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  • Title: [Association between GPX1 gene polymorphisms and noise-induced hearing loss].
    Author: Li JY, Jiao J, Chen GS, Gu GZ, Zhang HL, Yu SF.
    Journal: Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi; 2020 Feb 20; 38(2):116-120. PubMed ID: 32306674.
    Abstract:
    Objective: To identify association between genetic polymorphism in the Glutathione peroxidase 1 gene (GPX1) and noise-induced hearing loss (NIHL) . Methods: A nested case control study was conducted based on a cohort of noise-exposed subjects. 392 cases were selected from the steel factory in Henan Province, 392 matched control subjects for each case were designated on the basis of the matched criterion including same gender, age (±5years) and duration of exposure to noise (±2years) . Two single nucleotide polymorphisms (SNPs) of GPX1 were genotyped by SNPscanTM multiplex SNP genotyping kit. Hardy-Weinberg equilibrium (HWE) tests were performed using Pearson's χ(2) for each SNP among control group, effects of genotypes of GPX1 on NIHL were analyzed by logistic regression. Results: All two SNPs were in HWE. After adjustment for covariates including smoking status, rs1987628 polymorphism was statistically significantly associated with the NIHL risk under codominant and Dominant inheritance models; In the subjects carrying rs1987628 GA genotype had a higher NIHL risk than those carrying the GG genotype, the adjusted OR value was 1.803 (95%CI 1.215-2.676, P=0.003) . And meanwhile, rs1987628 GA+AA genotype had a higher NIHL risk than those carrying the GG genotype, the adjusted OR value was 1.762 (95%CI 1.197-2.593, P=0.004) . Conclusion: It was suggested that genetic polymorphism in the GPX1 gene might be the genetic susceptible factor for NIHL. 目的: 研究谷胱甘肽过氧化物酶1(glutathione peroxidase 1,GPX1)基因多态性与噪声性听力损失(noise-induced hearing loss,NIHL)易感性间的关系。 方法: 于2019年5月,采用1∶1巢式病例-对照研究方法在噪声暴露队列研究的基础上,选择双耳高频(3 000、4 000、6 000 Hz)≥40 dB者为听力损失组,纯音听力测试任一耳语频(500、1 000、2 000 Hz)的任一频段听阈场≤25 dB,且纯音听力测试高频平均听阈<35 dB者为对照组,听力损失组和对照组各392人。对调查对象进行一般体格检查和基本信息调查,进行纯音听力测试和作业现场噪声测量。采用中高通量单核苷酸多态性分型检测技术(SNPscan(TM)法)检测GPX1基因的2个单核苷酸位点的多态性。检验对照组人群的哈迪-温伯格平衡(Hardy-Weinberg equilibrium,HWE)。应用logistic回归方法分析基因单核苷酸多态性(single nucleotide polymorphism,SNP)与NIHL易感性之间的关系。 结果: 两组包括375名男性和17名女性,其中病例组平均年龄(40.9±8.2)岁,平均工龄(19.4±9.1)年,双耳高频平均听阈位移范围(51.3±8.9)dB;对照组平均年龄(40.3±8.2)岁,平均工龄(18.8±8.9)年,双耳高频平均听阈位移(12.5±10.2)dB,GPX1单核苷酸位点在对照组中的频率分布均符合Hardy-Weinberg平衡。调整研究样本吸烟因素后,发现rs1987628位点在共显性、显性遗传模型下与NIHL发生风险有关(P<0.05);与GG基因型携带者相比,听力损失组GA基因型携带者的NIHL的危险度显著升高,OR值为1.803(95%CI 1.215~2.676,P=0.003);GA+AA基因型携带者的NIHL的危险度显著升高,OR值为1.762(95%CI 1.197~2.593,P=0.004)。rs3448单核苷酸位点的基因型与NIHL危险度无相关性(P>0.05)。 结论: GPX1基因多态性可能是NIHL的遗传易感性因素。.
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