Dataset Information

Association of GST gene polymorphism and noise-induced hearing loss: GST gene polymorphism and NIHL.

ABSTRACT:

Background

It has been proposed that Noise-induced hearing loss is a complex disease that is combination of environmental and genetic factors. There are inconsistent results concerning the association between variation in glutathione S-transferase (GST) genetic polymorphisms (GSTT1 rs1049055 and GSTM1 rs10712361) and susceptibility to Noise-induced hearing loss.

Objective

This study was designed to assess the association between GST gene polymorphism and Noise-induced hearing loss among noise-exposed workers. Methods: In a case-control study, male workers from tile and ceramic factories were selected randomly. Subjects were classified into two groups according to the result of audiometry: 73 subjects showed Noise-induced hearing loss which was considered in the case group and 87 subjects without hearing loss was enrolled in the control group. The GSTT1 and GSTM1 polymorphism of both groups were assessed by multiplex polymerase chain reaction.

Results

Null GSTT1 and GSTM1 genotypes were more frequent in case group but no significant statistical difference was seen in case and control groups. No significant link between GSTT1 and GSTM1 genotypes was found.

Conclusion

This study suggests that the genetic variability of GSTT1 and GSTM1 has no effect on susceptibility to noise induced hearing loss.

SUBMITTER: Loukzadeh Z

PROVIDER: S-EPMC6940572 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Publications

Association of GST gene polymorphism and noise-induced hearing loss: GST gene polymorphism and NIHL.

Loukzadeh Ziba Z Sani Hadi Eshaghi HE Sheikhha Mohammad Hasan MH Ratki Farzaneh Morteza FM

AIMS public health 20191211 4

<h4>Background</h4>It has been proposed that Noise-induced hearing loss is a complex disease that is combination of environmental and genetic factors. There are inconsistent results concerning the association between variation in glutathione S-transferase (<i>GST</i>) genetic polymorphisms (<i>GSTT1</i> rs1049055 and <i>GSTM1</i> rs10712361) and susceptibility to Noise-induced hearing loss.<h4>Objective</h4>This study was designed to assess the association between <i>GST</i> gene polymorphism an ...[more]

PMID: 31909074

Similar Datasets

Project description: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.

Project description:Noise-induced hearing loss (NIHL) is a prevalent form of adult hearing impairment, characterized by oxidative damage to auditory sensory hair cells. Although certain dihydropyridines, the L-type calcium channel blockers, exhibit protective properties against such damage, the ability of third-generation dihydropryidines like lercanidipine to mitigate NIHL remains unclear.We utilized glucose oxidase (GO)-treated OC1 cell lines and cochlear explants to evaluate the protective influence of lercanidipine on hair cells. To further investigate its effectiveness, we exposed noise-stimulated mice in vivo and analyzed their hearing thresholds. Additionally, we assessed the antioxidative capabilities of lercanidipine by examining oxidation-related enzyme expression and levels of oxidative stress markers, including 3-nitrotyrosine (3NT) and 4-hydroxynonenal (4HNE). Our findings demonstrate that lercanidipine significantly reduces the adverse impacts of GO on both OC-1 cell viability (0.3 to 2.5 µM) and outer hair cell (OHC) survival in basal turn cochlear explants (7 µM). These results are associated with increased mRNA expression of antioxidant enzyme genes (HO-1, SOD1/2, and Txnrd1), along with decreased expression of oxidase genes (COX-2, iNOS). Crucially, lercanidipine administration prior to, and following, noise exposure effectively ameliorates NIHL, as evidenced by lowered hearing thresholds and preserved OHC populations in the basal turn, 14 days post-noise stimulation at 110 dB SPL. Moreover, our observations indicate that lercanidipine's antioxidative action persists even three days after simultaneous drug and noise treatments, based on 3-nitrotyrosine and 4-hydroxynonenal immunostaining in the basal turn. Based on these findings, we propose that lercanidipine has the capacity to alleviate NIHL and safeguard OHC survival in the basal turn, potentially via its antioxidative mechanism. These results suggest that lercanidipine holds promise as a clinically viable option for preventing NIHL in affected individuals.

Dataset Information

Association of GST gene polymorphism and noise-induced hearing loss: GST gene polymorphism and NIHL.

Background

Objective

Results

Conclusion

Publications

Association of GST gene polymorphism and noise-induced hearing loss: GST gene polymorphism and NIHL.

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