于培培, 焦洁, 谷桂珍, 陈国顺, 张焕玲, 周文慧, 吴辉, 李艳红, 郑玉新, 余善法. SOD2基因多态性与噪声性听力损失易感性的关系[J]. 环境与职业医学, 2018, 35(12): 1069-1075. DOI: 10.13213/j.cnki.jeom.2018.18387
引用本文: 于培培, 焦洁, 谷桂珍, 陈国顺, 张焕玲, 周文慧, 吴辉, 李艳红, 郑玉新, 余善法. SOD2基因多态性与噪声性听力损失易感性的关系[J]. 环境与职业医学, 2018, 35(12): 1069-1075. DOI: 10.13213/j.cnki.jeom.2018.18387
YU Peipei, JIAO Jie, GU Gui-zhen, CHEN Guo-shun, ZHANG Huan-ling, ZHOU Wen-hui, WU Hui, LI Yanhong, ZHENG Yu-xin, YU Shan-fa. Association between SOD2 polymorphisms and susceptibility to noise-induced hearing loss[J]. Journal of Environmental and Occupational Medicine, 2018, 35(12): 1069-1075. DOI: 10.13213/j.cnki.jeom.2018.18387
Citation: YU Peipei, JIAO Jie, GU Gui-zhen, CHEN Guo-shun, ZHANG Huan-ling, ZHOU Wen-hui, WU Hui, LI Yanhong, ZHENG Yu-xin, YU Shan-fa. Association between SOD2 polymorphisms and susceptibility to noise-induced hearing loss[J]. Journal of Environmental and Occupational Medicine, 2018, 35(12): 1069-1075. DOI: 10.13213/j.cnki.jeom.2018.18387

SOD2基因多态性与噪声性听力损失易感性的关系

Association between SOD2 polymorphisms and susceptibility to noise-induced hearing loss

  • 摘要: 目的 探讨超氧化物歧化酶2(SOD2)基因多态性与噪声性听力损失(NIHL)易感性之间的关系。

    方法 采用1: 2匹配的巢式病例-对照研究方法,从2006年建立的某钢铁厂噪声作业工人研究队列中,挑选听力损失组190例,并根据性别、工种相同,年龄相差≤5岁,接噪工龄相差≤2年的标准为每位病例匹配2名对照,共匹配380名对照。采用中高通量单核苷酸多态性(SNP)分型检测技术检测SOD2基因rs2758343、rs2758346、rs4880、rs5746105位点的多态性。构建共显性、显性、隐性3种基因模型,采用单因素条件logistic回归分析单个位点多态性与NIHL易感性之间的关系。采用COX回归分析不同基因型个体NIHL发生风险随着接噪工龄的增长而变化的情况。采用GMDR v0.9软件分析SOD2基因的4个SNP位点间的交互效应。

    结果 在隐性模型下,rs5746105位点AA基因型的个体发生NIHL的风险是GG和GA基因型个体的1.50倍(95%CI:1.02~2.21)。随着接噪工龄的延长,rs5746105位点AA基因型个体患NIHL的风险是GG基因型个体的1.67倍(95%CI:1.08~2.57);AA基因型的个体患NIHL的风险是GG和GA基因型个体的1.42倍(95%CI:1.04~1.94)。SOD2基因4个SNP位点的最优基因-基因交互作用模型分析结果显示未发现具统计学意义的交互作用模型(P > 0.05)。

    结论 SOD2基因的rs5746105位点突变型等位基因A可能是NIHL发生的一个危险因素。

     

    Abstract: Objective To explore the association between superoxide dismutase gene 2 (SOD2) polymorphisms and the susceptibility to noise-induced hearing loss (NIHL).

    Methods A 1:2 matched nested case-control study was conducted based on the cohort established in 2006 of workers with noise exposure in a steel factory, and a total of 190 NIHL cases and 380 controls were chosen according to the matching standards of same gender, same type of work, age difference ≤5 years, and noise exposure duration ≤2 years. The single nucleotide polymorphisms (SNPs) of rs2758343, rs2758346, rs4880, and rs5746105 in SOD2 were genotyped by high throughput SNP genotyping assay. Codominant, dominant, and recessive models were established to study SOD2 polymorphisms and the susceptibility to NIHL by single-factor conditional logistic regression analysis. The risk of NIHL in individuals with different genotypes along with the extending of noise exposure duration was analyzed by COX regression analysis. The interactive effect among the four SNPs was analyzed by GMDR v0.9 software.

    Results The risk of NIHL in individuals with AA genotype of rs5746105 was 1.50 times of those with GG and GA genotypes (95%CI:1.02-2.21). With the increase of noise exposure duration, individuals with AA genotype of rs5746105 had a higher risk of NIHL than those with GG genotype (HR=1.67, 95%CI:1.08-2.57) and those with GG and GA genotypes (HR=1.42, 95%CI:1.04-1.94). The results of optimal gene-gene interaction model did not show interactions among the four SNPs in SOD2 (P > 0.05).

    Conclusion The mutant allele A of rs5746105 in SOD2 may be a risk factor of NIHL.

     

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