肌动蛋白结合蛋白TRIOBP与噪声性听力损失易感的相关性研究

目的分析肌动蛋白结合蛋白TRIOBP基因的多态性与噪声性听力损失的关系,探索人群发生噪声性听力损失的遗传学机制。方法通过病例对照研究设计选取2020年1—12月汽车制造工厂接受职业健康检查的噪声暴露工人,将双耳高频听力阈值超过25 dB的工人作为高频听力损失组,根据年龄、噪声接触情况和工作岗位等变量进行匹配,选择双耳任一频段(500、1000、2000、3000、4000、6000 Hz)的听力阈值低于25 dB的工人作为对照组,每组234人。收集受试者的一般信息、职业史、个人史、既往史、体检结果和空腹全血样本,对两组工人的血样进行TRIOBP基因单核苷酸多态性测序,采用条件logistic回归分析TRIOBP的遗传变异与NIHL(噪声性听力损失)易感的相关性。结果单因素分析显示,高频听力损失组比对照组有更多的工人接触过混合溶剂,睡眠时间延长(P<0.05);对照组比高频听力损失组有更多的工人有听觉系统症状、ALT异常和LDL-C异常(P<0.05)。条件logistic回归分析显示,TRIOBP基因的5个SNP均不是NIHL易感性的影响因素(P>0.05)。结论混合溶剂接触、睡眠时间、听觉系统症状、ALT及LDL-C异常可能是噪声性听力损失的影响因素,尚不能认为TRIOBP的遗传变异与NIHL的易感性相关。

Correlation between actin-binding protein TRIOBP and susceptibility to noise-induced hearing loss

  Objective  To analyze the relationship between polymorphisms of the actin-binding protein TRIOBP gene and noise-induced hearing loss (NIHL), so as to explore the genetic mechanisms underlying the occurrence of NIHL.  Methods  Noise-exposed workers who had undergone occupational health screening at several automobile manufacturing plants in Guangzhou from January to December 2020 were studied through a case-control study design, the noise-exposed workers with binaural high-frequency hearing thresholds above 25 dB (A) were selected as the high frequency hearing loss group, while those with hearing thresholds below 25 dB (A) in any binaural frequency band (500, 1 000, 2 000, 3 000, 4 000, 6 000 Hz) based on matching variables such as age, noise exposure level and job position were selected as the control group. There were 234 subjects in each group. The general information, occupational history, personal history, previous disease history, physical examination results and fasting whole blood samples of the subjects were collected. Blood samples from both groups of workers were sequenced for single nucleotide polymorphisms of the TRIOBP gene, and conditional logistic regression was used to show the genetic variation in TRIOBP in relation to susceptibility to NIHL.  Results  Univariate analysis showed that more workers in the high frequency hearing loss group had been exposed to mixed solvents and had prolonged sleep than those in the control group (P < 0.05); more workers in the control group than those in the high frequency hearing loss case group had auditory system symptoms, ALT abnormalities and LDL-C abnormalities (P < 0.05). Conditional logistic regression analysis showed that the five SNPs of TRIOBP gene were not the influencing factors of NIHL susceptibility (P> 0.05).  Conclusions  Mixed solvent exposure, sleep time, auditory system symptoms, abnormal ALT and LDL-C may be influential factors in noise-induced hearing loss. It cannot be considered that the genetic variation of TRIOBP is related to the susceptibility of NIHL.