ArticleAmerican journal of respiratory cell and molecular biology2011
Chlorine gas exposure causes systemic endothelial dysfunction by inhibiting endothelial nitric oxide synthase-dependent signaling.
Article in American journal of respiratory cell and molecular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 49 citations in OpenAlex.
- A human airway-on-a-chip microphysiological system for modeling chlorine gas toxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Airborne chloride exposure and benign prostatic hyperplasia risk.BMC research notes · 2025Article
- Association of over-the-counter mouthwash use with markers of nitric oxide metabolism, inflammation, and endothelial function-a cross-sectional study.Frontiers in oral health · 2025Article
- Chlorine gas poisoning by trichloroisocyanuric acid and respiratory failure: a case report of a 49-year-old patient.Frontiers in medicine · 2025Article
- A rare case of acute respiratory distress syndrome due to chlorine gas inhalation: Rapid progression with favorable ICU outcome.Respiratory medicine case reports · 2025Article
- Safety and toxicology assessment of sodium nitrite administered by intramuscular injection.Toxicology and applied pharmacology · 2021Article
- Halogen-Induced Chemical Injury to the Mammalian Cardiopulmonary Systems.Physiology (Bethesda, Md.) · 2021Review
- Toxic effects of chlorine gas and potential treatments: a literature review.Toxicology mechanisms and methods · 2021Review
- Transient receptor potential channels in pulmonary chemical injuries and as countermeasure targets.Annals of the New York Academy of Sciences · 2020Article
- Vascular permeability disruption explored in the proteomes of mouse lungs and human microvascular cells following acute bromine exposure.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Suppressive Effects of theEvidence-based complementary and alternative medicine : eCAM · 2020Article
- Temporal Trends in Cardiovascular Hospital Discharges Following a Mass Chlorine Exposure Event in Graniteville, South Carolina.Frontiers in public health · 2019Article
- Halogen Inhalation-Induced Lung Injury and Acute Respiratory Distress Syndrome.Chinese medical journal · 2018Review
- The chlorinated lipidome originating from myeloperoxidase-derived HOCl targeting plasmalogens: Metabolism, clearance, and biological properties.Archives of biochemistry and biophysics · 2018Review
- Mechanisms and Treatment of Halogen Inhalation-Induced Pulmonary and Systemic Injuries in Pregnant Mice.Hypertension (Dallas, Tex. : 1979) · 2017Article
- Measuring nitrate reductase activity from human and rodent tongues.Nitric oxide : biology and chemistry · 2017Article
- Nitrite therapy prevents chlorine gas toxicity in rabbits.Toxicology letters · 2017Article
- Formation of chlorinated lipids post-chlorine gas exposure.Journal of lipid research · 2016Article
- Chlorine-induced cardiopulmonary injury.Annals of the New York Academy of Sciences · 2016Review
- Respiratory syncytial virus infection increases chlorine-induced airway hyperresponsiveness.American journal of physiology. Lung cellular and molecular physiology · 2015Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 2 countries.
Funding
Abstract
Chlorine gas (Cl(2)) exposure during accidents or in the military setting results primarily in injury to the lungs. However, the potential for Cl(2) exposure to promote injury to the systemic vasculature leading to compromised vascular function has not been studied. We hypothesized that Cl(2) promotes extrapulmonary endothelial dysfunction characterized by a loss of endothelial nitric oxide synthase (eNOS)-derived signaling. Male Sprague Dawley rats were exposed to Cl(2) for 30 minutes, and eNOS-dependent vasodilation of aorta as a function of Cl(2) dose (0-400 ppm) and time after exposure (0-48 h) were determined. Exposure to Cl(2) (250-400 ppm) significantly inhibited eNOS-dependent vasodilation (stimulated by acetycholine) at 24 to 48 hours after exposure without affecting constriction responses to phenylephrine or vasodilation responses to an NO donor, suggesting decreased NO formation. Consistent with this hypothesis, eNOS protein expression was significantly decreased (∼ 60%) in aorta isolated from Cl(2)-exposed versus air-exposed rats. Moreover, inducible nitric oxide synthase (iNOS) mRNA was up-regulated in circulating leukocytes and aorta isolated 24 hours after Cl(2) exposure, suggesting stimulation of inflammation in the systemic vasculature. Despite decreased eNOS expression and activity, no changes in mean arterial blood pressure were observed. However, injection of 1400W, a selective inhibitor of iNOS, increased mean arterial blood pressure only in Cl(2)-exposed animals, suggesting that iNOS-derived NO compensates for decreased eNOS-derived NO. These results highlight the potential for Cl(2) exposure to promote postexposure systemic endothelial dysfunction via disruption of vascular NO homeostasis mechanisms.
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Registered trials
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