Sublethal exposure to thiacloprid disrupts intestinal microbiota, digestion and detoxification functions in silkworms...

Concerns about neonicotinoids are growing due to their potential toxicity to non-target organisms. The toxic effects of trace residues in the environment may reveal the causes of their toxicity to non-target organisms.

In this study, the toxicity of sublethal dose of thiacloprid to silkworm was studied, and the potential mechanism of toxicity was analyzed from the four dimensions of intestinal electron microscopy structure, microbe, enzyme activity changes, and gene expression. Firstly, sublethal doses of thiacloprid inhibited the weight growth of silkworms by 40.9% and reduced the pre-pupation survival rate by 14.3%. Meanwhile, it caused structural damage to the midgut cells of silkworms. Exposure also altered the microbial community structure of the intestinal tract, increasing species richness while reducing species diversity and uniformity. The proportion of beneficial bacteria with anti-stress functions, such as Firmicutes (from 39.44% to 16.47%) and Staphylococcus (from 38.85% to 1.27%), was greatly reduced. Conversely, the proportions of pathogenic bacteria, including Tyzzerella (from 0.01% to 14.07%) and Achromobacter (from 2.76% to 7.16%), increased markedly. In addition, exposure significantly inhibited the gene expression and enzyme activity of digestion-related enzymes (amylase, lipase, and trypsin), among which the inhibition of lipase was particularly significant; it significantly activated the gene expression and enzyme activity of detoxification-related enzymes (P450, GST, and CarE).

In summary, these findings offer significant insights into the toxicity mechanisms of non-target organisms exposed to neonicotinoids at sublethal doses. © 2026 Society of Chemical Industry.