Polycyclic aromatic hydrocarbon exposure, miRNA genetic variations, and associated leukocyte mitochondrial DNA copy number: A cross-sectional study in China

Mitochondria DNA was preferentially attacked by the exogenous carcinogens including polycyclic aromatic hydrocarbons (PAHs) relative to nuclear DNA, and nuclear gene variants may account for variability in the mitochondrial DNA copy number (mtDNAcn). However, it remains unclear whether miRNA genetic...

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Veröffentlicht in:Chemosphere (Oxford) 2020-05, Vol.246, p.125773-125773, Article 125773
Hauptverfasser: Duan, Xiaoran, Yang, Yongli, Zhang, Hui, Liu, Bin, Wei, Wan, Wang, Liuya, Sun, Changqing, Yao, Wu, Cui, Liuxin, Zhou, Xiaoshan, Wang, Wei
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container_title Chemosphere (Oxford)
container_volume 246
creator Duan, Xiaoran
Yang, Yongli
Zhang, Hui
Liu, Bin
Wei, Wan
Wang, Liuya
Sun, Changqing
Yao, Wu
Cui, Liuxin
Zhou, Xiaoshan
Wang, Wei
description Mitochondria DNA was preferentially attacked by the exogenous carcinogens including polycyclic aromatic hydrocarbons (PAHs) relative to nuclear DNA, and nuclear gene variants may account for variability in the mitochondrial DNA copy number (mtDNAcn). However, it remains unclear whether miRNA genetic variations are associated with mitochondrial DNA damage in the PAH-exposed workers. Therefore, we measured the leukocyte mtDNAcn, urinary 1-hydroxypyrene (1-OHPYR), environmental PAH exposure, and miRNA genetic polymorphisms among 544 coke oven workers and 238 healthy control participants. We found that the mtDNAcn in the exposure group (0.60 ± 0.29) was significantly lower than that in the control group (1.03 ± 0.31) (t = 18.931, P 
doi_str_mv 10.1016/j.chemosphere.2019.125773
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However, it remains unclear whether miRNA genetic variations are associated with mitochondrial DNA damage in the PAH-exposed workers. Therefore, we measured the leukocyte mtDNAcn, urinary 1-hydroxypyrene (1-OHPYR), environmental PAH exposure, and miRNA genetic polymorphisms among 544 coke oven workers and 238 healthy control participants. We found that the mtDNAcn in the exposure group (0.60 ± 0.29) was significantly lower than that in the control group (1.03 ± 0.31) (t = 18.931, P &lt; 0.001). Spearman correlation analysis showed that the peripheral blood leukocyte mtDNAcn had significantly negative correlations with the levels of 1-OHPYR and environmental PAH exposure (P &lt; 0.001). Covariance analysis indicated that miR-210 rs11246190 AA, miR-210 rs7395206 CC, and miR-126 rs2297538 GG probably promoted a decrease in leukocyte mtDNAcn in the exposure or control groups (P &lt; 0.05). In generalized linear model, miR-210 rs11246190 GG was a protective factor of mtDNAcn, and environmental PAH exposure was the risk factor of the mtDNAcn. In conclusion, the decrease of leukocyte mtDNAcn is the result of a combination of environmental and genetic factors. [Display omitted] •mtDNAcn decreased with environmental PAH exposure.•miR-210 rs11246190 GG was a protective factor of mtDNAcn.•The other 14 polymorphisms in miRNA had null effects on mtDNAcn.</description><identifier>ISSN: 0045-6535</identifier><identifier>EISSN: 1879-1298</identifier><identifier>DOI: 10.1016/j.chemosphere.2019.125773</identifier><identifier>PMID: 31911328</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Adult ; Carcinogens - analysis ; China ; Coke - analysis ; Cross-Sectional Studies ; DNA Copy Number Variations ; DNA Damage ; DNA, Complementary ; DNA, Mitochondrial - genetics ; Environmental Exposure - analysis ; Environmental Exposure - statistics &amp; numerical data ; Environmental Pollutants - analysis ; Environmental Pollutants - toxicity ; Female ; Humans ; Leukocytes - chemistry ; Male ; MicroRNAs - metabolism ; Middle Aged ; miRNA ; Mitochondria - genetics ; Mitochondrial DNA copy number ; Occupational Exposure - analysis ; Polycyclic aromatic hydrocarbons ; Polycyclic Aromatic Hydrocarbons - analysis ; Polycyclic Aromatic Hydrocarbons - metabolism ; Polycyclic Aromatic Hydrocarbons - toxicity ; rs11246190 ; Young Adult</subject><ispartof>Chemosphere (Oxford), 2020-05, Vol.246, p.125773-125773, Article 125773</ispartof><rights>2020 Elsevier Ltd</rights><rights>Copyright © 2020 Elsevier Ltd. 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However, it remains unclear whether miRNA genetic variations are associated with mitochondrial DNA damage in the PAH-exposed workers. Therefore, we measured the leukocyte mtDNAcn, urinary 1-hydroxypyrene (1-OHPYR), environmental PAH exposure, and miRNA genetic polymorphisms among 544 coke oven workers and 238 healthy control participants. We found that the mtDNAcn in the exposure group (0.60 ± 0.29) was significantly lower than that in the control group (1.03 ± 0.31) (t = 18.931, P &lt; 0.001). Spearman correlation analysis showed that the peripheral blood leukocyte mtDNAcn had significantly negative correlations with the levels of 1-OHPYR and environmental PAH exposure (P &lt; 0.001). Covariance analysis indicated that miR-210 rs11246190 AA, miR-210 rs7395206 CC, and miR-126 rs2297538 GG probably promoted a decrease in leukocyte mtDNAcn in the exposure or control groups (P &lt; 0.05). In generalized linear model, miR-210 rs11246190 GG was a protective factor of mtDNAcn, and environmental PAH exposure was the risk factor of the mtDNAcn. In conclusion, the decrease of leukocyte mtDNAcn is the result of a combination of environmental and genetic factors. 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However, it remains unclear whether miRNA genetic variations are associated with mitochondrial DNA damage in the PAH-exposed workers. Therefore, we measured the leukocyte mtDNAcn, urinary 1-hydroxypyrene (1-OHPYR), environmental PAH exposure, and miRNA genetic polymorphisms among 544 coke oven workers and 238 healthy control participants. We found that the mtDNAcn in the exposure group (0.60 ± 0.29) was significantly lower than that in the control group (1.03 ± 0.31) (t = 18.931, P &lt; 0.001). Spearman correlation analysis showed that the peripheral blood leukocyte mtDNAcn had significantly negative correlations with the levels of 1-OHPYR and environmental PAH exposure (P &lt; 0.001). Covariance analysis indicated that miR-210 rs11246190 AA, miR-210 rs7395206 CC, and miR-126 rs2297538 GG probably promoted a decrease in leukocyte mtDNAcn in the exposure or control groups (P &lt; 0.05). In generalized linear model, miR-210 rs11246190 GG was a protective factor of mtDNAcn, and environmental PAH exposure was the risk factor of the mtDNAcn. In conclusion, the decrease of leukocyte mtDNAcn is the result of a combination of environmental and genetic factors. [Display omitted] •mtDNAcn decreased with environmental PAH exposure.•miR-210 rs11246190 GG was a protective factor of mtDNAcn.•The other 14 polymorphisms in miRNA had null effects on mtDNAcn.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>31911328</pmid><doi>10.1016/j.chemosphere.2019.125773</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0002-5278-5538</orcidid><orcidid>https://orcid.org/0000-0001-8533-7750</orcidid><orcidid>https://orcid.org/0000-0002-0708-8848</orcidid></addata></record>
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subjects Adult
Carcinogens - analysis
China
Coke - analysis
Cross-Sectional Studies
DNA Copy Number Variations
DNA Damage
DNA, Complementary
DNA, Mitochondrial - genetics
Environmental Exposure - analysis
Environmental Exposure - statistics & numerical data
Environmental Pollutants - analysis
Environmental Pollutants - toxicity
Female
Humans
Leukocytes - chemistry
Male
MicroRNAs - metabolism
Middle Aged
miRNA
Mitochondria - genetics
Mitochondrial DNA copy number
Occupational Exposure - analysis
Polycyclic aromatic hydrocarbons
Polycyclic Aromatic Hydrocarbons - analysis
Polycyclic Aromatic Hydrocarbons - metabolism
Polycyclic Aromatic Hydrocarbons - toxicity
rs11246190
Young Adult
title Polycyclic aromatic hydrocarbon exposure, miRNA genetic variations, and associated leukocyte mitochondrial DNA copy number: A cross-sectional study in China
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