热休克蛋白60基因多态性与噪声性听力损失易感性的关系

目的探讨热休克蛋白60（HSP60）基因多态性与噪声性听力损失的关系。方法采用横断面流行病学研究方法，对194名噪声暴露作业工人进行调查和听力测试，按听力学评价的结果将其分为听力损失组和听力正常组；用等位基因特异扩增法（ASA）和多聚酶链反应一限制性片断长度多态性法（PCR-RFLP）检测其HSP60基因上rs11551350和rs2340690两个单核苷酸位点的多态性。结果rs11551350位点在93名噪声性听力损失的工人中CG、AA和AG基因型的频率分别为1．1％、9．7％和89．2％，等位基因G和A的频率为45．7％和54．3％；在101名听力正常的工人中，基因型频率分别为5．9％（CG）、5．9％（AA）和88．1％（AG），等位基因频率为50．0％（G）和50．0％（A）。rs2340690位点在噪声性听力损失组CC、TT和CT基因型的频率分别为51．6％、7．5％和40．9％，等位基因C和T的频率为72．0％和28．0％；在听力正常组的基因型频率分别为45．5％CC）、4．0％（TT）和50．5％（CT）；等位基因频率为70．8％（C）和29．2％（T）。两位点的基因型分布及其等位基因频率在噪声性听力损失组与听力正常组之间差异均无显著性（P〉0．05）。采用多元Logistic回归对两组问年龄、性别、吸烟状况、爆震史和累积噪声暴露量等因素进行校正后，未发现两位点中任一基因型的噪声性听力损失的危险度有显著性升高（P〉0．05）。结论HSW60基因的rs11551350和rs2340690两个单核苷酸位点的多态性可能不是噪声性听力损失的遗传易感性因素。

Association of the heat shock protein 60 gene polymorphisms with noise-induced hearing loss in exposed workers

Objective To investigate the association of the heat shock protein 60(HSP60)gene polymorphisms with development of noise-induced hearing loss(NIHL)in workers exposed to noise.Method In total,194 workers occupationally exposed to noise were selected in a cross-sectional study.According to audiometric tests,they were divided into two groups,NIHL group and normal group.The HSP60 gene polymorphisms in the loci of two single nucleotides rs11551350 and rs2340690 were analyzed in 93 workers with NIHL and 101 normal workers by allele specific analysis(ASA)and polymerase chain reaction followed by restriction fragment length polymorphism(PCR-RFLP)analysis.Result There was no significant difference in frequencies of GG,AA and GA genotypes and G and A alleles of the rs11551350 locus between NIHL group(1.1%,9.7% and 89.2%,and 45.7% and 54.3%,respectively)and normal group(5.9%,5.9% and 88.1%,and 50.0% and 50.0%,repsectively)(P>0.05),as well as in frequencies of CC,TT and CT genotypes and C and T alleles of the rs2340690 locus between the two groups(51.6%,7.5% and 40.9%,and 72.0% and 28.0% in NIHL group,respectively;and 45.5%,4.0% and 50.5%,and 70.8% and 29.2% in normal group,respectively).After adjusted for age,sex,smoking status,history of exposure to explosive noise and cumulative noise exposure(CNE)with multivariate logistic regression analysis,no significant higher risk for NIHL was found in those with any genotype of the two loci(P>0.05).Conclusion It is suggested that genetic polymorphism of the rs11551350 and rs2340690 loci in the HSP60 gene might not be the genetic susceptible factor for NIHL.