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目的:检测p53基因第五外显子“CCGG”序列第二个胞嘧啶(C)的甲基化状况,探讨p53基因在地方性砷中毒(地砷病)发生发展中的作用。方法:采用甲基化敏感性限制性内切酶(methylation-sensitive restriction Endonuclease,MS-RE)-PCR法,检测118例砷中毒患者和126例正常对照p53基因第五外显子甲基化状况。结果:砷中毒组p53基因第五外显子甲基化率为50.85%,对照组中p53基因第五外显子甲基化率为88.89%,砷中毒组中p53基因第五外显子甲基化率明显低于对照组(P<0.01);在砷中毒不同病情组,甲基化率均低于对照组,差异均有统计学意义(P<0.01),且随着病情加重,甲基化率有降低的趋势,但差异无显著性(P>0.05)。结论:燃煤砷污染可致砷中毒组人群p53基因第五外显子低甲基化。
Objective: To detect the methylation status of the second cytosine (C) in the fifth exon “CCGG” of p53 gene and to explore the role of p53 gene in the development of endemic arsenism. Methods: The methylation-sensitive restriction endonuclease (MS-RE) -PCR method was used to detect methylation status of exon 5 in 118 arsenism patients and 126 normal controls . Results: The fifth exon methylation rate of p53 gene was 50.85% in arsenism group and the fifth exon methylation rate was 88.89% in control group. The fifth exon of p53 gene in arsenism group The rates of methylation were significantly lower in the arsenic poisoning group than in the control group (P <0.01), and the differences were statistically significant (P <0.01). As the disease progressed, There was a tendency of decrease in the rate of the degradation, but the difference was not significant (P> 0.05). Conclusion: Coal arsenic pollution can cause hypomethylation of exon 5 of p53 gene in arsenic poisoning group.