p16 启动子甲基化在 Pb2+ 暴露个体中。
p16 promoter methylation in Pb2+ -exposed individuals.
机构信息
Laboratory of Forensic Medicine and Toxicology, School of Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece.
出版信息
Clin Toxicol (Phila). 2010 Feb;48(2):124-8. doi: 10.3109/15563650903567091.
BACKGROUND
One of the principle symptoms of lead poisoning is the development of neurological disorders. Neuronal response is closely related to DNA methylation changes. Aim. In this study, we estimated p16 methylation in nine individuals exposed to lead using methylation-specific polymerase chain reaction followed by analysis of the methylated cytosine content of the product by thermal denaturation.
RESULTS
We found that, based on lead blood concentration, lead-exposed individuals were divided into two groups. Among highly exposed individuals (blood Pb(2+) concentration = 51-100 microg/dL), we observed complete CpG methylation, whereas for low Pb(2+) concentrations (blood Pb(2+) concentration = 6-11 microg/dL), we observed partial methylation.
CONCLUSION
Our results show that among lead-overexposed individuals, p16 methylation is frequent and extensive, and suggest that DNA methylation could be involved in the mechanism by which lead induces neurotoxicity.
背景
铅中毒的主要症状之一是神经系统疾病的发展。神经元反应与 DNA 甲基化变化密切相关。目的：在这项研究中，我们使用甲基化特异性聚合酶链反应估计了 9 名接触铅的个体的 p16 甲基化，然后通过热变性分析产物中甲基化胞嘧啶的含量。
结果
我们发现，根据血铅浓度，接触铅的个体分为两组。在高暴露个体（血铅浓度= 51-100μg/dL）中，我们观察到完全 CpG 甲基化，而在低 Pb（2+）浓度（血铅浓度= 6-11μg/dL）下，我们观察到部分甲基化。
结论
我们的结果表明，在铅超暴露个体中，p16 甲基化频繁且广泛，提示 DNA 甲基化可能参与了铅诱导神经毒性的机制。
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