Genetic association between methionine sulfoxide reductase B1 polymorphisms and risk of noise-induced hearing loss
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Hanin Alwaqfi 1 , Safa Alqudah 1 2 * , Amjad A Mahasneh 1 3 , Margaret Zuriekat 4
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1 Jordan University of Science and Technology, Irbid, JORDAN2 Taibah University, Median, SAUDI ARABIA3 American University of Sharjah, Sharjah, UAE4 The University of Jordan, Amman, JORDAN* Corresponding Author

Abstract

Purpose: Hearing loss is the loss of hearing function in one or both ears. Noise-induced hearing loss (NIHL) is the second most prevalent type of sensorineural hearing loss, adversely affects the functional and social lives of workers in noisy environments. This study aimed to confirm the relationship between methionine sulfoxide reductase B1 (MSRB1) expression in the human auditory system and noise exposure by searching for related pathogenic single-nucleotide polymorphisms (SNPs).
Methodology: The study included 90 workers with NIHL and 90 with normal hearing. A hearing test was administered to each participant, and blood samples were collected from both groups to conduct genetic analyses. A comparison of the genomes of workers with NIHL and those with normal hearing was performed.
Results: The results showed that rs732510 was found in NIHL participants, while the other SNPs (rs2815304, rs11640479, and rs9934331) were found in both controls and NIHL subjects. Among the NIHL group, 44 participants had heterozygous mutants (TC), 30 had homozygous mutants (CC), and 13 had homozygous wild-type alleles (TT). The heterozygous mutant allele had a statistically significantly higher prevalence (48.9%) compared to the homozygous wild-type allele (14.4%) and homozygous mutant allele (33.3%) among patients with NIHL (χ2[3] = 43.96, p < 0.05).
Conclusion: This study is the first to report an association between rs732510 in MSRB1 and NIHL in the human auditory system. This finding paves the way for future research to discover more about the gene’s role in the auditory function, suggesting it could be a promising biological biomarker associated with NIHL.

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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Article Type: Original Article

ELECTRON J GEN MED, Volume 22, Issue 6, December 2025, Article No: em691

https://doi.org/10.29333/ejgm/17048

Publication date: 01 Nov 2025

Online publication date: 16 Sep 2025

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