Cited by 145Air Quality and Health ImpactsNitric Oxide and Endothelin EffectsAtherosclerosis and Cardiovascular Diseases

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Pulmonary ozone exposure induces vascular dysfunction, mitochondrial damage, and atherogenesis

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Chuang, Gin C., Yang, Zhen, Westbrook, David G., Pompilius, Melissa, Ballinger, Carol A., White, C. Roger, Krzywanski, David M., Postlethwait, Edward M., Ballinger, Scott W.·2009·American Journal of Physiology-Lung Cellular and Molecular Physiology

DOI 10.1152/ajplung.00102.2009PMC PMC2742788

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Abstract

More than 100 million people in the United States live in areas that exceed current ozone air quality standards. In addition to its known pulmonary effects, environmental ozone exposures have been associated with increased hospital admissions related to cardiovascular events, but to date, no studies have elucidated the potential molecular mechanisms that may account for exposure-related vascular impacts. Because of the known pulmonary redox and immune biology stemming from ozone exposure, we hypothesized that ozone inhalation would initiate oxidant stress, mitochondrial damage, and dysfunction within the vasculature. Accordingly, these factors were quantified in mice consequent to a cyclic, intermittent pattern of ozone or filtered air control exposure. Ozone significantly modulated vascular tone regulation and increased oxidant stress and mitochondrial DNA damage (mtDNA), which was accompanied by significantly decreased vascular endothelial nitric oxide synthase protein and indices of nitric oxide production. To examine influences on atherosclerotic lesion formation, apoE-/- mice were exposed as above, and aortic plaques were quantified. Exposure resulted in significantly increased atherogenesis compared with filtered air controls. Vascular mitochondrial damage was additionally quantified in ozone- and filtered air-exposed infant macaque monkeys. These studies revealed that ozone increased vascular mtDNA damage in nonhuman primates in a fashion consistent with known atherosclerotic lesion susceptibility in humans. Consequently, inhaled ozone, in the absence of other environmental toxicants, promotes increased vascular dysfunction, oxidative stress, mitochondrial damage, and atherogenesis.

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Authors: Chuang, G. C., Yang, Z., Westbrook, D. G., Pompilius, M., Ballinger, C. A., White, C. R., Krzywanski, D. M., Postlethwait, E. M., & Ballinger, S. W.
Affiliations: University of Alabama at Birmingham (US)
ORCID: Chuang, Gin C.
Yang, Zhen
Pompilius, Melissa
White, C. Roger
Krzywanski, David M.
Ballinger, Scott W.
Venue: American Journal of Physiology-Lung Cellular and Molecular Physiology
Publisher: American Physiological Society
Published: 2009-08
Volume: 297
Issue: 2
Pages: L209-L216
ISSN: 1040-0605 (ISSN-L)
1522-1504
DOI: 10.1152/ajplung.00102.2009
PMC: PMC2742788
OpenAlex: W2016752913
Cited by: 145
References: 51
Citations by year: 2026: 4 · 2025: 5 · 2024: 7 · 2023: 4 · 2022: 9 · 2021: 12 · 2020: 11 · 2019: 6 · 2018: 4 · 2017: 13 · 2016: 3 · 2015: 14 · 2014: 5 · 2013: 14 · 2012: 8
FWCI: 8.05
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: American Journal of Physiology-Lung Cellular and Molecular Physiology (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Heart, Lung, and Blood Institute (HL 77419, HL-054696, R01HL054696, R01HL077419)
National Institute of Diabetes and Digestive and Kidney Diseases (DK079626)
National Institute of Environmental Health Sciences (P01-ES11617, ES11172, R01ES011172, P01ES011617)
Topics: Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Air Quality and Health Impacts
Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
Keywords: ozone inhalation, vascular dysfunction, mitochondrial DNA damage, oxidative stress, atherogenesis, endothelial nitric oxide synthase, nitric oxide production, vascular tone regulation, aortic plaque, ApoE-deficient mice, air pollution health effects, cardiovascular risk
MeSH terms: Superoxide Dismutase 2, Air Pollutants, Animals, Aorta, Blood Pressure, DNA Damage, DNA, Mitochondrial, Heart Rate, Lung Diseases, Macaca mulatta, Male, Mice, Inbred C57BL, Mitochondria, Nitrates, Nitric Oxide, Nitrites, Ozone, Superoxide Dismutase, Tyrosine, Oxidants, Oxidative Stress, Mitochondrial Diseases, Atherosclerosis, Mice, Nitric Oxide Synthase Type III

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Pulmonary ozone exposure induces vascular dysfunction, mitochondrial damage, and atherogenesis

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