Reduction in mitochondrial DNA methylation leads to compensatory increase in mitochondrial DNA content: novel blood-borne biomarkers for monitoring occupational noise.
- Author:
Jia-Hao YANG
1
;
Zhuo-Ran LI
1
;
Zhuo-Zhang TAN
2
;
Wu-Zhong LIU
3
;
Qiang HOU
3
;
Pin SUN
1
;
Xue-Tao ZHANG
3
Author Information
- Publication Type:Journal Article
- Keywords: Hearing abnormality; Mitochondrial DNA damage; Mitochondrial DNA methylation; Occupational noise exposure
- MeSH: Humans; DNA, Mitochondrial; DNA Methylation; Male; Adult; Noise, Occupational/adverse effects*; Middle Aged; Occupational Exposure/adverse effects*; Biomarkers/blood*; Female
- From:Environmental Health and Preventive Medicine 2025;30():40-40
- CountryJapan
- Language:English
-
Abstract:
BACKGROUND:Prolonged occupational noise exposure poses potential health risks, but its impact on mitochondrial DNA (mtDNA) damage and methylation patterns remains unclear.
METHOD:We recruited 306 factory workers, using average binaural high-frequency hearing thresholds from pure-tone audiometry to assess noise exposure. MtDNA damage was evaluated through mitochondrial DNA copy number (mtDNAcn) and lesion rate, and mtDNA methylation changes were identified via pyrophosphate sequencing.
RESULTS:There was a reduction in MT-RNR1 methylation of 4.52% (95% CI: -7.43% to -1.62%) among workers with abnormal hearing, whereas changes in the D-loop region were not statistically significant (β = -2.06%, 95% CI: -4.44% to 0.31%). MtDNAcn showed a negative association with MT-RNR1 methylation (β = -0.95, 95% CI: -1.23 to -0.66), while no significant link was found with D-loop methylation (β = -0.05, 95% CI: -0.58 to 0.48). Mediation analysis indicated a significant increase in mtDNAcn by 10.75 units (95% CI: 3.00 to 21.26) in those with abnormal hearing, with MT-RNR1 methylation mediating 35.9% of this effect.
CONCLUSIONS:These findings suggest that occupational noise exposure may influence compensatory increases in mtDNA content through altered MT-RNR1 methylation.
