Journal
ANTIOXIDANTS
Volume 11, Issue 10, Pages -Publisher
MDPI
DOI: 10.3390/antiox11102029
Keywords
copper; apoptosis; endoplasmic reticulum stress; oxidative stress; Eriocheir sinensis
Funding
- Central Public Interest Scientific Institution Basal Research Fund, Freshwater Fisheries Research Center, CAFS [2021JBFM12, 2020TD36]
- Key Project for Jiangsu Agricultural New Variety Innovation [PZCZ201749]
- Jiangsu Revitalization of Seed Industry [JBGS[2021]031]
Ask authors/readers for more resources
High concentrations of copper pose a threat to aquatic animals, but the response mechanisms of crustaceans to Cu2+ exposure are not well understood. This study investigated the physiological and molecular changes in Chinese mitten crabs after Cu2+ exposure. The results showed that Cu2+ exposure decreased antioxidative capacity and promoted lipid peroxidation in different tissues. It also induced apoptosis and autophagy, and triggered an immune response. The toxicity of Cu2+ may be associated with the activation of ERK, AMPK, and TLR2-MyD88-NF-kappa B pathways.
High concentrations of copper (Cu2+) pose a great threat to aquatic animals. However, the mechanisms underlying the response of crustaceans to Cu2+ exposure have not been well studied. Therefore, we investigated the alterations of physiological and molecular parameters in Chinese mitten crab (Eriocheir sinensis) after Cu2+ exposure. The crabs were exposed to 0 (control), 0.04, 0.18, and 0.70 mg/L of Cu2+ for 5 days, and the hemolymph, hepatopancreas, gills, and muscle were sampled. The results showed that Cu2+ exposure decreased the antioxidative capacity and promoted lipid peroxidation in different tissues. Apoptosis was induced by Cu2+ 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 Cu2+. Autophagy was considerably influenced by Cu2+ exposure, as evidenced by the upregulation of autophagy-related genes in the hepatopancreas and gills. Cu2+ exposure also caused an immune response in different tissues, especially the hepatopancreas, where the TLR2-MyD88-NF-kappa B pathway was initiated to mediate the inflammatory response. Overall, our results suggest that Cu2+ exposure induces oxidative stress, ER stress, apoptosis, autophagy, and immune response in E. sinensis, and the toxicity may be implicated following the activation of the ERK, AMPK, and TLR2-MyD88-NF-kappa B pathways.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available