ArticleToxicological sciences : an official journal of the Society of Toxicology2013
Chronic arsenic exposure in nanomolar concentrations compromises wound response and intercellular signaling in airway epithelial cells.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 32 citations in OpenAlex.
- Silica Nanoparticles Inhibit Responses to ATP in Human Airway Epithelial 16HBE Cells.International journal of molecular sciences · 2021Article
- Paradoxical effects of arsenic in the lungs.Environmental health and preventive medicine · 2021Review
- Chronic exposure to arsenite enhances influenza virus infection in cultured cells.Journal of applied toxicology : JAT · 2020Article
- Cerium dioxide (CeOEnvironmental research · 2018Article
- Betamethasone prevents human rhinovirus- and cigarette smoke- induced loss of respiratory epithelial barrier function.Scientific reports · 2018Article
- Estrogen Mitigates the Negative Effects of Arsenic Contamination in anApplied in vitro toxicology · 2018Article
- Effects of Orally Ingested Arsenic on Respiratory Epithelial Permeability to Bacteria and Small Molecules in Mice.Environmental health perspectives · 2017Article
- Arsenic alters transcriptional responses to Pseudomonas aeruginosa infection and decreases antimicrobial defense of human airway epithelial cells.Toxicology and applied pharmacology · 2017Article
- Editor's Highlight: Interactive Genotoxicity Induced by Environmentally Relevant Concentrations of Benzo(a)Pyrene Metabolites and Arsenite in Mouse Thymus Cells.Toxicological sciences : an official journal of the Society of Toxicology · 2016Article
- Airway epithelial cell exposure to distinct e-cigarette liquid flavorings reveals toxicity thresholds and activation of CFTR by the chocolate flavoring 2,5-dimethypyrazine.Respiratory research · 2016Article
- Arsenic compromises conducting airway epithelial barrier properties in primary mouse and immortalized human cell cultures.PloS one · 2013Article
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Paracrine ATP signaling in the lung epithelium participates in a variety of innate immune functions, including mucociliary clearance, bactericide production, and as an initiating signal in wound repair. We evaluated the effects of chronic low-dose arsenic relevant to U.S. drinking water standards (i.e., 10 ppb [130nM]) on airway epithelial cells. Immortalized human bronchial epithelial cells (16HBE14o-) were exposed to 0, 130, or 330nM arsenic (as Na-arsenite) for 4-5 weeks and examined for wound repair efficiency and ATP-mediated Ca(2+) signaling. We found that chronic arsenic exposure at these low doses slows wound repair and reduces ATP-mediated Ca(2+) signaling. We further show that arsenic compromises ATP-mediated Ca(2+) signaling by altering both Ca(2+) release from intracellular stores (via metabotropic P2Y receptors) and Ca(2+) influx mechanisms (via ionotropic P2X receptors). To better model the effects of arsenic on ATP-mediated Ca(2+) signaling under conditions of natural exposure, we cultured tracheal epithelial cells obtained from mice exposed to control or 50 ppb Na-arsenite supplemented drinking water for 4 weeks. Tracheal epithelial cells from arsenic-exposed mice displayed reduced ATP-mediated Ca(2+) signaling dynamics similar to our in vitro chronic exposure. Our findings demonstrate that chronic arsenic exposure at levels that are commonly found in drinking water (i.e., 10-50 ppb) alters cellular mechanisms critical to airway innate immunity.
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