F–53B induces hepatotoxic effects and slows self-healing in ulcerative colitis in mice

Abstract

Chlorinated polyfluorinated ether sulfonate (F–53 B) is a distinct substitute for perfluorooctane sulphonate. It has been reported to be biologically toxic to mammals, causing enteric toxicity, liver toxicity and neurotoxicity. However, studies about the effects of F–53 B on patients with gastrointestinal diseases such as inflammatory bowel disease are very limited. In this study, whether the toxic impacts of F–53 B on the gut and liver can be exacerbated in mice with colitis was explored. The sensitivity of mice with acute colitis caused by dextran sulfate sodium salt (DSS) to F–53 B was compared with that of healthy mice. The mice were administered water containing F–53 B at doses of 10 and 100 μg/L sequentially for two weeks, respectively. F–53 B exposure exacerbated DSS-induced colonic inflammation, including inducing shortening of colon length, inflammatory cell infiltration and more severe histopathological symptoms. In addition, F–53 B administration significantly increased the levels of inflammatory cytokines, including interleukin (IL)-1, IL-6 and tumour necrosis factor-α, in the plasma of mice with enteritis compared with control group. F–53 B impaired intestinal integrity of mice with colitis by downregulating Claudin-1 and antimicrobial peptide-related genes while elevating serum lipopolysaccharide levels. In addition, in mice with colitis, F–53 B increased the levels of serum total cholesterol, triglyceride, low-density lipoprotein cholesterol, aspartate aminotransferase, and alanine aminotransferase, resulted in more severe liver inflammation and increased the level of genes related to the Gasdermin D-mediated pyrolysis. Conclusively, our results indicated that F–53 B delayed the self-healing of ulcerative colitis (UC) and caused liver inflammation in mice. This study provided some new insights into the health risks of F–53 B and raises concerns about the health of individuals with UC.