Transcriptome and physiological analyses reveal the mechanism of the liver injury and pathological alterations in northern snakehead (Channa argus) after dietary exposure to aflatoxin B1

Aflatoxin B1 (AFB1) is the most toxic naturally occurring mycotoxin produced by Aspergillus flavus and Aspergillus parasiticus, has been regarded as a critical food contaminant in aquafeed. Furthermore, previous studies indicated that dietary AFB1 exposure could cause liver tissues injury in mammals and fish. However, the mechanism of dietary AFB1-induced liver injury of fish has not been fully elucidated. The aim of this study was to investigate the effects of dietary AFB1 exposure on the liver of northern snakehead (Channa argus) (7.52 ± 0.02 g) through hematological parameters, liver histopathology, and ultrastructural analysis and revealed the possible mechanism of AFB1-induced northern snakehead liver injury through RNA-Seq analysis. The results of serum biochemical indicators demonstrated that the aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), and alkaline phosphatase (ALP) as the biomarkers of liver damage, increased significantly at AFB1 exposure concentrations above 200 μg/kg. Liver histopathology and ultrastructural analysis demonstrated that different degrees of lesions were found in 100, 200, and 400 μg/kg groups. Liver transcriptomic analyses demonstrated that a total of 1307 differentially expressed genes (DEGs) were significantly expressed induced in response to the dietary AFB1 exposure, of which 540 were up- and 767 were down-regulated genes. Furthermore, Gene Ontology (GO) analysis showed that the ribosome biogenesis, ribonucleoprotein complex biogenesis, negative regulation of cellular process, and metabolic process were highly enriched in the biological process category. Meanwhile, 310 enriched pathways were identified in the Kyoto Encyclopedia of Genes and Genomes (KEGG) Pathway database analysis, of which the metabolism of xenobiotics by cytochrome P450, glutathione metabolism, protein processing in endoplasmic reticulum, and PI3K-Akt signaling pathway were the vital metabolic mechanisms related to dietary AFB1 exposure-induced liver injury in northern snakehead and were confirmed by qPCR. Overall, the findings provide more valuable information for further studies on the latent toxicity mechanisms of AFB1 in fish. •Dietary aflatoxin B1 caused Channa argus liver damage and dysfunction.•Dietary aflatoxin B1 caused Channa argus liver endoplasmic reticulum stress and mitochondrial swelling•Dietary aflatoxin B1 disturbed redox balance and changed antioxidant defense in Channa argus.•Dietary a