ArticleToxicology and applied pharmacology2012
Role of reactive nitrogen species generated via inducible nitric oxide synthase in vesicant-induced lung injury, inflammation and altered lung functioning.
Article in Toxicology and applied pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 43 citations in OpenAlex.
- Oxidative Stress: An Intersection Between Radiation and Sulfur Mustard Lung Injury.Disaster medicine and public health preparedness · 2024Article
- Role of macrophage bioenergetics in N-acetylcysteine-mediated mitigation of lung injury and oxidative stress induced by nitrogen mustard.Toxicology and applied pharmacology · 2024Article
- Oxy-Inflammation in Humans during Underwater Activities.International journal of molecular sciences · 2024Review
- Targeting Tumor Necrosis Factor Alpha to Mitigate Lung Injury Induced by Mustard Vesicants and Radiation.Disaster medicine and public health preparedness · 2023Review
- Article
- Melatonin as Modulator for Sulfur and Nitrogen Mustard-Induced Inflammation, Oxidative Stress and DNA Damage: Molecular Therapeutics.Antioxidants (Basel, Switzerland) · 2023Review
- Extra Virgin Olive Oil Phenolic Extract on Human Hepatic HepG2 and Intestinal Caco-2 Cells: Assessment of the Antioxidant Activity and Intestinal Trans-Epithelial Transport.Antioxidants (Basel, Switzerland) · 2021Article
- Transcriptional profiling of lung macrophages during pulmonary injury induced by nitrogen mustard.Annals of the New York Academy of Sciences · 2020Article
- Long-term Respiratory Effects of Mustard Vesicants.Toxicology letters · 2020Review
- Regulation of Macrophage Foam Cell Formation During Nitrogen Mustard (NM)-Induced Pulmonary Fibrosis by Lung Lipids.Toxicological sciences : an official journal of the Society of Toxicology · 2019Article
- Role of neuronal nitric oxide synthase (nNOS) at medulla in tachycardia induced by repeated administration of ethanol in conscious rats.Journal of biomedical science · 2018Article
- Antipleuritic and Vascular Permeability Inhibition of the Ethyl Acetate-Petroleum Ether Stem Bark Extract ofInternational journal of inflammation · 2018Article
- World Trade Center (WTC) dust exposure in mice is associated with inflammation, oxidative stress and epigenetic changes in the lung.Experimental and molecular pathology · 2017Article
- From the Cover: Catalytic Antioxidant Rescue of Inhaled Sulfur Mustard Toxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2016Article
- Mustard vesicant-induced lung injury: Advances in therapy.Toxicology and applied pharmacology · 2016Review
- Macrophages and inflammatory mediators in pulmonary injury induced by mustard vesicants.Annals of the New York Academy of Sciences · 2016Review
- Early indicators of survival following exposure to mustard gas: Protective role of 25(OH)D.Toxicology letters · 2016Article
- Inflammatory mechanisms of pulmonary injury induced by mustards.Toxicology letters · 2016Review
- Protective role of spleen-derived macrophages in lung inflammation, injury, and fibrosis induced by nitrogen mustard.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- Suppression of Hyperactive Immune Responses Protects against Nitrogen Mustard Injury.The Journal of investigative dermatology · 2015Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Pulmonary toxicity induced by sulfur mustard and related vesicants is associated with oxidative stress. In the present studies we analyzed the role of reactive nitrogen species (RNS) generated via inducible nitric oxide synthase (iNOS) in lung injury and inflammation induced by vesicants using 2-chloroethyl ethyl sulfide (CEES) as a model. C57Bl/6 (WT) and iNOS-/- mice were sacrificed 3 days or 14 days following intratracheal administration of CEES (6 mg/kg) or control. CEES intoxication resulted in transient (3 days) increases in bronchoalveolar lavage (BAL) cell and protein content in WT, but not iNOS-/- mice. This correlated with expression of Ym1, a marker of oxidative stress in alveolar macrophages and epithelial cells. In contrast, in iNOS-/- mice, Ym1 was only observed 14 days post-exposure in enlarged alveolar macrophages, suggesting that they are alternatively activated. This is supported by findings that lung tumor necrosis factor and lipocalin Lcn2 expression, mediators involved in tissue repair were also upregulated at this time in iNOS-/- mice. Conversely, CEES-induced increases in the proinflammatory genes, monocyte chemotactic protein-1 and cyclooxygenase-2, were abrogated in iNOS-/- mice. In WT mice, CEES treatment also resulted in increases in total lung resistance and decreases in compliance in response to methacholine, effects blunted by loss of iNOS. These data demonstrate that RNS, generated via iNOS play a role in the pathogenic responses to CEES, augmenting oxidative stress and inflammation and suppressing tissue repair. Elucidating inflammatory mechanisms mediating vesicant-induced lung injury is key to the development of therapeutics to treat mustard poisoning.
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