NRN1 and CAT Gene Polymorphisms, Complex Noise, and Lifestyles interactively Affect the Risk of Noise-induced Hearing Loss.

Shuang-yan Liu, J. Xin, Zheng Li, Song Lei, Yingmei Chen, T. Zhao, Hai-yan Wang, Liangwen Xu, Mei-bian Zhang, Lei Yang
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引用次数: 6

Abstract

Objective The effects of interactions between genetic and environmental factors on the noise-induced hearing loss (NIHL) are still unclear. This study aimed to assess interactions among gene polymorphisms, noise metrics, and lifestyles on the risk of NIHL. Methods A case-control study was conducted using 307 patients with NIHL and 307 matched healthy individuals from five manufacturing industries. General demographic data, lifestyle details, and noise exposure levels were recorded. The Kompetitive allele-specific polymerase chain reaction (KASP) was used to analyze the genotypes of 18 SNPs. Results GMDR model demonstrated a relevant interaction between NRN1 rs3805789 and CAT rs7943316 (P = 0.0107). Subjects with T allele of rs3805789 or T allele of rs7943316 had higher risks of NIHL than those with the SNP pair of rs3805789-CC and rs7943316-AA (P < 0.05). There was an interaction among rs3805789, rs7943316, and kurtosis (P = 0.0010). Subjects exposed to complex noise and carrying both rs3805789-CT and rs7943316-TT or rs3805789-CT/TT and rs7943316-AA had higher risks of NIHL than those exposed to steady noise and carrying both rs3805789-CC and rs7943316-AA (P < 0.05). The best six-locus model involving NRN1 rs3805789, CAT rs7943316, smoking, video volume, physical exercise, and working pressure for the risk of NIHL was found to be the interaction (P = 0.0010). An interaction was also found among smoking, video volume, physical exercise, working pressure, and kurtosis (P = 0.0107). Conclusion Concurrence of NRN1 and CAT constitutes a genetic risk factor for NIHL. Complex noise exposure significantly increases the risk of NIHL in subjects with a high genetic risk score. Interactions between genes and lifestyles as well as noise metrics and lifestyles affect the risk of NIHL.
NRN1和CAT基因多态性、复杂噪声和生活方式相互作用影响噪声性听力损失的风险
目的遗传和环境因素在噪声性听力损失中的相互作用尚不清楚。本研究旨在评估基因多态性、噪声指标和生活方式对NIHL风险的相互作用。方法采用病例对照研究方法,选取来自5个制造业的307例NIHL患者和307例匹配的健康人。一般人口统计数据、生活方式细节和噪音暴露水平被记录下来。采用竞争性等位基因特异性聚合酶链反应(KASP)对18个snp进行基因型分析。结果gmdr模型显示NRN1 rs3805789与CAT rs7943316之间存在相关交互作用(P = 0.0107)。携带rs3805789或rs7943316 T等位基因的受试者患NIHL的风险高于携带rs3805789- cc和rs7943316- aa SNP对的受试者(P < 0.05)。rs3805789、rs7943316与峰度存在交互作用(P = 0.0010)。暴露于复杂噪声环境中同时携带rs3805789-CT和rs7943316-TT或rs3805789-CT/TT和rs7943316-AA的受试者NIHL风险高于暴露于稳定噪声环境中同时携带rs3805789-CC和rs7943316-AA的受试者(P < 0.05)。发现NRN1 rs3805789、CAT rs7943316、吸烟、视频播放量、体育锻炼和工作压力与NIHL风险的最佳6位点模型为交互作用(P = 0.0010)。吸烟、视频量、体育锻炼、工作压力和峰度之间也存在交互作用(P = 0.0107)。结论NRN1与CAT同时存在是NIHL的遗传危险因素。复杂噪声暴露显著增加遗传风险评分高的受试者患NIHL的风险。基因和生活方式之间的相互作用以及噪声指标和生活方式影响NIHL的风险。
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