Integrated multiomics approach and pathological analyses provide new insights into hepatic injury and metabolic alterations in Saanen goats after dietary exposure to aflatoxin B1

Exploring the toxicity and metabolic mechanisms of aflatoxin B₁ (AFB₁) in ruminants can help to develop strategies to prevent or reduce the transfer of the toxin and its metabolites to milk and meat. This study aimed to explore the effects of 3 concentrations of dietary AFB₁ (0, 50, and 500 μg/kg) on hepatic injury and metabolism in Saanen goats via histological examination, western blot analysis, as well as integrated multiomics techniques. Eighteen Saanen goats were assigned to 1 of 3 treatments and the AFB₁ challenge lasted for 14 d. Results showed that the liver tissue was enlarged and the relative organ index of the liver was linearly increased with elevated AFB₁ levels. The hepatocyte apoptosis rate was significantly increased after AFB₁ exposure, and the western blotting results revealed that both the external apoptotic pathway and mitochondrial-mediated intrinsic apoptotic pathway might be involved in AFB₁-induced hepatocyte apoptosis. We identified 251, 269, and 154 significant differentially expressed genes (DEG) and 340, 596, and 127 significant differential metabolites in comparisons between the control (CON; 0 μg/kg) and low-dose (LO; 50 μg/kg) groups, the CON and high-dose (HI; 500 μg/kg) groups, and the LO and HI groups, respectively. The DEG annotated were mainly involved in the cell part, cell, single-organism process, cellular process, binding, and other functional categories. The identified metabolites primarily belonged to glycerophospholipids, prenol lipids, carboxylic acids, and derivatives. Integrative analysis of transcriptomics and metabolomics revealed that glycerophospholipids metabolism and choline metabolism in cancer were the most affected pathways related to AFB₁ exposure. The identified differential metabolites, DEG, and pathways might have played a crucial role in the hepatic injury induced by AFB₁ in goats.