双特异性磷酸酶 22 启动子的低甲基化与消防员的服役时间相关，并且可被低剂量苯并[a]芘诱导。
Hypomethylation of dual specificity phosphatase 22 promoter correlates with duration of service in firefighters and is inducible by low-dose benzo[a]pyrene.
机构信息
Division of Environmental Genetics and Molecular Toxicology, Department of Environmental Health, Center for Environmental Genetics, University of Cincinnati Cancer Institute, College of Medicine, University of Cincinnati, Cincinnati, OH, USA.
出版信息
J Occup Environ Med. 2012 Jul;54(7):774-80. doi: 10.1097/JOM.0b013e31825296bc.
Abstract
OBJECTIVE
Firefighters (FFs) are chronically exposed to smoke and products of incomplete combustion, which frequently contain polycyclic aromatic hydrocarbons (PAHs). This study examined the possibility of an association between PAH-induced epigenetic alterations and occupational firefighting exposure.
METHODS
Promoter methylation was analyzed in four genes in blood DNA from 18 FFs and 20 non-FFs (controls). Jurkat and human normal prostate epithelial cells were treated with benzo[a]pyrene to ascertain the epigenetic effects of this type of agent.
RESULTS
Firefighters had a higher prevalence of dual specificity phosphatase 22-promoter hypomethylation in blood DNA (P = 0.03) and the extent of hypomethylation correlated with duration of firefighting service (P = 0.04) but not with age. Benzo[a]pyrene reduced promoter methylation and increased gene expression of the same gene in Jurkat and normal prostate epithelial cells.
CONCLUSIONS
Cumulative occupational exposure to combustion-derived PAHs during firefighting can cause epigenetic changes in promoters of specific genes.
摘要
目的
消防员长期接触烟雾和不完全燃烧产物，其中常含有多环芳烃（PAHs）。本研究探讨了 PAH 引起的表观遗传改变与职业消防暴露之间可能存在的关联。
方法
分析了 18 名消防员和 20 名非消防员（对照组）血液 DNA 中四个基因的启动子甲基化。用苯并[a]芘处理 Jurkat 和人正常前列腺上皮细胞，以确定此类物质的表观遗传效应。
结果
消防员血液 DNA 中双特异性磷酸酶 22 启动子低甲基化的发生率更高（P = 0.03），低甲基化程度与消防服务年限相关（P = 0.04），但与年龄无关。苯并[a]芘降低了 Jurkat 和正常前列腺上皮细胞中同一基因的启动子甲基化程度，并增加了基因表达。
结论
在消防过程中累积的职业性接触燃烧衍生的 PAHs 可能会导致特定基因启动子的表观遗传改变。
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