Hazards of noise-induced hearing loss (NIHL) to crowd who are long-term exposured and work in the noisy environment is increasingly prominent. But just part of the individuals who are exposed to the same noisy environment have hearing loss, and the severity of hearing loss are different, which indicates genetic predisposition might be associated with NIHL. In recent years, many experts and scholars at home and abroad have done a lot of research in this field, this article summarizes all available studies.
Genetic Predisposition to Disease ; Hearing Loss, Noise-Induced ; genetics ; Humans ; Noise, Occupational ; adverse effects

OBJECTIVETo evaluate the association of glutathione S-transferase M1 (GSTM1) and glutathione S-transferase T1 (GSTT1) polymorphisms with noise-induced hearing loss.

METHODSThe Cochrane library, PubMed, OVID, EMBASE, Springer, Wanfang Data, VIP, CNKI, and CBM were searched to collect case-control studies on GSTM1 or GSTT1 polymorphism and noise-induced hearing loss. The articles meeting the inclusion criteria were reviewed systematically, and the reported data were aggregated using Revman 5.0.

RESULTSFive studies were included in the meta-analysis. The meta-analysis and subgroup analysis showed that the persons with GSTM1 null genotype had an increased risk of noise-induced hearing loss compared with those with GSTM1 wild genotype (OR = 1.37, 95%CI: 1.13∼1.66); in the Chinese population, the risk of noise-induced hearing loss was higher in persons with GSTM1 null genotype than in those with GSTM1 wild genotype (OR = 1.5, 95%CI: 1.2∼1.86); there was no significant difference in the risk of noise-induced hearing loss between persons with GSTT1 null and wild genotypes.

CONCLUSIONGSTM1 polymorphism is related to noise-induced hearing loss, but GSTT1 polymorphism is unrelated to this condition.

Glutathione Transferase ; genetics ; Hearing Loss, Noise-Induced ; genetics ; Humans ; Polymorphism, Single Nucleotide

Animals ; Gene Expression Profiling ; Genetic Predisposition to Disease ; genetics ; Genetic Testing ; Hearing Loss, Noise-Induced ; genetics ; Humans

Noise-induced hearing loss (NIHL) is a complex disease caused by interactions between environmental and genetic factors. This study investigated whether genetic variability in protocadherin related 15 (PCDH15) underlies an increased susceptibility to the development of NIHL in a Chinese population. The results showed that compared with the TT genotype of rs11004085, CT/CC genotypes were associated with an increased risk of NIHL [adjusted odds ratio (OR) = 2.64; 95% confidence interval (CI): 1.14-6.11, P = 0.024]. Additionally, significant interactions between the rs11004085 and rs978842 genetic variations and noise exposure were observed in the high-level exposure groups (P < 0.05). Furthermore, the risk haplotype TAGCC was observed when combined with higher levels of noise exposure (P < 0.05). Thus, our study confirms that genetic variations in PCDH15 modify the susceptibility to NIHL development in humans.
Cadherins ; genetics ; China ; Genetic Predisposition to Disease ; Genetic Variation ; Hearing Loss, Noise-Induced ; epidemiology ; genetics ; Humans ; Risk Factors

OBJECTIVE: To study the clinical and sequence character of the entire mitochondrial genome in five subjects with mitochondrial 12SrRNA T1095C mutation, and to analyze its relationship with the military noise-induced hearing loss (NIHL). METHOD: Three hundreds and four soldiers exposed to military noise were selected in Yunan and Beijing, including susceptible (experimental) and tolerance (control) groups. Mitochondrial 12SrRNA T1095C mutation were found in 5 subjects. Then the complete nucleotide sequence of five subjects were sequenced and its clinical character were analyzed. RESULT: m12SrRNA T1095C mutation were identified in 5 subjects of experimental group,and none were found in control group. There was significant difference between them (P < 0.05). All five soldiers had the history of military noise exposure and showed sensorineural deafness of different degrees. Sequence analysis of the complete mitochondrial genomes showed the distinct sets of mtDNA polymorphism besides T1095C mutation in five subjects. CONCLUSION The T1095C mutation in hearing loss subjects with various genetic background and history of military noise exposure, is involved in the pathogenesis of hearing impairment. It indicates that the T1095C mutation do relate well with military noise induced-hearing loss.
Adult ; Base Sequence ; DNA, Mitochondrial ; genetics ; Hearing Loss, Noise-Induced ; genetics ; Humans ; Male ; Military Personnel ; Mutation ; Young Adult

Objective: To explore the relationship between DNA methylation and occupational noise-induced hearing loss. Methods: A case-control study was conducted. People with hearing loss induced by occupational noise were recruited as the case group and those with normal hearing but still exposed to occupational noise were recruited as the control group. A total of 60 participants were included, of which 30 participants were in the case group and 30 in the control group. The methylation level was detected by 850k genome-wide DNA methylation chip technology. The significance of differential methylated position (DMP) was tested by R-packet 'Champ'. The differential methylated region (DMR) was analyzed by using Champ's Bumphunter algorithm. Cluster profiler was used to analyze the gene list for GO and KEGG pathway enrichment. Results: There was significant difference between two groups in binaural high-frequency average hearing threshold (P<0.05), but there was no significant difference in age, smoking, drinking, hypertension, physical exercise and cumulative noise exposure. The results of DMP and DMR analysis showed that 713875 sites were detected in the case group and the control group, and 439 methylation sites with significant difference, accounting for 0.06%; 650 regions were detected, and 72 methylation regions with significant differences, accounting for 11.08%. Compared with the control group, the results of GO enrichment analysis showed that the case group had statistically significant differences in four pathways: axogenesis of projection neurons in the central nervous system, neuronal development in the central nervous system, axogenesis of neurons in the central nervous system and neuronal differentiation in the central nervous system. KEGG enrichment analysis showed that there were significant differences in sphingolipid metabolism, aldosterone synthesis and secretion, primary bile acid biosynthesis pathway between the case group and the control group. Conclusion: The occurrence of occupational noise-induced hearing loss may be related to the regulation of gene expression related to axogenesis of projection neurons in the central nervous system, development of neurons in the central nervous system, axogenesis of neurons in the central nervous system, differentiation of neurons in the central nervous system, sphingolipid metabolism, aldosterone synthesis and secretion, primary bile acid biosynthesis and gene methylation related to metabolism.
Aldosterone ; Bile Acids and Salts ; Case-Control Studies ; DNA Methylation ; Hearing Loss, Noise-Induced/genetics* ; Humans ; Noise, Occupational/adverse effects* ; Occupational Diseases ; Occupational Exposure ; Sphingolipids

The effects of genetic factors on the noise-induced hearing loss (NIHL) are still unclear. In the present study, eight single-nucleotide polymorphisms (SNPs) included rs1227049 and rs3802711 (CDH23), rs1695 (GSTP1), rs137852540 (GJB2), rs2289274 (PMCA2), rs4880 (SOD2), rs7943316, and rs769214 within CAT that might associated with NIHL were further validated in Chinese workers. The results showed that the carriers of the T allele (AT+TT) of rs7943316 and A allele (GA+AA) of rs769214, were significantly associated with an increased risk of NIHL compared to those with AA genotype (P<0.05) and GG genotype (P<0.05). Moreover, a significant three-locus model (P=0.0107) involving rs2016520, rs9794, and rs1805192 were observed that might associated with NIHL, with 53.95% of testing accuracy. Thus, our present study provided the evidence that GJB2, SOD2, and CAT genes might account for the NIHL development in independently and/or in an interactive manner.
Asian Continental Ancestry Group ; genetics ; Case-Control Studies ; Catalase ; genetics ; China ; Connexin 26 ; Connexins ; genetics ; Genetic Predisposition to Disease ; Hearing Loss, Noise-Induced ; genetics ; Humans ; Male ; Superoxide Dismutase ; genetics

Asian Continental Ancestry Group ; genetics ; Case-Control Studies ; Genetic Predisposition to Disease ; Hearing Loss, Noise-Induced ; genetics ; Humans ; NF-E2-Related Factor 2 ; genetics ; Occupational Exposure

OBJECTIVETo investigate the association between single nucleotide polymorphisms (SNPs) in glutathione peroxidase 1 (GPX-1) gene, rs3448, rs1050450, rs1800668, and rs1987628, and the susceptibility to noise-induced hearing loss (NIHL) among Chinese Han population.

METHODSA case-control study was conducted to investigate the threshold shift of the left ear at 3000 Hz among the workers of Chinese Han population who were exposed to the same level of sound pressure. Two hundred and one (10%) of the subjects with the highest level of threshold shift were recruited in susceptible group, while 202 of (10%) of the subjects with the lowest level of threshold shift were recruited in tolerant group. Targeted occupational health survey and questionnaire survey were performed among these people. For each individual, genome DNA was extracted from 5 ml of fasting peripheral venous blood. Four SNPs (GPX-1 rs3448, rs1050450, rs1800668, and rs1987628) were genotyped by the TaqMan SNP genotyping kit. The main effects of SNPs and the association between NIHL susceptibility and SNPs were analyzed by logistic regression.

RESULTSThe C allele of rs1987628 was a risk factor for NIHL, with an odds ratio (OR) of 2.531 (95%CI: 1.878-3.411) as compared with the T allele. The CC genotype of rs1987628 was more associated with NIHL than the TT genotype (OR = 3.500, 95% CI: 1.984-6.174; adjusted OR = 3.544, 95% CI: 1.974 ∼ 6.364).

CONCLUSIONAmong Chinese Han population, GPX-1 SNP rs1987628 may be associated with the susceptibility to NIHL.

Adult ; Case-Control Studies ; Female ; Genetic Predisposition to Disease ; Glutathione Peroxidase ; genetics ; Hearing Loss, Noise-Induced ; genetics ; Humans ; Male ; Polymorphism, Single Nucleotide ; Young Adult

Numerous studies have shown that the health of spiral ganglion neurons is highly important for hearing. As a trophic factor of spiral ganglion neurons, neurotrophin 3 (NT3) is a potential candidate for prevention of spiral ganglion neuron degeneration in human. In our experiments, efficient transduction and long term expression of foreign gene of cochlea cells has been found with adenovirus carried lacZ gene (Ad-lacZ). A model of guinea pig deafness was made by intense noise exposure, which destroyed the entire organ of Corti in the middle part of the cochlea. Seven days after noise exposure, the animals were anesthetized and 1 10(8) recombinant adenoviral particles were injected into the scala tympani through the round window membrane. Animals inoculated with neurotrophin 3 adenovirus(Ad-NT3) were designated as the experimental group, animals inoculated with Ad-lacZ vector served as the control group. Four weeks after the inoculation of the virus, NT3 immunoreactivity was observed in the Ad-NT3 inoculated group. HE histochemical staining results showed that in the Ad-lacZ injected group, the neuronal degeneration was severer and the density of spiral ganglion neurons was significantly lower than those in the Ad-NT3 injected group. Our results demonstrate that with adenovirus-mediated overexpression NT3 may be developed into a new treatment to prevent secondary spiral ganglion degeneration following the damage to Corti organ.
Adenoviridae ; genetics ; Animals ; Cochlea ; pathology ; Gene Transfer Techniques ; Genetic Therapy ; Guinea Pigs ; Hearing Loss, Noise-Induced ; pathology ; In Vitro Techniques ; Neurotrophin 3 ; genetics ; Recombination, Genetic