title: Polycyclic aromatic hydrocarbons-associated microRNAs and their interactions with the environment: influences on oxidative DNA damage and lipid peroxidation in coke oven workers.
abstract: We previously identified five polycyclic aromatic hydrocarbons (PAHs)-associated microRNAs (miRNAs) and found they were associated with chromosome damage. As oxidative damage is the common contributory cause of various PAHs-related diseases, we further investigated the influences of these miRNAs and their interactions with environmental factors on oxidative DNA damage and lipid peroxidation. We measured PAHs internal exposure biomarkers [urinary monohydroxy-PAHs (OH-PAHs) and plasma benzo[a]pyrene-r-7,t-8,t-9,c-10-tetrahydotetrol-albumin (BPDE-Alb) adducts], the expression levels of PAHs-associated plasma miRNAs (miR-24-3p, miR-27a-3p, miR-142-5p, miR-28-5p, and miR-150-5p), and urinary biomarkers of oxidative DNA damage [8-hydroxydeoxyguanosine (8-OH-dG)] and lipid peroxidation [8-iso-prostaglandin-F2α (8-iso-PGF2α)] in 365 healthy male coke oven workers. These miRNAs were associated with a dose-response increase in 8-OH-dG (β > 0), and with a dose-response decrease in 8-iso-PGF2α (β < 0), especially in workers with lower PAHs exposure levels, in nonsmokers, and in nondrinkers. These miRNAs interacted antagonistically with ΣOH-PAHs and BPDE-Alb adducts (βinteraction < 0) and synergistically with drinking status (βinteraction > 0) to influence 8-OH-dG, while they interacted synergistically with BPDE-Alb adducts (βinteraction > 0) and antagonistically with smoking status (βinteraction < 0) to influence 8-iso-PGF2α. Our results suggested that miRNAs and their interactions with environmental factors might be novel mechanisms mediating the effects of PAHs exposure on oxidative DNA damage and lipid peroxidation.
authors.affiliation: Key Laboratory of Environment and Health, Ministry of Education & Ministry of Environmental Protection, and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology , Wuhan 430030, Hubei, China.
authors.forename: Qifei
authors.initials: Q
authors.lastname: Deng
authors.forename: Xiayun
authors.initials: X
authors.lastname: Dai
authors.forename: Huan
authors.initials: H
authors.lastname: Guo
authors.forename: Suli
authors.initials: S
authors.lastname: Huang
authors.forename: Dan
authors.initials: D
authors.lastname: Kuang
authors.forename: Jing
authors.initials: J
authors.lastname: Feng
authors.forename: Tian
authors.initials: T
authors.lastname: Wang
authors.forename: Wangzhen
authors.initials: W
authors.lastname: Zhang
authors.forename: Kun
authors.initials: K
authors.lastname: Huang
authors.forename: Die
authors.initials: D
authors.lastname: Hu
authors.forename: Huaxin
authors.initials: H
authors.lastname: Deng
authors.forename: Xiaomin
authors.initials: X
authors.lastname: Zhang
authors.forename: Tangchun
authors.initials: T
authors.lastname: Wu
mesh_terms: D000080242:8-Hydroxy-2'-Deoxyguanosine; D000328:Adult; D015415:Biomarkers / Q000652:urine; D003077:Coke; D004249:DNA Damage; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000652:urine; D015237:Dinoprost / Q000031:analogs & derivatives / Q000652:urine; D005786:Gene Expression Regulation; D006801:Humans; D008019:Life Style; D015227:Lipid Peroxidation / Q000235:genetics*; D008297:Male; D035683:MicroRNAs / Q000235:genetics / Q000378:metabolism*; D016273:Occupational Exposure / Q000032:analysis*; D010084:Oxidation-Reduction; D011084:Polycyclic Aromatic Hydrocarbons / Q000378:metabolism*
chemical_list: D015415:Biomarkers; D003077:Coke; D035683:MicroRNAs; D011084:Polycyclic Aromatic Hydrocarbons; C075750:8-epi-prostaglandin F2alpha; D000080242:8-Hydroxy-2'-Deoxyguanosine; D015237:Dinoprost; D003849:Deoxyguanosine