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Published on: November 1, 2013
Hormesis Effect of Methyl Triclosan on Cell Proliferation and Migration in Human Hepatocyte L02 Cells
Jing An1, Weiwei Yao1, Waner Tang1
1Institute of Environmental Pollution and Health, School of Environmental and Chemical Engineering, Shanghai University, Shanghai 200444, P. R. China.
Abstract:
Methyl triclosan (mTCS) is a methylated derivative of triclosan (TCS), which is extensively used as an antimicrobial component of various nursing products and disinfectants. Current research studies of mTCS mainly focused on the environmental persistence and bioaccumulation potential. Knowledge regarding the toxicity and carcinogenicity of mTCS is limited until now. In this study, the human hepatocyte L02 cells were used to investigate the cellular effects of mTCS under different concentrations (0.1-60 μM). The hormesis effect was observed where a low dose of mTCS (≤5 μM) exposure stimulated the cell proliferation ability, while high-dose exposure (≥20 μM) inhibited cell proliferation. In the same time, low doses of mTCS (0.5 and 1 μM) induced enhanced anchorage-independent proliferation ability and cell migration ability, indicating a positive effect on malignant transformation in L02 cells. Moreover, reactive oxygen species productions were significantly increased after mTCS exposure (≥1 μM), as compared with the control group. Furthermore, expressions of tumor-related genes, mouse double minute 2 (MDM2), matrix metalloproteinase 9 (MMP9), and proliferating cell nuclear antigen (PCNA), and proto-oncogene MYC (c-Myc), Jun, and FosB were significantly upregulated, while no significant changes were observed on expressions of apoptosis-related and cell cycle-related genes in L02 cells after exposure of low-dose mTCS. In conclusion, these results indicated that a low dose of mTCS had a hormesis effect in L02 cells on cell proliferation and malignant transformation in vitro, which might be mediated through oxidative stress response.
Insights
Low doses of methyl triclosan (mTCS) stimulate human liver cell proliferation and malignant transformation, potentially via oxidative stress. High doses inhibit proliferation, indicating a hormesis effect in cellular response to mTCS.
Area of Science:
- Toxicology
- Cell Biology
- Environmental Health
Background:
- Methyl triclosan (mTCS), a derivative of triclosan (TCS), is widely used in consumer products.
- Existing research on mTCS primarily addresses environmental persistence and bioaccumulation.
- Limited data exists on the toxicity and carcinogenic potential of mTCS.
Purpose of the Study:
- To investigate the cellular effects of methyl triclosan (mTCS) on human hepatocyte L02 cells.
- To determine the dose-dependent toxicity and potential for malignant transformation induced by mTCS.
Main Methods:
- Human hepatocyte L02 cells were exposed to varying concentrations of mTCS (0.1-60 μM).
- Cell proliferation, anchorage-independent growth, and cell migration were assessed.
- Reactive oxygen species (ROS) production and gene expression (tumor-related, apoptosis, cell cycle) were analyzed.
Main Results:
- A hormesis effect was observed: low mTCS doses (≤5 μM) stimulated cell proliferation, while high doses (≥20 μM) inhibited it.
- Low mTCS doses (0.5-1 μM) enhanced anchorage-independent proliferation and cell migration, suggesting potential for malignant transformation.
- mTCS exposure (≥1 μM) significantly increased ROS production and upregulated tumor-related genes (MDM2, MMP9, PCNA, c-Myc, Jun, FosB).
Conclusions:
- Low-dose methyl triclosan (mTCS) exhibits a hormesis effect on human liver cells, promoting proliferation and malignant transformation in vitro.
- The observed effects may be mediated by oxidative stress response pathways.
- Further investigation into the carcinogenicity of mTCS at low environmental concentrations is warranted.

