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Upregulated liver toxicity mediated by intestinal flora antibiotic resistance following exposure to triclosan and aged microplastics
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Combined exposure of Xenopus tropicalis to aged polystyrene microplastics and triclosan significantly enriched intestinal antibiotic resistance genes and disrupted short-chain fatty acid-producing bacteria, which in turn inhibited the GPR41-AMPK lipid metabolism pathway and caused liver lipid accumulation. This study reveals a gut-liver axis mechanism by which microplastics and antimicrobial agents synergistically drive metabolic disease risk in aquatic vertebrates.
Liver toxicity in aquatic organisms and the generation of antibiotic resistance genes (ARGs) caused by microplastics (MPs) and antibacterial contaminants have been widely reported. However, the mechanisms linking intestinal microbiota resistance to host liver metabolic dysregulation under combined exposure to MPs and antimicrobial agents remain unclear. In this study, Xenopus tropicalis was exposed to aged polystyrene MPs combined with triclosan (aPS + TCS). Compared with single-exposure groups, the aPS + TCS group showed more significant structural alterations in the gut microbiota and an increased abundance of ARGs, including linB , tetM , and ANT(6)-Ia . Notably, the abundance of tetM increased 7.37-fold compared with that in the control group. In the aPS + TCS group, drug-resistant bacteria carrying ARGs replaced short-chain fatty acid (SCFA)-producing functional bacteria, resulting in a 55% reduction in intestinal SCFAs compared with the control group. Molecular docking results revealed that reduced levels of SCFAs, such as butyric acid and propionic acid, inhibited the GPR41-AMPK lipid metabolism pathway. This inhibition led to increased lipid droplet size and elevated levels of lipid metabolites in the liver, thereby posing a risk of fatty liver disease. This study highlights the health risks associated with the disruption of intestinal microbiota function by aged MPs combined with bacteriostatic agents or antibiotics. • The resistance mechanism induced by aPS + TCS is resistance target protection. • ARG expression in the gut is most significantly promoted by aPS + TCS. • Increased drug-resistant bacteria inhibits the SCFA producing functional bacteria. • SCFA content in the gut was significantly reduced by aPS + TCS exposure. • Fatty liver disease is exacerbated through intestinal flora-SCFAs-GPR41 pathway.
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Researchers exposed frogs to aged microplastics carrying triclosan, an antimicrobial chemical commonly found in personal care products, and found the combination was more toxic to the gut than either pollutant alone. The microplastics increased triclosan absorption in the gut by 89%, disrupting gut bacteria and bile acid metabolism, which led to intestinal inflammation. This study shows that microplastics can act as carriers that amplify the harmful effects of other chemicals already present in the environment.
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