氧乐果暴露工人端粒途径基因多态性与过氧化氢水平的关联
Association between genetic polymorphisms of telomere pathway genes and hydrogen peroxide level in omethoate exposure workers.
作者信息
Zhou Xiaoshan, Li Xinling, Wei Wan, Duan Xiaoran, Zhang Hui, Ding Mingcui, Yao Wu, Wang Qi, Wang Wei, Yang Yongli
机构信息
Department of Occupational Health and Occupational Diseases, College of Public Health, Zhengzhou University, Zhengzhou, China.
Department of Occupational Health and Occupational Diseases, College of Public Health, Zhengzhou University, Zhengzhou, China; The Key Laboratory of Nanomedicine and Health Inspection of Zhengzhou, Zhengzhou, China.
出版信息
Environ Toxicol Pharmacol. 2021 Feb;82:103541. doi: 10.1016/j.etap.2020.103541. Epub 2020 Nov 5.
OBJECTIVE
The aim of this study was to explore the association between genetic variations in telomere pathway genes and the level of hydrogen peroxide (HO) in omethoate exposure workers.
METHODS
A total of 180 omethoate exposure workers and 115 healthy controls were recruited. The level of HO in plasma was determined with molybdenic acid colorimetry. Polymerase chain reaction and restriction fragment length was used to detect polymorphisms in POT1 rs1034794, POT1 rs10250202, TERF1 rs3863242, and TERT rs2736098.
RESULTS
The level of HO in exposure group (4.26 ± 0.71) was significantly higher than that in control group (3.29 ± 0.46). Generalized linear models indicated that risk factors for the increase HO level were exposure [β(95 % CI) = 0.951 (0.806, 1.096), P < 0.001] and AA + AT genotype in POT1 rs034794 [β(95 % CI) = 0.397 (0.049, 0.745), P = 0.025].
CONCLUSION
The increase HO level was associated with omethoate exposure and AA + AT genotypes in POT1 gene rs1034794. It provided a new idea that polymorphisms in telomere pathway genes may indirectly regulate telomere length by influencing oxidative stress.
目的
本研究旨在探讨甲拌磷接触工人端粒途径基因的遗传变异与过氧化氢（HO）水平之间的关联。
方法
共招募了180名甲拌磷接触工人和115名健康对照者。采用钼酸比色法测定血浆中HO的水平。运用聚合酶链反应和限制性片段长度法检测POT1 rs1034794、POT1 rs10250202、TERF1 rs3863242和TERT rs2736098的多态性。
结果
接触组HO水平（4.26±0.71）显著高于对照组（3.29±0.46）。广义线性模型表明，HO水平升高的危险因素为接触[β（95%CI）=0.951（0.806，1.096），P<0.001]和POT1 rs034794中的AA+AT基因型[β（95%CI）=0.397（0.049，0.745），P=0.025]。
结论
HO水平升高与甲拌磷接触及POT1基因rs1034794中的AA+AT基因型有关。这为端粒途径基因多态性可能通过影响氧化应激间接调节端粒长度提供了新思路。
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