Abstract
Lambda-cyhalothrin (LCY), a widely used pyrethroid insecticide, is toxic to bees-vital pollinators experiencing global declines; however, its molecular effects during early development remain poorly understood. We investigated the molecular mechanisms underlying chronic sublethal exposure to LCY in the larval and adult stages. Larvae were exposed to LCY (0.004 µg active ingredient/larva), with four groups examined: solvent-treated larvae group (SLG), solvent-treated adult group (SAG), LCY-treated larvae group (LLG), and LCY-treated adult group (LAG). We identified 1128 and 168 significantly altered genes in LLG vs. SLG and LAG vs. SAG, respectively, with 125 larval- and 25 adult-specific DEGs, indicating stage-dependent toxicity. LCY dysregulated processes such as cuticle formation, sulfur metabolism, oxidoreductase activity, and neuropeptide signaling in larvae, while adults exhibited altered redox balance, peptide receptor signaling, and monoamine transport. Neuroactive signaling disruptions were observed in both stages, with additional effects on motor function, amino acid metabolism, and glycolysis in larvae; whereas adults exhibited altered lipid biosynthesis and energy metabolism. Downregulated genes involved in chitin metabolism and antioxidant defenses in larvae suggested compromised exoskeletal integrity and increased vulnerability. Overall, our findings highlight the long-term molecular consequences of early-life exposure and emphasize the need for safer pesticide practices to protect pollinator health.
Keywords:
Apis mellifera; Gene Ontology; KEGG pathway analysis; lambda-cyhalothrin; sublethal pesticide toxicity; transcriptomic analysis.