ArticleThe Journal of biological chemistry2010
Inhibition of lung fluid clearance and epithelial Na+ channels by chlorine, hypochlorous acid, and chloramines.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
32 citing papers in PubMed, 54 citations in OpenAlex.
- Chlorinated pool air, airway mucosal immunity, and respiratory health in competitive swimmers: a mini review.Frontiers in immunology · 2026Review
- Connexin-hemichannels-mediated ATP release causes lung injury following chlorine inhalation.American journal of physiology. Cell physiology · 2025Article
- Epithelial NaComprehensive Physiology · 2024Review
- Halogen-Induced Chemical Injury to the Mammalian Cardiopulmonary Systems.Physiology (Bethesda, Md.) · 2021Review
- Hyaluronan and halogen-induced airway hyperresponsiveness and lung injury.Annals of the New York Academy of Sciences · 2020Review
- Monocyte-derived alveolar macrophage apolipoprotein E participates in pulmonary fibrosis resolution.JCI insight · 2020Article
- Heme scavenging reduces pulmonary endoplasmic reticulum stress, fibrosis, and emphysema.JCI insight · 2018Observational
- Halogen Inhalation-Induced Lung Injury and Acute Respiratory Distress Syndrome.Chinese medical journal · 2018Review
- Influenza virus infection alters ion channel function of airway and alveolar cells: mechanisms and physiological sequelae.American journal of physiology. Lung cellular and molecular physiology · 2017Review
- 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
- Heme Attenuation Ameliorates Irritant Gas Inhalation-Induced Acute Lung Injury.Antioxidants & redox signaling · 2016Article
- Respiratory syncytial virus infection increases chlorine-induced airway hyperresponsiveness.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- Upregulation of autophagy decreases chlorine-induced mitochondrial injury and lung inflammation.Free radical biology & medicine · 2015Article
- Hyaluronan mediates airway hyperresponsiveness in oxidative lung injury.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- Postexposure aerosolized heparin reduces lung injury in chlorine-exposed mice.American journal of physiology. Lung cellular and molecular physiology · 2014Article
- Chlorine gas exposure disrupts nitric oxide homeostasis in the pulmonary vasculature.Toxicology · 2014Article
- Chlorine induces the unfolded protein response in murine lungs and skin.American journal of respiratory cell and molecular biology · 2013Article
- Ethanol alters alveolar fluid balance via Nadph oxidase (NOX) signaling to epithelial sodium channels (ENaC) in the lung.PloS one · 2013Article
- Targeted aerosolized delivery of ascorbate in the lungs of chlorine-exposed rats.Journal of aerosol medicine and pulmonary drug delivery · 2012Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
We investigated the mechanisms by which chlorine (Cl(2)) and its reactive byproducts inhibit Na(+)-dependent alveolar fluid clearance (AFC) in vivo and the activity of amiloride-sensitive epithelial Na(+) channels (ENaC) by measuring AFC in mice exposed to Cl(2) (0-500 ppm for 30 min) and Na(+) and amiloride-sensitive currents (I(Na) and I(amil), respectively) across Xenopus oocytes expressing human alpha-, beta-, and gamma-ENaC incubated with HOCl (1-2000 microm). Both Cl(2) and HOCl-derived products decreased AFC in mice and whole cell and single channel I(Na) in a dose-dependent manner; these effects were counteracted by serine proteases. Mass spectrometry analysis of the oocyte recording medium identified organic chloramines formed by the interaction of HOCl with HEPES (used as an extracellular buffer). In addition, chloramines formed by the interaction of HOCl with taurine or glycine decreased I(Na) in a similar fashion. Preincubation of oocytes with serine proteases prevented the decrease of I(Na) by HOCl, whereas perfusion of oocytes with a synthetic 51-mer peptide corresponding to the putative furin and plasmin cleaving segment in the gamma-ENaC subunit restored the ability of HOCl to inhibit I(Na). Finally, I(Na) of oocytes expressing wild type alpha- and gamma-ENaC and a mutant form of beta ENaC (S520K), known to result in ENaC channels locked in the open position, were not altered by HOCl. We concluded that HOCl and its reactive intermediates (such as organic chloramines) inhibit ENaC by affecting channel gating, which could be relieved by proteases cleavage.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.