Exploring Biomarkers for Noise-Induced Hearing Loss through Mitochondrial DNA Methylation Analysis

Dianpeng Wang^1,2*Caiping Li²Liuwei Shi^1,3Dafeng Lin¹Shaofan Weng¹Xiangli Yang¹Peimao Li¹Zhimin Zhang¹Wen Zhang¹Yan Guo¹Guangtao Yang¹Zhenlie Huang^2*Naixing Zhang^1*

• ¹Shenzhen Prevention and Treatment Center for Occupational Diseases,China, Shenzhen, China
• ²Southern Medical University, Guangzhou, Guangdong, China
• ³Jilin University, Changchun, Hebei Province, China

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.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).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).