine (P <0.05). The methylation rate of +80 CpG sites and urine Arsenic levels were positively correlated (P <0.05). Conclusion There is a correlation between arsenic-mediated oxidative stress and abnormal methylation of arsenic-induced genes. The related mechanisms need to be further explored.