ArticleProceedings of the National Academy of Sciences of the United States of America2012
Triclosan impairs excitation-contraction coupling and Ca2+ dynamics in striated muscle.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 48 papers.
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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.
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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
48 citing papers in PubMed, 162 citations in OpenAlex.
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- Conceptualizing the Role of the Microbiome as a Mediator and Modifier in Environmental Health Studies: A Scoping Review of Studies of Triclosan and the Microbiome.Current environmental health reports · 2024Article
- S2k-Guideline hand antisepsis and hand hygiene.GMS hygiene and infection control · 2024Article
- Triclosan and Its Consequences on the Reproductive, Cardiovascular and Thyroid Levels.International journal of molecular sciences · 2022Review
- Role of neurotoxicants in the pathogenesis of Alzheimer's disease: a mechanistic insight.Annals of medicine · 2021Review
- Role of environmental pollutants in Alzheimer's disease: a review.Environmental science and pollution research international · 2020Review
- Effect of Triclosan on the Functioning of Liver Mitochondria and Permeability of Erythrocyte Membranes of Marsh Frog (Pelophylax ridibundus (Pallas, 1771)).The Journal of membrane biology · 2020Article
- Antimicrobial agent triclosan suppresses mast cell signaling via phospholipase D inhibition.Journal of applied toxicology : JAT · 2019Article
- Triclosan induces PC12 cells injury is accompanied by inhibition of AKT/mTOR and activation of p38 pathway.Neurotoxicology · 2019Article
- Interactions of Dichlorodiphenyltrichloroethane (DDT) and Dichlorodiphenyldichloroethylene (DDE) With Skeletal Muscle Ryanodine Receptor Type 1.Toxicological sciences : an official journal of the Society of Toxicology · 2019Article
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- Development and Characterization of Bioactive Glass Containing Composite Coatings with Ion Releasing Function for Antibiotic-Free Antibacterial Surgical Sutures.Materials (Basel, Switzerland) · 2019Article
- Triclosan: An Update on Biochemical and Molecular Mechanisms.Oxidative medicine and cellular longevity · 2019Review
- The pH-dependent toxicity of triclosan to five aquatic organisms (Daphnia magna, Photobacterium phosphoreum, Danio rerio, Limnodrilus hoffmeisteri, and Carassius auratus).Environmental science and pollution research international · 2018Article
- Functional cardiotoxicity assessment of cosmetic compounds using human-induced pluripotent stem cell-derived cardiomyocytes.Archives of toxicology · 2018Article
- Triclosan Impairs Hippocampal Synaptic Plasticity and Spatial Memory in Male Rats.Frontiers in molecular neuroscience · 2018Article
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
Triclosan (TCS), a high-production-volume chemical used as a bactericide in personal care products, is a priority pollutant of growing concern to human and environmental health. TCS is capable of altering the activity of type 1 ryanodine receptor (RyR1), but its potential to influence physiological excitation-contraction coupling (ECC) and muscle function has not been investigated. Here, we report that TCS impairs ECC of both cardiac and skeletal muscle in vitro and in vivo. TCS acutely depresses hemodynamics and grip strength in mice at doses ≥12.5 mg/kg i.p., and a concentration ≥0.52 μM in water compromises swimming performance in larval fathead minnow. In isolated ventricular cardiomyocytes, skeletal myotubes, and adult flexor digitorum brevis fibers TCS depresses electrically evoked ECC within ∼10-20 min. In myotubes, nanomolar to low micromolar TCS initially potentiates electrically evoked Ca(2+) transients followed by complete failure of ECC, independent of Ca(2+) store depletion or block of RyR1 channels. TCS also completely blocks excitation-coupled Ca(2+) entry. Voltage clamp experiments showed that TCS partially inhibits L-type Ca(2+) currents of cardiac and skeletal muscle, and [(3)H]PN200 binding to skeletal membranes is noncompetitively inhibited by TCS in the same concentration range that enhances [(3)H]ryanodine binding. TCS potently impairs orthograde and retrograde signaling between L-type Ca(2+) and RyR channels in skeletal muscle, and L-type Ca(2+) entry in cardiac muscle, revealing a mechanism by which TCS weakens cardiac and skeletal muscle contractility in a manner that may negatively impact muscle health, especially in susceptible populations.
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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.