Reduction in mitochondrial DNA methylation leads to compensatory increase in mitochondrial DNA content: novel blood-borne biomarkers for monitoring occupational noise

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...

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Bibliographic Details
Main Authors: Jia-Hao Yang, Zhuo-Ran Li, Zhuo-Zhang Tan, Wu-Zhong Liu, Qiang Hou, Pin Sun, Xue-Tao Zhang
Format: Article
Language:English
Published: Komiyama Printing Co. Ltd 2025-05-01
Series:Environmental Health and Preventive Medicine
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Online Access:https://www.jstage.jst.go.jp/article/ehpm/30/0/30_25-00006/_html/-char/en
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Summary: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.
ISSN:1342-078X
1347-4715