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长期职业性低水平接触苯后两个抑癌基因和的异常DNA甲基化

Aberrant DNA Methylation of Two Tumor Suppressor Genes, and , after Chronic Occupational Exposure to Low Level of Benzene.

作者信息

Jamebozorgi Iraj, Majidizadeh Tayebeh, Pouryagoub Gholamreza, Mahjoubi Frouzandeh

机构信息

Petroleum Industry Health Organization, Assaluyeh, Bushehr, Iran.

Department of Medical Biotechnology, National Institute for Genetic Engineering and Biotechnology, Tehran, Iran.

出版信息

Int J Occup Environ Med. 2018 Jul;9(3):145-151. doi: 10.15171/ijoem.2018.1317.

DOI:10.15171/ijoem.2018.1317
PMID:29995020
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6466977/
Abstract

BACKGROUND

Exposure to benzene would be associated with many diseases including leukemia. Epigenetic alterations seem to be among the main mechanisms involved.

OBJECTIVE

To determine if chronic occupational exposure to low level of benzene would be associated with DNA methylation.

METHODS

Global DNA methylation and promoter-specific methylation of the two tumor suppressor genes, and , were assessed employing methylation-specific PCR using the DNA extracted from 40 petrochemical workers exposed to ambient benzene levels of <1 ppm, and 31 office workers not exposed to benzene or its derivatives.

RESULTS

While an increase in global DNA methylation of 5% in (p=0.501) and 28% in (p=0.02) genes was observed in the exposed group, no hypermethylation in either of the studied genes was observed in the unexposed group. No significant association was found between the frequency of aberrant methylation and either of age, work experience, and smoking habit in the exposed group.

CONCLUSION

Chronic occupational exposure to lower than the permissible exposure limit of benzene may still result in DNA methylation of tumor suppressor genes that may ultimately lead to development of cancer.

摘要

背景

接触苯会引发包括白血病在内的多种疾病。表观遗传改变似乎是其中的主要机制之一。

目的

确定长期职业性低水平接触苯是否与DNA甲基化有关。

方法

采用甲基化特异性PCR,利用从40名接触环境苯水平<1 ppm的石化工人以及31名未接触苯或其衍生物的办公室工作人员提取的DNA,评估两个抑癌基因的全基因组DNA甲基化和启动子特异性甲基化情况。

结果

在接触组中,观察到 基因的全基因组DNA甲基化增加5%(p = 0.501), 基因增加28%(p = 0.02),而在未接触组中,未观察到所研究基因中的任何一个发生高甲基化。在接触组中,异常甲基化频率与年龄、工作经验和吸烟习惯之间均未发现显著关联。

结论

长期职业性接触低于苯允许接触限值的苯仍可能导致抑癌基因的DNA甲基化,最终可能导致癌症发生。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f3d/6466977/0bee8044ad27/ijoem-9-145-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f3d/6466977/649bf099e519/ijoem-9-145-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f3d/6466977/0bee8044ad27/ijoem-9-145-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f3d/6466977/649bf099e519/ijoem-9-145-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f3d/6466977/0bee8044ad27/ijoem-9-145-g002.jpg

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