To explore the toxicological mechanism of benz[a]opyrene (B[a]P) in gall bladder for aquatic animals, common carp (Cyprinus carpio) was used as the experimental material in this study. A 15-day chronic toxicity test was conducted with different concentrations of B[a]P (0,0.025 and 0.25 mg/L) exposure to examine the toxicological mechanisms of B[a]P on carp gall bladder by measuring the content of B[a]P, antioxidant parameters, transcriptional response and immune gene expressions in common carp gall bladder. Results show that the accumulation of B[a]P in gall bladder tissues increased significantly with the concentration of B[a]P stress, which indicates that gall bladder plays an important role in detoxification. The activities of antioxidant enzymes (superoxide dismutase, catalase and glutathione peroxidase) and the concentration of malondialdehyde increased after B[a]P exposure, indicating that the gall bladder can respond to oxidative stress by activating the antioxidant oxidase system. In addition, exposure to low concentrations of B[a]P can induce immune responses in common carp gall bladder tissues, activating the Notch receptor signaling pathway, thereby causing apoptosis and eliminating excessive or abnormal cells in their own tissues. However, high-concentration exposure to B[a]P can inhibit the RIG-I and Notch receptor signaling pathways, causing an imbalance in gall bladder immune homeostasis. This inhibition of cell apoptosis prolongs the survival time of abnormal cells, and further activates immune cells, leading to self-tissue damage. This study provides preliminary insights into the potention self-protective mechanisms of common carp gall bladder cells in response to B[a]P exposure, laying the fundation for early warning and ecological risk assessment of polycyclic aromatic hydrocarbon pollution in water environment.