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Published on: March 23, 2019
Triclosan Disrupts SKN-1/Nrf2-Mediated Oxidative Stress Response in C. elegans and Human Mesenchymal Stem Cells
Dong Suk Yoon1,2, Yoorim Choi2,3, Dong Seok Cha1,4
1Department of Internal Medicine, Brody School of Medicine at East Carolina University, Greenville, NC, 27834, USA.
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.
Insights
Triclosan (TCS) harms C. elegans and human cells by disrupting the SKN-1/Nrf2 antioxidant response. This discovery offers new therapeutic targets for aging and disease treatment.
Area of Science:
- Toxicology
- Cell Biology
- Developmental Biology
Background:
- Triclosan (TCS) is an antimicrobial agent with suspected endocrine-disrupting effects.
- Potential risks of TCS exposure include impaired embryonic development and adult cellular homeostasis.
Purpose of the Study:
- To investigate the molecular mechanisms underlying TCS-induced toxicity.
- To determine the role of the SKN-1/Nrf2 pathway in TCS toxicity.
- To explore potential therapeutic interventions for TCS exposure.
Main Methods:
- Utilized the nematode C. elegans and human mesenchymal stem cells (hMSCs) as model systems.
- Assessed TCS effects on survival, proliferation, and SKN-1/Nrf2 pathway activation.
- Investigated the impact of antioxidant treatment and SKN-1/Nrf2 modulation on TCS toxicity.
Main Results:
- TCS exposure caused dose-dependent toxicity in C. elegans and hMSCs.
- TCS inhibited nuclear localization of SKN-1/Nrf2 and its downstream target gene expression.
- Antioxidant treatment or enhanced SKN-1/Nrf2 activity significantly mitigated TCS-induced toxicity.
Conclusions:
- TCS disrupts the SKN-1/Nrf2-mediated oxidative stress response, leading to cellular toxicity.
- The SKN-1/Nrf2 pathway is a critical mediator of TCS toxicity.
- Targeting the SKN-1/Nrf2 pathway presents a novel therapeutic strategy for TCS-related health risks and potentially aging-related diseases.
