ArticleProceedings of the National Academy of Sciences of the United States of America2009
The antioxidant role of thiocyanate in the pathogenesis of cystic fibrosis and other inflammation-related diseases.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.
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Who cites it
54 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Meta-analysis Reveals Potential Influence of Oxidative Stress on the Airway Microbiomes of Cystic Fibrosis Patients.Genomics, proteomics & bioinformatics · 2019Pooled it
- Myeloperoxidase impairs mucociliary transport on human airway epithelium.Disease models & mechanisms · 2026Article
- Myeloperoxidase impairs mucociliary transport on human airway epithelium.bioRxiv : the preprint server for biology · 2025Article
- Analytical developments in the synergism of copper particles and cysteine: a review.Nanoscale advances · 2024Review
- Design a Friendly Nanoscale Chemical Sensor Based on Gold Nanoclusters for Detecting Thiocyanate Ions in Food Industry Applications.Biosensors · 2024Article
- The Roles of Neutrophil-Derived Myeloperoxidase (MPO) in Diseases: The New Progress.Antioxidants (Basel, Switzerland) · 2024Review
- CFTR dysfunction leads to defective bacterial eradication on cystic fibrosis airways.Frontiers in physiology · 2024Review
- Associations of perchlorate, nitrate, and thiocyanate exposure with arthritis and inflammation indicators in young and middle-aged adults, NHANES 2005-2016.Frontiers in immunology · 2024Article
- Substrate-dependent metabolomic signatures of myeloperoxidase activity in airway epithelial cells: Implications for early cystic fibrosis lung disease.Free radical biology & medicine · 2023Article
- Hypothiocyanite and host-microbe interactions.Molecular microbiology · 2023Article
- Characterization of a novel dual murine model of chemotherapy-induced oral and intestinal mucositis.Scientific reports · 2023Article
- Extraction of Bioactive Compounds from Different Vegetable Sprouts and Their Potential Role in the Formulation of Functional Foods against Various Disorders: A Literature-Based Review.Molecules (Basel, Switzerland) · 2022Review
- Advances in PSMA theranostics.Translational oncology · 2022Article
- Positively Charged Gold Quantum Dots: An Nanozymatic "Off-On" Sensor for Thiocyanate Detection.Foods (Basel, Switzerland) · 2022Article
- Resistance of Streptococcus pneumoniae to Hypothiocyanous Acid Generated by Host Peroxidases.Infection and immunity · 2022Article
- Article
- Mucosal Immunity in Cystic Fibrosis.Journal of immunology (Baltimore, Md. : 1950) · 2021Review
- Heme Peroxidases at Unperturbed and Inflamed Mucous Surfaces.Antioxidants (Basel, Switzerland) · 2021Review
- CFTR Protein: Not Just a Chloride Channel?Cells · 2021Review
- Reverse Ordered Sequential Mechanism for Lactoperoxidase with Inhibition by Hydrogen Peroxide.Antioxidants (Basel, Switzerland) · 2021Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Cystic fibrosis (CF) is a pleiotropic disease, originating from mutations in the CF transmembrane conductance regulator (CFTR). Lung injuries inflicted by recurring infection and excessive inflammation cause approximately 90% of the morbidity and mortality of CF patients. It remains unclear how CFTR mutations lead to lung illness. Although commonly known as a Cl(-) channel, CFTR also conducts thiocyanate (SCN(-)) ions, important because, in several ways, they can limit potentially harmful accumulations of hydrogen peroxide (H(2)O(2)) and hypochlorite (OCl(-)). First, lactoperoxidase (LPO) in the airways catalyzes oxidation of SCN(-) to tissue-innocuous hypothiocyanite (OSCN(-)), while consuming H(2)O(2). Second, SCN(-) even at low concentrations competes effectively with Cl(-) for myeloperoxidase (MPO) (which is released by white blood cells), thus limiting OCl(-) production by the enzyme. Third, SCN(-) can rapidly reduce OCl(-) without catalysis. Here, we show that SCN(-) and LPO protect a lung cell line from injuries caused by H(2)O(2); and that SCN(-) protects from OCl(-) made by MPO. Of relevance to inflammation in other diseases, we find that in three other tested cell types (arterial endothelial cells, a neuronal cell line, and a pancreatic beta cell line) SCN(-) at concentrations of > or =100 microM greatly attenuates the cytotoxicity of MPO. Humans naturally derive SCN(-) from edible plants, and plasma SCN(-) levels of the general population vary from 10 to 140 microM. Our findings raise the possibility that insufficient levels of antioxidant SCN(-) provide inadequate protection from OCl(-), thus worsening inflammatory diseases, and predisposing humans to diseases linked to MPO activity, including atherosclerosis, neurodegeneration, and certain cancers.
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