Liu_2026_Aquat.Toxicol_298_107917

Fenvalerate (FEN), a widely used synthetic pyrethroid pesticide that poses substantial risks to aquatic ecosystems. This study systematically compared the toxic effects of FEN exposure through food and water pathways in the abalone Haliotis discus hannai, with specific focus on the gills. Our results demonstrated detectable FEN accumulation in the gills under both exposure routes, and water exposure led to significantly higher accumulation, particularly at higher concentrations. Proteomic analysis revealed that both exposure routes induced substantial molecular alterations, with food exposure primarily disrupting Metabolic processes, while water exposure caused more extensive disruptions, including Genetic Information Processing pathways. Both exposure routes induced oxidative stress in the gills, evidenced by significantly elevated superoxide dismutase (SOD) and glutathione S-transferase (GST) activities and increased malondialdehyde (MDA) levels, though acetylcholinesterase (AChE) activity remained unchanged across all groups. Molecular analysis showed that both food and water exposure upregulated genes related to antioxidant defense (Nuclear factor erythroid 2-related factor 2, Nrf2), apoptosis (BCL2-Associated X Protein, BAX; Cysteine-Aspartic Acid Protease 3, Caspase-3), immune inflammation (Toll-Like Receptor 2, TLR2; Toll-Like Receptor 4, TLR4; Tumor Necrosis Factor Alpha, TNF-alpha), and cellular signaling (Phosphatidylinositol 3-Kinase, PI3K), while downregulating the anti-apoptotic gene (B-cell Lymphoma 2, Bcl-2), with these effects being most pronounced under water exposure. Integrated biomarker response (IBR) and principal component analysis (PCA) consistently demonstrated that both exposure routes disrupted gill physiological homeostasis, with water exposure causing the most severe toxicological effects. These findings establish that while food exposure induces significant toxicity in abalone gills, water exposure represents the predominant risk factor through interconnected oxidative, immune, and apoptotic pathways.