Abstract

The increasing environmental release of cerium oxide nanoparticles (CeO2 NPs) raised concerns about their potential risks to aquatic organisms, yet their chronic effects remained poorly understood. This study investigated the impact of CeO2 NPs on the glucose and lipid metabolic homeostasis of the gut-liver axis and their bioaccumulation patterns in adult zebrafish. Exposure to 100 μg/L and 1000 μg/L CeO2 NPs for 26 days inhibited the growth of zebrafish and caused intestinal damage. The analysis of inductively coupled plasma mass spectrometry (ICP-MS) indicated that Ce was concentrated in the intestinal tract and liver, with less bioaccumulation in muscle. In the groups treated with 100 and 1000 μg/L CeO2 NPs, the expression of glycolipid-related genes was downregulated in liver of zebrafish. Hepatic biochemical assays showed that exposure to CeO2 NPs (100 and 1000 μg/L) resulted in decreased levels of pyruvate and elevated levels of glucose. It also led to increased content of lipid in the liver, manifesting as increased levels of triglycerides (TG) and low-density lipoprotein (LDL). In addition, sequencing of intestinal 16S rRNA amplicons revealed that CeO2 NPs significantly altered the microbial community composition and induced intestinal injury. This study demonstrated that CeO2 NPs disrupted the gut-liver axis metabolic homeostasis and induced tissue-specific accumulation in zebrafish, illustrating its multifaceted toxicological impact.