Triclosan Disrupts SKN-1/Nrf2-Mediated Oxidative Stress Response in C. elegans and Human Mesenchymal Stem Cells

Sci Rep. 2017 Oct 3;7(1):12592. doi: 10.1038/s41598-017-12719-3.


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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antioxidants / pharmacology
  • Caenorhabditis elegans / drug effects
  • Caenorhabditis elegans / genetics
  • Caenorhabditis elegans Proteins / genetics*
  • DNA-Binding Proteins / genetics*
  • Dose-Response Relationship, Drug
  • Endocrine Disruptors / pharmacology
  • Gene Expression Regulation / drug effects
  • Humans
  • Mesenchymal Stem Cells / drug effects
  • NF-E2-Related Factor 2 / genetics*
  • Oxidative Stress / drug effects
  • Oxidative Stress / genetics*
  • Transcription Factors / genetics*
  • Triclosan / pharmacology*


  • Antioxidants
  • Caenorhabditis elegans Proteins
  • DNA-Binding Proteins
  • Endocrine Disruptors
  • NF-E2-Related Factor 2
  • NFE2L2 protein, human
  • Transcription Factors
  • skn-1 protein, C elegans
  • Triclosan