Toosendanin inhibits the growth of Spodoptera litura by inducing metabolic dysfunction in the midgut

The Spodoptera litura, a crucial polyphagous pest, has emerged as a major threat to the agricultural sector. Regrettably, despite ongoing efforts, scientists have yet to uncover a safe and efficient control medication to tackle this pressing issue. Toosendanin (TSN), a commercial insecticidal active ingredient used to manage various pests in the field, has adverse effects on Spodoptera litura. However, the effects of TSN on the midgut of S. litura larvae remain unclear. This study explored the mechanism of TSN-induced toxicity and its inhibitory effects on larval growth and development using intestinal pathology, intestinal digestive enzyme activity determination, and intestinal transcriptome sequencing. The results indicated that TSN treatment led to pathological changes in the midgut structure. Analysis of digestive enzyme activity revealed that TSN inhibited the activities of acetyl CoA carboxylase, lipase, α-amylase, and trypsin. Simultaneously, it upregulated superoxide dismutase and reduced malondialdehyde content. Transcriptome analysis revealed that 2151 genes were significantly differentially expressed in the midgut after TSN exposure; the analysis highlighted significant enrichment of DEGs in areas such as hydrolase activity, carbohydrate metabolism, and peptide metabolism. Notably, some key enzymes involved in lipid metabolism, protein metabolism, and carbohydrate metabolism, such as pancreatic triacylglycerol lipase-like, pancreatic lipid-related protein 2-like, lipase3, alpha-amylase, trypsin, and chymotrypsin were downregulated following TSN treatment. This study's findings suggest that TSN causes midgut damage and inhibits larval growth by inducing metabolic dysfunction in the midgut.