Nrf2 protects against diverse PM2.5 components-induced mitochondrial oxidative damage in lung cells

Pardo, Michal; Xu, Fanfan; Shemesh, Michal; Qiu, Xinghua; Barak, Yoav; Zhu, Tong; Rudich, Yinon

doi:10.1016/j.scitotenv.2019.01.436

Cited by 79Genomics, phytochemicals, and oxidative stressAir Quality and Health ImpactsEnvironmental Justice and Health Disparities

Nrf2 protects against diverse PM2.5 components-induced mitochondrial oxidative damage in lung cells

Pardo, Michal, Xu, Fanfan, Shemesh, Michal, Qiu, Xinghua, Barak, Yoav, Zhu, Tong, Rudich, Yinon·2019·Science of The Total Environment

DOI 10.1016/j.scitotenv.2019.01.436

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Abstract

Nrf2 is an important transcription factor implicated in the oxidative stress response, which has been reported to play an important role in the way by which air pollution particulate matter (PM 2.5 ) induces adverse health effects. This study investigates the mechanism by which Nrf2 exerts its protective effect in PM 2.5 induced toxicity in lung cells. Lung cells silenced for Nrf2 (shNrf2) demonstrated diverse susceptibility to various PM extracts; water extracts containing high levels of dissolved metals exhibited higher capacity to generate mitochondrial reactive oxygen species (ROS) and hence increased oxidative stress levels. Organic extracts containing high levels of polycyclic aromatic hydrocarbons (PAHs) increased mortality and reduced ROS production in the silenced cells. shNrf2 cells exhibited a higher basal mitochondrial respiration rate compared to the control cells. Following exposure to water extracts, the mitochondrial respiration increased, which was not observed with the organic extracts. shNrf2 cells exposed to the organic extracts showed lower mitochondrial membrane potential and lower mtDNA copy number. Nrf2 may act as a signaling mediator for the mitochondria function following PM 2.5 exposure.

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Metals and organic constituents, like PAHs, adsorbed to PM2.5 and PM0.1 have high oxidative potential and ability to generate mitochondrial damage.
“Metals and organic constituents, like PAHs, adsorbed to PM2.5 and PM0.1 have high oxidative potential and ability to generate mitochondrial damage [141, 142].”
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Background
Sestrin2/Keap1/Nrf2 pathway regulates mucus hypersecretion in pulmonary epithelium induced by traffic-related PM2.5 and water-soluble extracts.
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Background
Artemisia gmelinii Extract Attenuates Particulate Matter-Induced Neutrophilic Inflammation in a Mouse Model of Lung Injury
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Background
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Systematic Review of Particulate Matter-Induced Upper Respiratory Disease with Mechanistic Signaling Pathway
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Authors: Pardo, M., Xu, F., Shemesh, M., Qiu, X., Barak, Y., Zhu, T., & Rudich, Y.
Affiliations: Weizmann Institute of Science (IL)
Peking University (CN)
Corresponding author: Pardo, Michal
ORCID: Pardo, Michal
Qiu, Xinghua
Barak, Yoav
Zhu, Tong
Rudich, Yinon
Venue: Science of The Total Environment
Publisher: Elsevier BV
Published: 2019-06
Volume: 669
Pages: 303-313
ISSN: 0048-9697 (ISSN-L)
DOI: 10.1016/j.scitotenv.2019.01.436
OpenAlex: W2922353834
Cited by: 79
References: 0
Citations by year: 2026: 2 · 2025: 7 · 2024: 11 · 2023: 11 · 2022: 9 · 2021: 15 · 2020: 20 · 2019: 4
FWCI: 3.97
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: The Science of The Total Environment (publishedVersion)
PubMed (publishedVersion)
Funders: Israel Science Foundation (#2229/15)
National Natural Science Foundation of China (41561144007)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics, phytochemicals, and oxidative stress
Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Air Quality and Health Impacts
Social Sciences › Sociology and Political Science › Environmental Justice and Health Disparities
Keywords: Nrf2, PM2.5, particulate matter toxicity, mitochondrial oxidative damage, reactive oxygen species, polycyclic aromatic hydrocarbons, dissolved metals, mitochondrial respiration, mitochondrial membrane potential, mitochondrial DNA copy number, oxidative stress response, lung cells, air pollution health effects
MeSH terms: A549 Cells, Air Pollutants, Air Pollution, Humans, Lung, Mitochondria, Particle Size, Oxidative Stress, Respiratory Mucosa, NF-E2-Related Factor 2, Particulate Matter

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Nrf2 protects against diverse PM2.5 components-induced mitochondrial oxidative damage in lung cells

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