Imidacloprid Exposure Induced Impaired Intestinal Immune Function in Procambarus clarkii: Involvement of Oxidative Stress, Inflammatory Response, and Autophagy

Imidacloprid (IMI), a widely used neonicotinoid insecticide, has raised environmental concerns due to its potential impact on non-target aquatic organisms. This study investigates the effects of IMI exposure on the intestinal immune function of red swamp crayfish (Procambarus clarkii, P. clarkii), focusing on oxidative stress, inflammatory response, and autophagy. The P. clarkii was exposed to different doses of IMI (0, 10.93, 21.86, 43.73, 87.45 μg/L) for 96 h. Our findings reveal that IMI exposure leads to a survival rate of less than 70% when the concentration was 87.45 μg/L at 96 h. Hemolymph LZM and AKP contents were significantly decreased at the medium and high concentrations, and the expressions of hsp70 and nf-κb genes were significantly up-regulated. The expression of the lysozyme gene was significantly down-regulated. Additionally, the activities of SOD, CAT, and GPX were significantly decreased, the contents of MDA were significantly increased, and the gene expressions of CuZnsod, mMnsod, cat, and gpx in the gut were significantly down-regulated after exposure to medium-high IMI. The expression of autophagy-related genes showed that the expressions of beclin1, atg5, atg13, and lc3c genes in the medium- and high-concentration groups were significantly up-regulated. In summary, this study elucidates that medium-high levels of IMI exposure impair intestinal immune function in P. clarkii through mechanisms involving oxidative stress, inflammatory response, and autophagy.