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

Area of Science:

• Molecular Biology
• Genetics
• Audiology

Background:

• Noise-induced hearing loss (NIHL) is a prevalent occupational disease.
• Occupational noise exposure damages cochlear cells via mitochondrial oxidative stress and reactive oxygen species (ROS).
• Mitochondrial dysfunction and apoptosis are key mechanisms in NIHL pathogenesis.

Purpose of the Study:

• To investigate the impact of noise-induced oxidative stress on mitochondrial DNA methylation.
• To identify potential molecular biomarkers for NIHL.
• To explore the relationship between mitochondrial DNA methylation patterns and NIHL.

Main Methods:

• Genome-wide methylation sequencing of mitochondrial DNA was performed on 40 NIHL cases and 40 controls.
• Targeted region sequencing utilized bisulfite multiplex PCR capture and high-depth next-generation sequencing (NGS).
• Analysis focused on differential methylation sites within mitochondrial genes.

Main Results:

• Significant differences in mitochondrial DNA methylation were observed at 53 sites in NIHL cases compared to controls.
• Lower methylation levels were found in genes like ATP6 and CYB in the NIHL group.
• The CYB gene demonstrated high diagnostic potential with an AUC of 0.807 in ROC analysis.

Conclusions:

• Mitochondrial DNA methylation, particularly in ATP6 and CYB genes, is reduced in individuals with NIHL.
• The CYB gene methylation pattern emerges as a promising potential biomarker for NIHL diagnosis.
• Further research is warranted to explore complex interactions and develop advanced diagnostic and therapeutic strategies for NIHL.