System Maintenance Notice

Please note that maintenance work is scheduled between 4 AM and 5 AM - CET. During this time, you may experience reduced performance. Thanks for your patience.

Publications

Journal Article Epublish

PubMed: 40689209 DOI: 10.3389/fphar.2025.1561791

Exploring biomarkers for noise-induced hearing loss through mitochondrial DNA methylation analysis.

Front Pharmacol 16:1561791

Authors: Dianpeng Wang, Caiping Li, Liuwei Shi, Dafeng Lin, Shaofan Weng, Xiangli Yang, Peimao Li, Zhimin Zhang, Wen Zhang, Yan Guo, Guangtao Yang, Zhenlie Huang, Naixing Zhang

Affiliations

  • School of Public Health, Southern Medical University, Guangzhou, China. Shenzhen Prevention and Treatment Center for Occupational Diseases, Shenzhen, China.
  • Shenzhen Prevention and Treatment Center for Occupational Diseases, Shenzhen, China. School of Public Health, Jilin University, Changchun, China.
  • Shenzhen Prevention and Treatment Center for Occupational Diseases, Shenzhen, China.
  • School of Public Health, Southern Medical University, Guangzhou, China.

Abstract

Objective

Noise-induced hearing loss (NIHL), resulting from occupational noise exposure, is a significant health concern with considerable economic and social implications. It is the most commonly reported occupational disease in developing countries. Noise causes cochlear cell damage by inducing mitochondrial oxidative stress elevating reactive oxygen species (ROS), ultimately leading to cell apoptosis. This study explores the impact of noise-induced oxidative stress on mitochondrial DNA methylation and aims to identify potential molecular biomarkers for NIHL.

Methods

This study included 40 cases of NIHL and 40 controls. Mitochondrial genome-wide methylation sequencing was performed using a targeted region approach with bisulfite multiplex PCR capture technology and high-depth next-generation sequencing (NGS).

Results

The analysis revealed significant differences in methylation levels at 53 sites within mitochondrial genes, including 12S_rRNA, 16S_rRNA, tRNA-Ile, ND2, tRNA-Trp, CO1, CO2, ATP6, and CYB, with lower methylation levels observed in the case group compared to controls. In contrast, methylation levels at 31 sites, including 12S_rRNA, tRNA-Val, 16S_rRNA, CO1, CO3, ND3, tRNA-Arg, ND4, and ND5, were significantly higher in the case group. Receiver Operating Characteristic (ROC) curve analysis showed that the CYB gene had an area under the curve (AUC) of 0.807, with high sensitivity (0.90) and reasonable specificity (0.70).

Conclusion

This study demonstrates a reduction in mitochondrial DNA methylation, particularly in the ATP6 and CYB genes, among individuals with NIHL. These findings suggest that mitochondrial DNA methylation, especially in the CYB gene, could serve as a potential biomarker for NIHL. However, given the complex interplay of various factors, including genetic, environmental, and lifestyle influences, further research is needed to fully understand the role of mitochondrial DNA methylation and oxidative stress in NIHL. Future studies should focus on identifying additional biomarkers and elucidating their mechanistic relationships, which could lead to more accurate diagnostic tools and therapeutic strategies.

MeSH

Cells, Genes, Hearing Loss, Noise-Induced, Stress, Physiological, Hearing, Oxidative Stress, Biomarkers, Dna Methylation, Dna, Mitochondrial, Hearing Loss, Dna