Inflammation response, oxidative stress and DNA damage caused by urban air pollution exposure increase in the lack of DNA repair XPC protein

•PM2.5 inflammatory response has been studied on mice with or without XPC protein.•XPC-knockout mice show an increased oxidative stress response to PM2.5 exposure.•XPC mice induced 2-fold increase of γ-H2AX foci relative to wild type mice.•A high carcinogenic risk was estimated to PAHs and metals ex...

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Published in:	Environment international Vol. 145; p. 106150
Main Authors:	de Oliveira Alves, Nilmara, Martins Pereira, Guilherme, Di Domenico, Marlise, Costanzo, Giovanna, Benevenuto, Sarah, de Oliveira Fonoff, Adriana M., de Souza Xavier Costa, Natália, Ribeiro Júnior, Gabriel, Satoru Kajitani, Gustavo, Cestari Moreno, Natália, Fotoran, Wesley, Iannicelli Torres, Janaína, de Andrade, Jailson Bittencourt, Matera Veras, Mariana, Artaxo, Paulo, Menck, Carlos Frederico Martins, de Castro Vasconcellos, Pérola, Saldiva, Paulo
Format:	Journal Article
Language:	English
Published:	Netherlands Elsevier Ltd 01-12-2020 Elsevier
Subjects:	Air Pollutants - analysis Air Pollutants - toxicity Air Pollution - adverse effects Air Pollution - analysis Animals Brazil DNA Damage DNA damage and PAHs DNA Repair Inflammation - chemically induced Inflammatory response Life Sciences Mice Nucleotide excision repair Oxidative Stress Particulate matter Particulate Matter - analysis Particulate Matter - toxicity Polycyclic Aromatic Hydrocarbons - analysis Brazil Oxidative stress XPA Inflammatory response HQ ICAM-1 XPC BaPE nitro-PAHs HAPC LPS BPDE PM2.5 SPMA UR WHO Nucleotide excision repair ECinh DNA damage and PAHs CR oxy-PAHs Particulate matter ROS PAHs LCR NER PM 8-oxodGuo
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Summary:	•PM2.5 inflammatory response has been studied on mice with or without XPC protein.•XPC-knockout mice show an increased oxidative stress response to PM2.5 exposure.•XPC mice induced 2-fold increase of γ-H2AX foci relative to wild type mice.•A high carcinogenic risk was estimated to PAHs and metals exposure in the SPMA. Air pollution represents a considerable threat to health worldwide. The São Paulo Metropolitan area, in Brazil, has a unique composition of atmospheric pollutants with a population of nearly 20 million people and 9 million passenger cars. It is long known that exposure to particulate matter less than 2.5 µm (PM2.5) can cause various health effects such as DNA damage. One of the most versatile defense mechanisms against the accumulation of DNA damage is the nucleotide excision repair (NER), which includes XPC protein. However, the mechanisms by which NER protects against adverse health effects related to air pollution are largely unknown. We hypothesized that reduction of XPC activity may contribute to inflammation response, oxidative stress and DNA damage after PM2.5 exposure. To address these important questions, XPC knockout and wild type mice were exposed to PM2.5 using the Harvard Ambient Particle concentrator. Results from one-single exposure have shown a significant increase in the levels of anti-ICAM, IL-1β, and TNF-α in the polluted group when compared to the filtered air group. Continued chronic PM2.5 exposure increased levels of carbonylated proteins, especially in the lung of XPC mice, probably as a consequence of oxidative stress. As a response to DNA damage, XPC mice lungs exhibit increased γ-H2AX, followed by severe atypical hyperplasia. Emissions from vehicles are composed of hazardous substances, with polycyclic aromatic hydrocarbons (PAHs) and metals being most frequently cited as the major contributors to negative health impacts. This analysis showed that benzo[b]fluoranthene, 2-nitrofluorene and 9,10-anthraquinone were the most abundant PAHs and derivatives. Taken together, these findings demonstrate the participation of XPC protein, and NER pathway, in the protection of mice against the carcinogenic potential of air pollution. This implicates that DNA is damaged directly (forming adducts) or indirectly (Reactive Oxygen Species) by the various compounds detected in urban PM2.5.
ISSN:	0160-4120 1873-6750
DOI:	10.1016/j.envint.2020.106150