Sub-Lethal Concentration of Metamifop Exposure Impair Gut Health of Zebrafish (Danio Rerio)

The gut-liver-axis has close relationship with the occurrence of metabolism disorder in liver and gut. Previous study has demonstrated that metamifop exposure at sublethal concentration induced hepatic lipid metabolism disorder in zebrafish. Whether metamifop will cause adverse effects in zebrafish intestine is unknown. In the present study, effects of metamifop on gut heath of zebrafish were investigated after sublethal concentration (0.025, 0.10 and 0.40 mg/L) exposure. Histopathology analysis showed that metamifop induced inflammation and reduction of goblet cells in gut of zebrafish, indicating the gut health might be impaired. The activities of digestive enzymes (Lipase and Alkline Phosphatase) and content of FABP2 (Fatty Acid-Binding Protein 2) and expression levels of genes ( apoa-1a , apoe-b , fatp4 , lpl and fabp2 ) related to lipid transported were decreased in metamifop-treated group, indicating the capacity of lipid absorption and transportation were impaired. The transcripts of genes associated with inflammation ( il-17c , nk-kb and tnf-α ) were obviously increased in metamifop treatment groups, suggesting that metamifop induced inflammatory response in zebrafish intestine. Moreover, reduction of mRNA levels of cldn-15 and elevation of lipopolysaccharides (LPS) content were observed in metamifop-treated groups, which suggested that metamifop exposure increased the intestinal permeability. Furthermore, metamifop exposure decreased the relative abundance of beneficial bacteria ( Psychrobacter and Aeromonas ) and elevated the abundance of pathogenic bacteria ( Rhodobacter and Ralstonia ) in zebrafish intestine. These results indicated that metamifop exposure at sublethal concentrations would cause adverse effects on zebrafish gut health, via reduction of lipids absorption, inflammatory response, elevation of permeability and microbiota disorder