ArticleAmerican journal of physiology. Lung cellular and molecular physiology2007
A role for CFTR in the elevation of glutathione levels in the lung by oral glutathione administration.
Article in American journal of physiology. Lung cellular and molecular physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 43 citations in OpenAlex.
- Randomized controlled trial of oral glutathione supplementation on body stores of glutathione.European journal of nutrition · 2015Trial
- Redox Imbalance in Cystic Fibrosis: The Multifaceted Role of Oxidative Stress.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Polysulfur-based bulking of dynamin-related protein 1 prevents ischemic sulfide catabolism and heart failure in mice.Nature communications · 2025Article
- Mapping the oxidative landscape in cystic fibrosis: methodological frontiers and application.Frontiers in pharmacology · 2025Review
- Oxidative Stress and Endoplasmic Reticulum Stress in Rare Respiratory Diseases.Journal of clinical medicine · 2021Review
- Distinctive metabolic profiles between Cystic Fibrosis mutational subclasses and lung function.Metabolomics : Official journal of the Metabolomic Society · 2021Article
- Oral supplementation with liposomal glutathione elevates body stores of glutathione and markers of immune function.European journal of clinical nutrition · 2018Article
- Response to Letter to the Editor from Dr. Guilford.European journal of nutrition · 2015Article
- Redox balance in cystic fibrosis.The international journal of biochemistry & cell biology · 2014Review
- Purification of the cystic fibrosis transmembrane conductance regulator protein expressed in Saccharomyces cerevisiae.Journal of visualized experiments : JoVE · 2014Article
- Protection against oxidative stress in beta thalassemia/hemoglobin E erythrocytes by inhibitors of glutathione efflux transporters.PloS one · 2013Article
- CFTR is the primary known apical glutathione transporter involved in cigarette smoke-induced adaptive responses in the lung.Free radical biology & medicine · 2012Article
- Sulfur mustard analog, 2-chloroethyl ethyl sulfide-induced skin injury involves DNA damage and induction of inflammatory mediators, in part via oxidative stress, in SKH-1 hairless mouse skin.Toxicology letters · 2011Article
- Targeting maladaptive glutathione responses in lung disease.Biochemical pharmacology · 2011Article
- Dimethylthiourea protects against chlorine induced changes in airway function in a murine model of irritant induced asthma.Respiratory research · 2010Article
- Hypertonic saline increases lung epithelial lining fluid glutathione and thiocyanate: two protective CFTR-dependent thiols against oxidative injury.Respiratory research · 2010Article
- Glutathione deficient C57BL/6J mice are not sensitized to ozone-induced lung injury.Biochemical and biophysical research communications · 2010Article
- Oxidative stress and glutathione in TGF-beta-mediated fibrogenesis.Free radical biology & medicine · 2010Review
- Reduced NHE3-mediated Na+ absorption increases survival and decreases the incidence of intestinal obstructions in cystic fibrosis mice.American journal of physiology. Gastrointestinal and liver physiology · 2009Article
- Dependence of cAMP meditated increases in Cl- and HCO(3)- permeability on CFTR in bovine corneal endothelial cells.Experimental eye research · 2008Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
The cystic fibrosis transmembrane conductance regulator (CFTR) protein is the only known apical glutathione (GSH) transporter in the lung. The purpose of these studies was to determine whether oral GSH or glutathione disulfide (GSSG) treatment could increase lung epithelial lining fluid (ELF) GSH levels and whether CFTR plays a role in this process. The pharmacokinetic profile of an oral bolus dose of GSH (300 mg/kg) was determined in mice. Plasma, ELF, bronchoalveolar lavage (BAL) cells, and lung tissue were analyzed for GSH content. There was a rapid elevation in the GSH levels that peaked at 30 min in the plasma and 60 min in the lung, ELF, and BAL cells after oral GSH dosing. Oral GSH treatment produced a selective increase in the reduced and active form of GSH in all lung compartments examined. Oral GSSG treatment (300 mg/kg) resulted in a smaller increase of GSH levels. To evaluate the role of CFTR in this process, Cftr knockout (KO) mice and gut-corrected Cftr KO-transgenic (Tg) mice were given an oral bolus dose of GSH (300 mg/kg) and compared with wild-type mice for changes in GSH levels in plasma, lung, ELF, and BAL cells. There was a twofold increase in plasma, a twofold increase in lung, a fivefold increase in ELF, and a threefold increase in BAL cell GSH levels at 60 min in wild-type mice; however, GSH levels only increased by 40% in the plasma, 60% in the lung, 50% in the ELF, and twofold in the BAL cells within the gut-corrected Cftr KO-Tg mice. No change in GSH levels was observed in the uncorrected Cftr KO mice. These studies suggest that CFTR plays an important role in GSH uptake from the diet and transport processes in the lung.
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Registered trials
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