Bioconcentration, oxidative stress and molecular mechanism of the toxic effect of acetamiprid exposure on Xenopus laevis tadpoles.

• Acetamiprid showed low bioconcentration potential in Xenopus laevis tadpoles. • Acetamiprid may have toxic effects on Xenopus laevis tadpoles. • Exposure to acetamiprid induces disorders in the antioxidant defense system. • Exposure to acetamiprid alters transcriptome and metabolome profiles in tadpoles. • Imbalances in purine metabolism and amino acid metabolism are potential molecular mechanisms. Acetamiprid is a neonicotinoid commonly detected in aquatic ecosystems, with residual concentrations of up to 0.41 mg/L in surface water, posing a threat to the health of nontarget aquatic organisms. However, studies on the potential toxicity and underlying mechanisms of action of acetamiprid on nontarget aquatic organisms are limited. This study investigated the acute and short-term toxicity of acetamiprid to Xenopus laevis tadpoles. A 96-h acute toxicity test determined the LC 50 of acetamiprid to be 32.1 mg/L. After 28 days of exposure to 1/10 and 1/100 LC 50 concentrations, tadpole samples were collected for bioconcentration elimination analysis, biochemical analyses, transcriptomics, and metabolomics studies to comprehensively evaluate the toxic effects of acetamiprid and its underlying mechanisms. The results, indicating bioconcentration factors (BCFs) < 1, suggest that acetamiprid has a low bioconcentration in tadpoles. Additionally, oxidative stress was observed in treated Xenopus laevis tadpoles. Transcriptomic and nontargeted metabolomic analyses identified 979 differentially expressed genes (DEGs) and 95 differentially metabolites in the 0.321 mg/L group. The integrated analysis revealed that disruption of purine and amino acid metabolic pathways potentially accounts for acetamiprid-induced toxic effects in tadpoles. The disruptive effects of acetamiprid on valine, leucine and isoleucine biosynthesis; and aminoacyl-tRNA biosynthesis metabolic pathways in tadpoles were validated through targeted metabolomics analysis. These findings are crucial for assessing the risk of acetamiprid to nontarget aquatic organisms. [ABSTRACT FROM AUTHOR]