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Formation of Covalent DNA Adducts by Enzymatically Activated Carcinogens and Drugs In Vitro and Their Determination by 32P-postlabeling
Published on: March 20, 2018
Urinary polycyclic aromatic hydrocarbon metabolites, peripheral blood mitochondrial DNA copy number, and
Juanjuan Du1, Baolong Pan2, Xiaomin Cao1
1Department of Occupational Health, School of Public Health, Shanxi Medical University, Taiyuan, Shanxi, 030001, China.
Background:
Polycyclic aromatic hydrocarbons (PAHs) are the risk factors for workers' neurological performance, which were widely exist in the occupational environment.
Objective:
We aimed to investigate the dose-response relationship between various PAH metabolites and workers' neurobehavioral changes and to explore whether mitochondrial DNA copy number (mtDNAcn) can be used as a potential biomarker to reflect changes in neurobehavioral behavior.
Method:
A total of 697 workers were recruited from a coke oven plant. The concentrations of eleven PAHs metabolites were determined by HPLC-MS/MS. Peripheral blood mtDNAcn was measured using QPCR. Neurobehavioral function was measured by NCTB questionnaire. The dose-response relationships were evaluated using restricted cubic spline models. Mediation analysis was also carried out.
Results:
We found dose-response relationships between urinary 2-hydroxynaphthalene (2-OH Nap), sum of PAH metabolites (Ʃ -OH PAHs) and total digit span (DSP), backward digit span (DSPB), forward digit span (DSPF) and mtDNAcn. Each one-unit increase in ln-transformed of 2-OH Nap or Ʃ -OH PAHs was associated with a 2.64 or 3.22 decrease in DSP, a 1.20 or 1.58 decrease in DSPF, a 1.44 or 1.62 decrease in DSPB and a 0.13 or 0.12 decrease in mtDNAcn. However, we did not find a significant mediation effect of mtDNAcn between PAHs metabolites and DSP, DSPF, or DSPB.
Conclusion:
Our data indicated that workers urinary 2-hydroxynaphthalene and sum of PAH metabolites levels were inversely associated with mtDNAcn and neurobehavior, especially their auditory memory. However, there was no significant mediation effect of mtDNAcn between urinary PAHs metabolites and neurobehavior.

