Gene-Environment Interactions Between Environmental Response Genes Polymorphisms and Mitochondrial DNA Copy Numbers
Buqiang Ji1, Long Yan Xiao, Jing-Chao Ren
1Department of Hematology, Linyi People's Hospital, 27 Jifang Road, Linyi, China (Ji, Xiao), School of Public Health, Xinxiang Medical University, 601 Jinsui Road, Xinxiang, China (Ren, Zhang, Wang, Dong, Li, Zhang), Department of Occupational Health and Toxicology, School of Public Health, Fudan University, 138 Yixueyuan Road, Shanghai, China (Xia).
Objective:
To determine the effect of mitochondrial DNA copy number (mtDNAcn) as a biomarker of benzene exposure.
Methods:
A total of 294 benzene-exposed workers and 102 controls were recruited. Biomarkers of mtDNAcn, cytokinesis-block micronucleus (MN) frequency, and peripheral blood white blood cells (WBC) were detected. Eighteen polymorphism sites in DNA damage repair and metabolic genes were analyzed.
Results:
Benzene exposure increased mtDNAcn and indicated a dose-response relationship (P < 0.001). mtDNAcn was negatively correlated with WBC count and DNA methylation and positively correlated with MN frequency. The AG type in rs1695 interacted with benzene exposure to aggravate mtDNAcn (β = 0.006, 95% CI: 0, 0.012, P = 0.050). rs13181, rs1695, rs1800975, and GSTM1 null were associated with benzene-induced mtDNAcn. Rs1695 interacted with benzene to increase mitochondrial damage.
Conclusions:
Benzene exposure increases mtDNAcn levels in benzene-exposed workers.
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