ArticleJournal of thoracic disease2016
PON2 and ATP2B2 gene polymorphisms with noise-induced hearing loss.
Article in Journal of thoracic disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed, 18 citations in OpenAlex.
- Comparison between logistic regression and machine learning algorithms on prediction of noise-induced hearing loss and investigation of SNP loci.Scientific reports · 2025Article
- Identification of oxidative stress-related diagnostic markers and immune infiltration features for idiopathic pulmonary fibrosis by bibliometrics and bioinformatics.Frontiers in medicine · 2024Review
- Occupational epidemiological characteristics of noise-induced hearing loss and the impact of combined exposure to noise and dust on workers' hearing-a retrospective study.Frontiers in public health · 2024Article
- The Role of Genetic Variants in the Susceptibility of Noise-Induced Hearing Loss.Frontiers in cellular neuroscience · 2022Review
- Polymorphisms in the FAS gene are associated with susceptibility to noise-induced hearing loss.Environmental science and pollution research international · 2021Article
- Human Paraoxonase-2 (PON2): Protein Functions and Modulation.Antioxidants (Basel, Switzerland) · 2021Review
- An overview of research trends and genetic polymorphisms for noise-induced hearing loss from 2009 to 2018.Environmental science and pollution research international · 2019Review
- Open chromatin dynamics in prosensory cells of the embryonic mouse cochlea.Scientific reports · 2019Article
- Paraoxonases Activities and Polymorphisms in Elderly and Old-Age Diseases: An Overview.Antioxidants (Basel, Switzerland) · 2019Review
- Cross-sectional associations between genetic polymorphisms in metabolic enzymes and longer leukocyte telomere length induced by omethoate.Oncotarget · 2017Article
- Review
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11 authors at 5 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundNoise-induced hearing loss (NIHL) is a complex disease induced by a combination of genetic and environmental factors. Paraoxonase2 (PON2) gene involved in the regulation of reactive oxygen species, and affecting the vulnerability of cochlea to NIHL, and ATPase, calcium-transporting, plasma membrane 2 (ATP2B2) gene which encodes plasma membrane calcium-transporting ATPase isoform 2 (PMCA2) are the candidate genes relating to the attack of NIHL. In this study, we investigated whether ATP2B2 and PON2 polymorphisms were associated with NIHL in Chinese of Han nationality population.
methodsWe performed a case-control study between six single nucleotide polymorphisms (SNPs) (rs1719571, rs3209637 and rs4327369 within ATP2B2, rs12026, rs7785846 and rs12704796 within PON2) and NIHL in 454 subjects. All the SNPs were genotypes, using the TaqMan MGB probe assay. Odds ratios (ORs) were calculated with 95% confidence intervals (95% CIs) with logistic regression analysis to test the level of association for SNPs.
resultsIn our study, 221 subjects with hearing loss and 233 subjects without hearing loss were recruited. The frequencies of the CG and CG + GG genotype of rs12026 (PON2) conferred risk factors for NIHL with adjusted OR values of 2.62 (95% CI, 1.69-4.06) and 2.48 (95% CI, 1.63-3.78), respectively. This kind of significance was also found at locus rs7785846, where genotypes CT and CT + TT were the risk types, with adjusted ORs of 2.52 (95% CI, 1.62-3.93) and 2.35 (95% CI, 1.54-3.58), respectively. We performed stratified analysis per noise exposure level, when it came to rs7785846 and rs12026 in the >92 dB(A) noise exposure group, the subjects who carried heterozygote were of significantly (P<0.01) higher susceptibility to NIHL than homozygote carriers. By contrast, no significantly higher risk was found for any rs12704796 genotypes or any genotypes in ATP2B2 (P>0.05), which may suggest that these SNPs did not have significant effects on noise susceptibility across noise exposure.
conclusionsOur research suggested that PON2 might play a role in the etiology of NIHL in Chinese of Han nationality population.
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