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

Dong Suk Yoon, Yoorim Choi, Dong Seok Cha, Peng Zhang, Seong Mi Choi, Mohammad Abdulmohsen Alfhili, Joseph Ryan Polli, De Qwon Pendergrass, Faten A. Taki, Brahmam Kapalavavi, Xiaoping Pan, Baohong Zhang, T. Keith Blackwell, Jin Woo Lee, Myon Hee Lee

Research output: Contribution to journalArticle

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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.

Original languageEnglish
Article number12592
JournalScientific reports
Volume7
Issue number1
DOIs
Publication statusPublished - 2017 Dec 1

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Triclosan
Mesenchymal Stromal Cells
Oxidative Stress
Embryonic Development
Homeostasis
Antioxidants
Cell Proliferation
Survival
Genes

All Science Journal Classification (ASJC) codes

  • General

Cite this

Yoon, D. S., Choi, Y., Cha, D. S., Zhang, P., Choi, S. M., Alfhili, M. A., ... Lee, M. H. (2017). Triclosan Disrupts SKN-1/Nrf2-Mediated Oxidative Stress Response in C. elegans and Human Mesenchymal Stem Cells. Scientific reports, 7(1), [12592]. https://doi.org/10.1038/s41598-017-12719-3
Yoon, Dong Suk ; Choi, Yoorim ; Cha, Dong Seok ; Zhang, Peng ; Choi, Seong Mi ; Alfhili, Mohammad Abdulmohsen ; Polli, Joseph Ryan ; Pendergrass, De Qwon ; Taki, Faten A. ; Kapalavavi, Brahmam ; Pan, Xiaoping ; Zhang, Baohong ; Blackwell, T. Keith ; Lee, Jin Woo ; Lee, Myon Hee. / Triclosan Disrupts SKN-1/Nrf2-Mediated Oxidative Stress Response in C. elegans and Human Mesenchymal Stem Cells. In: Scientific reports. 2017 ; Vol. 7, No. 1.
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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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Yoon, DS, Choi, Y, Cha, DS, Zhang, P, Choi, SM, Alfhili, MA, Polli, JR, Pendergrass, DQ, Taki, FA, Kapalavavi, B, Pan, X, Zhang, B, Blackwell, TK, Lee, JW & Lee, MH 2017, 'Triclosan Disrupts SKN-1/Nrf2-Mediated Oxidative Stress Response in C. elegans and Human Mesenchymal Stem Cells', Scientific reports, vol. 7, no. 1, 12592. https://doi.org/10.1038/s41598-017-12719-3

Triclosan Disrupts SKN-1/Nrf2-Mediated Oxidative Stress Response in C. elegans and Human Mesenchymal Stem Cells. / Yoon, Dong Suk; Choi, Yoorim; Cha, Dong Seok; Zhang, Peng; Choi, Seong Mi; Alfhili, Mohammad Abdulmohsen; Polli, Joseph Ryan; Pendergrass, De Qwon; Taki, Faten A.; Kapalavavi, Brahmam; Pan, Xiaoping; Zhang, Baohong; Blackwell, T. Keith; Lee, Jin Woo; Lee, Myon Hee.

In: Scientific reports, Vol. 7, No. 1, 12592, 01.12.2017.

Research output: Contribution to journalArticle

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AU - Yoon, Dong Suk

AU - Choi, Yoorim

AU - Cha, Dong Seok

AU - Zhang, Peng

AU - Choi, Seong Mi

AU - Alfhili, Mohammad Abdulmohsen

AU - Polli, Joseph Ryan

AU - Pendergrass, De Qwon

AU - Taki, Faten A.

AU - Kapalavavi, Brahmam

AU - Pan, Xiaoping

AU - Zhang, Baohong

AU - Blackwell, T. Keith

AU - Lee, Jin Woo

AU - Lee, Myon Hee

PY - 2017/12/1

Y1 - 2017/12/1

N2 - 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.

AB - 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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