Copper (Cu) is an important metal pollutant commonly found in aquatic environment owing to its inherent bioaccumulation and biomagnification potentials and long-term persistence in environmental compartments. The application of novel fabricated copper nanoparticles (Cu-NPs) has led to cytotoxicity in aquatic animals. However, the differences in underlying toxicity mechanisms between Cu-NPs and waterborne Cu (such as CuSO4) remain unelucidated. Herein, the mechanisms underlying the CuSO4/Cu-NPs-mediated perturbation of the hepatopancreatic mitochondrial function at different concentrations were investigated and compared. After exposing Eriocheir sinensis to 0 (control), 5, 50, and 500 μg/L CuSO4 and 10 μg/L Cu-NPs for 21 days, hepatopancreases were retrieved. The results revealed that Cu-NPs or CuSO4 (50 and 500 μg/L) induced ultrastructural damage following a time-dose effect, as indicated by swelling and degeneration of the lumen of hepatic tubules. Excess CuSO4 or Cu-NPs exposure decreased the antioxidative capacity and led to the over-accumulation of mitochondrial ROS. Moreover, the mitochondrial membrane potential (ΔΨm) was reduced and apoptosis induced. Additionally, both CuSO4 and Cu-NPs increased the numbers of mitophagosomes and the mRNA and protein levels of LC3B, and triggered mitophagy through PRKN-independent pathway; however, mostly the BNIP3L/Beclin1 pathway was involved in excess CuSO4-induced mitophagy. Altogether, this study provides a basis for exploring Cu-mediated potential mitochondrial autophagy activation mechanisms and their effects on environmental toxicity.
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