微粒空气污染对人类呼出气体冷凝物和 BEAS-2B 细胞中 BPDE-DNA 加合物、端粒长度和线粒体 DNA 拷贝数的影响。

IF 4.5 2区 医学 Q1 INFECTIOUS DISEASES
Naruporn Pedklang , Panida Navasumrit , Chalida Chompoobut , Jeerawan Promvijit , Potchanee Hunsonti , Mathuros Ruchirawat
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引用次数: 0

摘要

与交通有关的颗粒物(PM)和多环芳烃(PAHs)与人类的呼吸系统疾病和癌症风险有关。基因组损伤(包括苯并[a]芘二环氧化物(BPDE)-DNA 加合物)以及端粒长度(TL)和线粒体 DNA 拷贝数(mtDNA-CN)的改变与呼吸系统疾病有关。本研究旨在调查人类受试者和支气管上皮细胞系(BEAS-2B)暴露于交通相关颗粒污染物与呼出气体冷凝物(EBC)中基因组损伤之间的关系。在招募的 60 名健康受试者中,居住在交通高度拥挤地区的居民暴露于较高浓度的 PM2.5(1.66 倍,p 2.5-PAHs)、UFPs、PM2.5-PAHs 和 UFPs-PAHs 中,上述生物效应在一项体外细胞研究中得到了证实,该研究用含有细微和超细 PM 及 PAHs 的柴油废气颗粒物(DEP)处理 BEAS-2B 细胞。在处理过的 BEAS-2B 细胞中还发现了 BPDE-DNA 加合物水平升高、TL 缩短和 mtDNA-CN 降低。TL缩短和mtDNA-CN降低的部分原因是hTERT和SIRT1转录水平的降低,它们分别参与端粒酶活性和线粒体生物生成。这些结果表明,暴露于与交通相关的颗粒污染物会导致呼吸细胞基因组不稳定,从而可能增加呼吸系统疾病和癌症发生的健康风险。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effects of particulate air pollution on BPDE-DNA adducts, telomere length, and mitochondrial DNA copy number in human exhaled breath condensate and BEAS-2B cells
Traffic-related particulate matter (PM) and polycyclic aromatic hydrocarbons (PAHs) have been linked to respiratory diseases and cancer risk in humans. Genomic damage, including benzo[a]pyrene diolepoxide (BPDE)-DNA adducts as well as alterations in telomere length (TL) and mitochondrial DNA copy number (mtDNA-CN) are associated with respiratory diseases. This study aimed to investigate the association between exposure to traffic-related particulate pollutants and genomic damage in exhaled breath condensate (EBC) in human subjects and a bronchial epithelial cell line (BEAS-2B). Among the 60 healthy recruited subjects, residents living in high-traffic-congested areas were exposed to higher concentrations of PM2.5 (1.66-fold, p < 0.01), UFPs (1.79-fold, p < 0.01), PM2.5-PAHs (1.50-fold, p < 0.01), and UFPs-PAHs (1.35-fold, p < 0.05), than those in low-traffic-congested areas. In line with increased exposure to particulate air pollution, the high-traffic-exposed group had significantly increased BPDE-DNA adducts (1.40-fold, p < 0.05), TL shortening (1.24-fold, p < 0.05), and lower mtDNA-CN (1.38-fold, p < 0.05) in EBC. The observations in the human study linking exposure to PM2.5, UFPs, PM2.5-PAHs, and UFPs-PAHs with the aforementioned biological effects were confirmed by an in vitro cell-based study, in which BEAS-2B cells were treated with diesel exhaust particulate matter (DEP) containing fine and ultrafine PM and PAHs. Increased BPDE-DNA adducts levels, shortened TL, and decreased mtDNA-CN were also found in treated BEAS-2B cells. The shortened TL and decreased mtDNA-CN were in part mediated by decreased transcript levels of hTERT, and SIRT1, which are involved in telomerase activity and mitochondrial biogenesis, respectively. These results suggest that exposure to traffic-related particulate pollutants can cause genomic instability in respiratory cells, which may increase the health risk of respiratory diseases and the development of cancer.
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来源期刊
CiteScore
11.50
自引率
5.00%
发文量
151
审稿时长
22 days
期刊介绍: The International Journal of Hygiene and Environmental Health serves as a multidisciplinary forum for original reports on exposure assessment and the reactions to and consequences of human exposure to the biological, chemical, and physical environment. Research reports, short communications, reviews, scientific comments, technical notes, and editorials will be peer-reviewed before acceptance for publication. Priority will be given to articles on epidemiological aspects of environmental toxicology, health risk assessments, susceptible (sub) populations, sanitation and clean water, human biomonitoring, environmental medicine, and public health aspects of exposure-related outcomes.
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