Table 4.
Summary of intestinal toxicity of triclosan.
| Models | Enterotoxic effects | References |
|---|---|---|
| C57BL/6 mice | TCS exacerbated colitis through a gut microbiota-dependent mechanism by which gut microbial GUS proteins mediated the colonic reactivation of TCS from its inactive glucosinolate metabolites and drove the intestinal toxicity of TCS in the process. | Zhang et al., 2022b |
| C57BL/6 mice | TCS exposure triggered low-grade colonic inflammation, increased colitis, and exacerbated colitis-associated colon cancer in mice, and it adversely influenced colonic inflammation and associated colon tumorigenesis primarily by modulating intestinal microbiota and TLR4 signaling. | Yang et al., 2018 |
| Sprague Dawley (SD) rats | Low-dose TCS treatment disordered the intestinal microbiota in adolescent rats and led to an increase in the abundance of Spirochetes. | Hu et al., 2016 |
| C57/B6 mice Balb/c mice |
TCS exposure changed the diversity and composition of the intestinal microbiota in Balb/c mice. TCS treatment upregulated levels of sexual cytokines in the DSS-induced mouse model, decreased Occludin levels, and exacerbated the extent of intestinal mucosal and crypt damage, inflammatory cell infiltration, and glandular cell heterotype. | Liu et al., 2022c |
| Zebrafish | TCS exposure led to the disorder of zebrafish intestinal metabolism, as well as abnormalities in the intestinal mucosal immune system, while TCS treatment resulted in upregulation of pro-inflammatory genes (IL-1β, TNF-α) and elevated MDA concentrations. | Zang et al., 2019 |
| Zebrafish | TCS exposure impaired the structure and ecodynamics of the adult zebrafish gastrointestinal microbiome. | Gaulke et al., 2016 |
| Pimephales promelas | The Pimephales promelas gut microbiome was rapidly and significantly altered after exposure to low levels of environmentally relevant TCS, but recovered from this short-term perturbation in a fairly short period of time. | Narrowe et al., 2015 |
| Raw264.7/ HeLa cells | TCS mediated autophagy of HeLa and Raw264.7 cells probably via the AMPK/ULK1 and JNK/ERK/p38 pathways in a dose-dependent fashion. | Wang et al., 2018c |