Table 3.

Summary of liver toxicity of triclosan.

Models	Hepatotoxic effects	References
C57BL/6 mice	TCS-exposed mice showed hepatic hypertrophy, increase in liver lipid levels, and upregulation of fatty acid oxidation and inflammation-related genes.	Huang et al., 2020
C57BL/6 mice	TCS aggravated high-fat diet-induced metabolic disorders by disrupting the regulation of FGF21 expression.	Yueh et al., 2020
Sprague Dawley (SD) rats	More upregulated genes in carbohydrate and lipid metabolic pathways were observed in aged rats as TCS exposure contributed to metabolic disturbance and these effects would accumulate over time.	Ma et al., 2020
C57/B6 mice	TCS transmission through lactation resulted in adipogenesis, ER stress, PPARα activation, immune inflammation in the neonatal liver, and nonalcoholic fatty liver disease in neonatal C57/B6 mice.	Weber et al., 2022
Zebrafish	TCS regulated fto-mediated m6 methylation by inhibiting miR-30b expression, which led to the disturbance of lipid metabolism and elevation of TG and TC levels in zebrafish.	Sun et al., 2021a
Zebrafish	Severe hepatocyte atrophy and necrosis in the liver tissue of zebrafish larvae after TCS exposure, with a marked increase in the gap between the liver plates.	Liu et al., 2019
Mosquito fish	TCS exposure perturbed the antioxidant system in mosquito fish liver tissues, and a number of oxidative stress-related biomarkers were displayed in a concentration-dependent (e.g. NQO1 mRNA, CAT mRNA) and/or time-dependent (e.g. GSH content) manner.	Bao et al., 2021
HepG2 cells	TCS treatment significantly restrained DNA methylation levels and suppressed DNA methyltransferase 1 activity in HepG2 cells.	Ma et al., 2013