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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-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GG、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%(GG)、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回归对两组间年龄、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HSP60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。
Objective To investigate the relationship between heat shock protein 60 (HSP60) gene polymorphism and noise-induced hearing loss. Methods A total of 194 noise exposure workers were surveyed and audiologically tested by the method of cross-sectional epidemiology. According to the results of audiometry, they were divided into hearing loss group and normal hearing group. Allele-specific amplification ASA) and polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) were used to detect the polymorphism of rs11551350 and rs2340690 two single nucleotide polymorphisms in HSP60 gene. Results The frequency of GG, AA and AG genotypes at rs11551350 was 1.1%, 9.7% and 89.2% in 93 workers with noise-induced hearing loss, and the frequencies of alleles G and A were 45.7% and 54.3% Among 101 workers with normal hearing, the genotype frequencies were 5.9% (GG), 5.9% (AA) and 88.1% (AG), and the allele frequencies were 50.0% (G) and 50.0% (A). The frequencies of CC, TT and CT genotypes of rs2340690 locus were 51.6%, 7.5% and 40.9% respectively in patients with noise-induced hearing loss. The frequencies of alleles C and T were 72.0% and 28.0% The genotype frequencies were 45.5% (CC), 4.0% (TT) and 50.5% (CT), respectively. The allele frequencies were 70.8% (C) and 29.2% (T). There was no significant difference in genotype distribution and allele frequencies between the two groups (P> 0.05) and normal hearing group (P> 0.05). Using multivariate logistic regression to correct the age, sex, smoking status, detonation history and accumulated noise exposure between the two groups, no significant risk of noise-induced hearing loss was found in either of the two genotypes Increased (P> 0.05). Conclusion Polymorphism of rs11551350 and rs2340690 two single nucleotide polymorphisms in HSP60 gene may not be the genetic susceptibility to noise-induced hearing loss.