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Tytuł:
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Global H3K79 di-methylation mediates DNA damage response to PAH exposure in Chinese coke oven workers.
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Autorzy:
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Zhang Z; Guangdong Provincial Key Laboratory of Food, Nutrition and Health, Department of Toxicology, School of Public Health, Sun Yat-sen University, Guangzhou, 510080, China; Food Safety and Health Research Center, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health, Southern Medical University, Guangzhou, 510515, China.
Xing X; Guangdong Provincial Key Laboratory of Food, Nutrition and Health, Department of Toxicology, School of Public Health, Sun Yat-sen University, Guangzhou, 510080, China.
Jiang S; Guangdong Provincial Key Laboratory of Food, Nutrition and Health, Department of Toxicology, School of Public Health, Sun Yat-sen University, Guangzhou, 510080, China.
Qiu C; Department of Intensive Care Unit, The First Affiliated Hospital of Sun Yat-sen University, 58, Zhongshan Road 2, Guangzhou, China.
Mo Z; Guangdong Provincial Key Laboratory of Food, Nutrition and Health, Department of Toxicology, School of Public Health, Sun Yat-sen University, Guangzhou, 510080, China.
Chen S; Guangdong Provincial Key Laboratory of Food, Nutrition and Health, Department of Toxicology, School of Public Health, Sun Yat-sen University, Guangzhou, 510080, China.
Chen L; Guangdong Provincial Key Laboratory of Food, Nutrition and Health, Department of Toxicology, School of Public Health, Sun Yat-sen University, Guangzhou, 510080, China.
Wang Q; Guangdong Provincial Key Laboratory of Food, Nutrition and Health, Department of Toxicology, School of Public Health, Sun Yat-sen University, Guangzhou, 510080, China.
Xiao Y; Guangdong Provincial Key Laboratory of Food, Nutrition and Health, Department of Toxicology, School of Public Health, Sun Yat-sen University, Guangzhou, 510080, China.
Dong G; Guangdong Provincial Key Laboratory of Food, Nutrition and Health, Department of Toxicology, School of Public Health, Sun Yat-sen University, Guangzhou, 510080, China.
Zheng Y; Qingdao University, Qingdao, 266021, China.
Chen W; Guangdong Provincial Key Laboratory of Food, Nutrition and Health, Department of Toxicology, School of Public Health, Sun Yat-sen University, Guangzhou, 510080, China.
Li D; Guangdong Provincial Key Laboratory of Food, Nutrition and Health, Department of Toxicology, School of Public Health, Sun Yat-sen University, Guangzhou, 510080, China. Electronic address: .
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Źródło:
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Environmental pollution (Barking, Essex : 1987) [Environ Pollut] 2021 Jan 01; Vol. 268 (Pt B), pp. 115956. Date of Electronic Publication: 2020 Oct 29.
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Typ publikacji:
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Journal Article
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Język:
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English
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Imprint Name(s):
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Original Publication: Barking, Essex, England : Elsevier Applied Science Publishers, c1987-
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MeSH Terms:
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Coke*
Occupational Exposure*/analysis
Polycyclic Aromatic Hydrocarbons*/analysis
Polycyclic Aromatic Hydrocarbons*/toxicity
Asian People ; DNA Damage ; Humans ; Male ; Methylation ; Pyrenes/analysis
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Contributed Indexing:
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Keywords: Coke oven workers; DNA damage Response; DOT1L; Histone H3 lysine 79 di-methylation; Polycyclic aromatic hydrocarbons
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Substance Nomenclature:
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0 (Coke)
0 (Polycyclic Aromatic Hydrocarbons)
0 (Pyrenes)
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Entry Date(s):
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Date Created: 20201107 Date Completed: 20201218 Latest Revision: 20221207
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Update Code:
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20240105
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DOI:
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10.1016/j.envpol.2020.115956
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PMID:
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33158619
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Polycyclic aromatic hydrocarbons (PAHs) are the main contaminants of coke oven emissions which can induce serious genetic damage in coke oven workers. Epigenetic alternations play essential roles in the regulation of DNA damage effect of PAHs. Previous studies indicate that H3K79 di-methylation (H3K79me2) is integral in DNA damage repair. However, the potential role of H3K79me2 in DNA damage response (DDR) following PAHs exposure is still unclear. In this study, we recruited 256 male coke oven workers and control workers, and examined H3K79me2 and DNA damage in their peripheral blood lymphocytes (PBLCs). The results showed that global H3K79me2 of coke oven workers was 29.3% less than that of the controls (P < 0.001). The H3K79me2 was negatively correlated with the concentration of urinary 1-hydroxypyrene (1-OHP) (β = -0.235, P < 0.001) and level of genetic damage evaluated by comet assay (β Tail DNA % = -0.313, P < 0.001; β OTM = -0.251, P = 0.008). Consistently, we found that benzo(a)pyrene (BaP) inhibited H3K79me2 in immortalized human bronchial epithelial (HBE) cells in a time-dependent manner. In order to explore the function of H3K79me2 in PAHs DDR, we established histone 3.1/3.3 K79A mutant cells (H3K79 A) to suppress H3K79me2. H3K79 A cells showed more serious DNA damage and decreased cell viability than control cells after BaP treatment. In addition, we also found that the expression of DOT1L, the only methyltransferase in H3K79, was repressed by BaP dose-dependently. DOT1L knockdown resulted in decreased H3K79me2 level and aggravated DNA damage after BaP exposure. This suggests that BaP induces H3K79me2 repression via inhibiting DOT1L expression. In conclusion, these findings indicate that PAH exposure decreases the level of global H3K79me2, which is integral for DNA damage response regulation of PAHs.
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2020 Elsevier Ltd. All rights reserved.)
