ArticleOxidative medicine and cellular longevity2013
Exacerbated airway toxicity of environmental oxidant ozone in mice deficient in Nrf2.
Article in Oxidative medicine and cellular longevity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 38 citations in OpenAlex.
- Lung injury, oxidative stress, and impaired functioning in a model of prolonged ozone exposure in female mice are associated with macrophage proinflammatory and profibrotic activation and altered bioenergetics.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Ozone Saline Solution Polarizes Microglial Cells Towards an Anti-Inflammatory Phenotype.Molecules (Basel, Switzerland) · 2025Article
- Aerosol physicochemical determinants of carbon black and ozone inhalation co-exposure induced pulmonary toxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2023Article
- Murine Neonatal Oxidant Lung Injury: NRF2-Dependent Predisposition to Adulthood Respiratory Viral Infection and Protection by Maternal Antioxidant.Antioxidants (Basel, Switzerland) · 2021Article
- Ozone-induced changes in the murine lung extracellular vesicle small RNA landscape.Physiological reports · 2021Article
- Role for Mucin-5AC in Upper and Lower Airway Pathogenesis in Mice.Toxicologic pathology · 2021Article
- Association of Nuclear Factor Erythroid-2-Related Actor 2 Gene Polymorphisms with Diabetic Nephropathy in Chinese Patients.International journal of general medicine · 2021Article
- Evaluation of oxidative damage and Nrf2 activation by combined pollution exposure in lung epithelial cells.Environmental science and pollution research international · 2020Article
- Roles of Nrf2 in Protecting the Kidney from Oxidative Damage.International journal of molecular sciences · 2020Review
- Role of Nrf2 in inflammatory response in lung of mice exposed to zinc oxide nanoparticles.Particle and fibre toxicology · 2019Article
- Androgens augment pulmonary responses to ozone in mice.Physiological reports · 2019Article
- The Role of Nrf2 in the Antioxidant Cellular Response to Medical Ozone Exposure.International journal of molecular sciences · 2019Review
- Sulforaphane enriched transcriptome of lung mitochondrial energy metabolism and provided pulmonary injury protection via Nrf2 in mice.Toxicology and applied pharmacology · 2019Article
- Transcriptional Effects of Ozone and Impact on Airway Inflammation.Frontiers in immunology · 2019Review
- Adrenal-derived stress hormones modulate ozone-induced lung injury and inflammation.Toxicology and applied pharmacology · 2017Article
- Live-cell imaging approaches for the investigation of xenobiotic-induced oxidant stress.Biochimica et biophysica acta · 2016Review
- The Next Generation of Risk Assessment Multi-Year Study-Highlights of Findings, Applications to Risk Assessment, and Future Directions.Environmental health perspectives · 2016Review
- Role of Nrf2 and Autophagy in Acute Lung Injury.Current pharmacology reports · 2016Article
- Association of Nrf2 with airway pathogenesis: lessons learned from genetic mouse models.Archives of toxicology · 2015Review
- Can cell proliferation of umbilical cord blood cells reflect environmental exposures?SpringerPlus · 2015Article
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Ozone (O3) is a strong oxidant in air pollution that has harmful effects on airways and exacerbates respiratory disorders. The transcription factor Nrf2 protects airways from oxidative stress through antioxidant response element-bearing defense gene induction. The present study was designed to determine the role of Nrf2 in airway toxicity caused by inhaled O3 in mice. For this purpose, Nrf2-deficient (Nrf2(-/-)) and wild-type (Nrf2(+/+)) mice received acute and subacute exposures to O3. Lung injury was determined by bronchoalveolar lavage and histopathologic analyses. Oxidation markers and mucus hypersecretion were determined by ELISA, and Nrf2 and its downstream effectors were determined by RT-PCR and/or Western blotting. Acute and sub-acute O3 exposures heightened pulmonary inflammation, edema, and cell death more severely in Nrf2(-/-) mice than in Nrf2(+/+) mice. O3 caused bronchiolar and terminal bronchiolar proliferation in both genotypes of mice, while the intensity of compensatory epithelial proliferation, bronchial mucous cell hyperplasia, and mucus hypersecretion was greater in Nrf2(-/-) mice than in Nrf2(+/+) mice. Relative to Nrf2(+/+), O3 augmented lung protein and lipid oxidation more highly in Nrf2(-/-) mice. Results suggest that Nrf2 deficiency exacerbates oxidative stress and airway injury caused by the environmental pollutant O3.
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