Noise induced hearing loss (NIHL), a multifactorial disease involving both genetic and environmental factors, is one of the most important occupational health hazards. Nonetheless, the influence of FOXO3 variants on NIHL risk have not been illuminated. This research was conducted to explore the effects of FOXO3 polymorphisms on individual susceptibility to NIHL. A total of 2689 industrial workers from one textile factory of east China were recruited to participate in the current research. Venous blood was collected, questionnaire and pure-tone audiometry (PTA) was conducted by specialist physicians. Then, we performed genotyping of three selected SNPs (rs2802292, rs10457180, and rs12206094) in FOXO3 gene in 566 NIHL patients and 566 controls. Subsequently, the main effects of genotype and its interactions were evaluated. Our results revealed that individuals with the allele of rs2802292, allele of rs10457180, allele of rs12206094 (OR = 1.43, 1.43, and 1.31 respectively) and the haplotype and others () (rs2802292-rs10457180-rs12206094) (OR = 1.49 and 2.09 respectively) are associated with an increased risk of NIHL in a Chinese population. Stratified analysis showed that an increased NIHL risk was found in the subjects who exposed to noise >16 years with rs2802292 and rs10457180 AG/GG genotype with an OR of 1.62 and 1.66 respectively. Multifactor dimensionality reduction analysis indicated that rs10457180, rs2802292, and rs12206094 have interactions and are related to increased NIHL risk (OR = 1.53). The genetic polymorphism rs2802292, rs10457180, and rs12206094 within FOXO3 gene are associated with an increased risk of NIHL in a Chinese population and have potential to be biomarkers for noise exposed workers.

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Objectives. e purpose of this study was to investigate the correlation between single-nucleotide polymorphism (SNP) in 3′UTR of XPO5 gene and the occurrence of noise-induced hearing loss (NIHL), and to further explore the regulatory mechanism of miRNAs in NIHL on XPO5 gene. Methods.We conducted a case-control study involving 1040 cases and 1060 controls. e effects of SNPs on XPO5 expression were studied by genotyping, real-time polymerase chain reaction (qPCR), cell transfection, and the dual-luciferase reporter assay. Results.We genotyped four SNPs (rs2257082, rs11077, rs7755135, and rs1106841) in the XPO5 gene. e rs2257082 AG/GG carriers have special connection to an increased risk of noise-induced hearing loss compared to the AA carriers. e rs11077TG/GG carriers had a significantly increased association with NIHL susceptibility than the TT carriers. ere was a higher risk of NIHL in the XPO5 gene rs7755135 CC carriers than in the TT carriers. No statistically significant correlation was obtained with respect to SNPrs1106841. Functional experiments showed that the rs11077 change might inhibit the interaction between miRNAs (miRNA-4763-5p, miRNA-5002-3p, and miRNA-617) and XPO5, with rs11077G allele resulting in overexpression of XPO5. Conclusion. e genetic polymorphism, rs11077, within XPO5 is associated with the risk of noise-induced hearing loss in a Chinese population.

ObjectiveWe aim to investigate whether genetic mutations in three important base excision repair genes (OGG1, APEX1, and XRCC1) may influence susceptibility to noise-induced hearing loss. MethodsThree SNPs in OGG1, APEX1, and XRCC1 were genotyped from noise exposed workers who were classified into susceptible and resistant individuals. Results: Results showed that the rs1799782 TT genotype located in the XRCC1 coding region and rs1130409 GG/GT in the APEX1 coding region were associated with increased risk for noise-induced hearing loss. Compared to the rs1799782 C allele frequency, the T allele frequency increased in the sensitive group (OR = 1.51). Rs1130409 G allele frequency also increased in the sensitive group compared to the resistant group (OR = 1.59). ConclusionsXRCC1 rs1799782 and APEX1 rs1130409 may have potential as biomarkers for screening susceptibility to NIHL in workers exposed severe noise. hearing loss in a Chinese population. International archives of occupational and environmental health 2016, 89(4):621-628. 19. Lou XY, Chen GB, Yan L, Ma JZ, Zhu J, Elston RC, Li MD: A generalized combinatorial approach for detecting gene-by-gene and gene-byenvironment interactions with application to nicotine dependence. American journal of human genetics 2007, 80(6):1125-1137. 20. Shi YY, He L: SHEsis, a powerful software platform for analyses of linkage disequilibrium, haplotype construction, and genetic association at polymorphism loci. Cell Res 2005, 15(2):97-98. 21. Lamerdin JE, Montgomery MA, Stilwagen SA, Scheidecker LK, Tebbs RS, Brookman KW, Thompson LH, Carrano AV: Genomic sequence comparison of the human and mouse XRCC1 DNA repair gene regions. Genomics 1995, 25(2):547-554. (5):801-807. 23. Hadi MZ, Coleman MA, Fidelis K, Mohrenweiser HW, Wilson DM, 3rd: Functional characterization of Ape1 variants identified in the human population. Nucleic acids research 2000, 28(20):3871-3879. 24.Au WW, Salama SA, Sierra-Torres CH: Functional characterization of polymorphisms in DNA repair genes using cytogenetic challenge assays.