Physiology and transcriptomic reveals the toxic effect of acute acetamiprid exposure on noble scallop Chlamys nobilis.

Neonicotinoid insecticides such as acetamiprid are increasingly detected in coastal environments, yet their sublethal impacts on non-target marine bivalves remain poorly understood. Here, we integrated histopathology, enzymatic assays, and weighted gene co-expression network analysis (WGCNA) to elucidate the acute toxicological mechanisms of ACE in the noble scallop Chlamys nobilis. Exposure to 5 mg/L ACE for 72 h induced pronounced gill filament deformation, identifying the gill as a sensitive target tissue. At the biochemical level, superoxide dismutase (SOD) and catalase (CAT) activities were elevated at both 1 and 5 mg/L, whereas glutathione S-transferase (GST) activity decreased at the higher concentration, suggesting an overwhelmed antioxidant defense system. Transcriptomic analysis further revealed disruption of vitamin B12 uptake (e.g., downregulation of CUBN and ABCC1) and impairment of ABC transporter-mediated xenobiotic efflux, potentially exacerbating intracellular toxicant accumulation and oxidative stress. Meanwhile, ACE exposure triggered lipid metabolic reprogramming (arachidonic and linoleic acid pathways) and enhanced amino acid catabolism, indicating a shift toward energy reallocation to sustain stress responses. Notably, ACE also induced neurotoxicity via dual pathways: acetylcholinesterase (AChE) inhibition and GABAergic synapse dysregulation (GABRA upregulation). Collectively, these results demonstrate that ACE disrupts detoxification capacity, redox homeostasis, neural function, and energy metabolism in marine bivalves, providing mechanistic insights into the ecological risks of neonicotinoids in coastal ecosystems.