Open AccessTriclosan Disrupts SKN-1/Nrf2-Mediated Oxidative Stress Response in C. elegans and Human Mesenchymal Stem Cells
Author(s) -
Dong Suk Yoon,
Yoorim Choi,
Dong Seok,
Peng Zhang,
SungJa Choi,
Mohammad A. Alfhili,
Joseph Ryan Polli,
De Qwon Pendergrass,
Faten Taki,
Brahmam Kapalavavi,
Xiaoping Pan,
Baohong Zhang,
T. Keith Blackwell,
Jin Woo Lee,
MyonHee Lee
Publication year - 2017
Publication title -
scientific reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.24
H-Index - 213
ISSN - 2045-2322
DOI - 10.1038/s41598-017-12719-3
Subject(s) - oxidative stress , mesenchymal stem cell , triclosan , microbiology and biotechnology , toxicity , biology , stem cell , caenorhabditis elegans , oxidative phosphorylation , antioxidant , chemistry , biochemistry , gene , medicine , pathology , organic chemistry
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.