ArticleScientific reports2017
Triclosan Disrupts SKN-1/Nrf2-Mediated Oxidative Stress Response in C. elegans and Human Mesenchymal Stem Cells.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 41 citations in OpenAlex.
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- Incorporation of paclitaxel in mesenchymal stem cells using nanoengineering upregulates antioxidant response, CXCR4 expression and enhances tumor homing.Materials today. Bio · 2023Article
- Triclosan: A Small Molecule with Controversial Roles.Antibiotics (Basel, Switzerland) · 2022Review
- The Role of NRF2 in Bone Metabolism - Friend or Foe?Frontiers in endocrinology · 2022Review
- Triclosan induces apoptosis in Burkitt lymphoma-derived BJAB cells through caspase and JNK/MAPK pathways.Apoptosis : an international journal on programmed cell death · 2021Article
- Triclosan depletes the membrane potential in Pseudomonas aeruginosa biofilms inhibiting aminoglycoside induced adaptive resistance.PLoS pathogens · 2020Article
- The teratogenic effect of Triclosan on embryogenesis is attenuated by Tween 20 inmicroPublication biology · 2020Article
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- Triclosan: An Update on Biochemical and Molecular Mechanisms.Oxidative medicine and cellular longevity · 2019Review
- Non-Ionic Surfactants Antagonize Toxicity of Potential Phenolic Endocrine-Disrupting Chemicals, Including Triclosan inMolecules and cells · 2018Article
- Toxic Effects of Bisphenol A, Propyl Paraben, and Triclosan on Caenorhabditis elegans.International journal of environmental research and public health · 2018Article
- Measurement of Intracellular ROS inBio-protocol · 2018Article
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 3 countries.
Funding
Abstract
Triclosan (TCS), an antimicrobial chemical with potential endocrine-disrupting properties, may pose a risk to early embryonic development and cellular homeostasis during adulthood. Here, we show that TCS induces toxicity in both the nematode C. elegans and human mesenchymal stem cells (hMSCs) by disrupting the SKN-1/Nrf2-mediated oxidative stress response. Specifically, TCS exposure affected C. elegans survival and hMSC proliferation in a dose-dependent manner. Cellular analysis showed that TCS inhibited the nuclear localization of SKN-1/Nrf2 and the expression of its target genes, which were associated with oxidative stress response. Notably, TCS-induced toxicity was significantly reduced by either antioxidant treatment or constitutive SKN-1/Nrf2 activation. As Nrf2 is strongly associated with aging and chemoresistance, these findings will provide a novel approach to the identification of therapeutic targets and disease treatment.
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Registered trials
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