Effects of Copper Exposure on Oxidative Stress, Apoptosis, Endoplasmic Reticulum Stress, Autophagy and Immune Response in Different Tissues of Chinese Mitten Crab ().

High concentrations of copper (Cu) pose a great threat to aquatic animals. However, the mechanisms underlying the response of crustaceans to Cu exposure have not been well studied. Therefore, we investigated the alterations of physiological and molecular parameters in Chinese mitten crab () after Cu exposure. The crabs were exposed to 0 (control), 0.04, 0.18, and 0.70 mg/L of Cu for 5 days, and the hemolymph, hepatopancreas, gills, and muscle were sampled. The results showed that Cu exposure decreased the antioxidative capacity and promoted lipid peroxidation in different tissues. Apoptosis was induced by Cu exposure, and this activation was associated with the mitochondrial and ERK pathways in the hepatopancreas. ER stress-related genes were upregulated in the hepatopancreas but downregulated in the gills at higher doses of Cu. Autophagy was considerably influenced by Cu exposure, as evidenced by the upregulation of autophagy-related genes in the hepatopancreas and gills. Cu exposure also caused an immune response in different tissues, especially the hepatopancreas, where the TLR2-MyD88-NF-κB pathway was initiated to mediate the inflammatory response. Overall, our results suggest that Cu exposure induces oxidative stress, ER stress, apoptosis, autophagy, and immune response in , and the toxicity may be implicated following the activation of the ERK, AMPK, and TLR2-MyD88-NF-κB pathways.