MAPK-CncC Signaling Pathways Regulate the Antitoxic Response to Avermectin-Induced Oxidative Stress in Juvenile Chinese Mitten Crab, Eriocheir sinensis.

Abstract

This study delves into the adverse effects of AVM, emphasizing oxidative stress induction in the Chinese mitten crab, Erocheir sinensis, and the role of the MAPK-CncC signaling pathway in mediating the antioxidative response. Our findings reveal a dose-dependent impairment in growth performance, alongside occurrence of oxidative stress. The activity of CAT and superoxide dismutase increased significantly in all treatments (0.2, 2, and 20 μg/L) while the lipid peroxidation level rose in median (2 μg/L) and high (20 μg/L) concentration groups. The T-AOC levels decreased in all treatments while the reactive oxygen species levels increased significantly. Transcriptomic insights indicated the activation of the MAPK-CncC signaling pathway, critical in upregulating genes associated with detoxification and oxidative stress defense. Knocking down CncC, a homologue of vertebrate Nrf2 gene, by dsRNA in E. sinensis resulted in down-regulation of antioxidative genes and reduced survival tolerance to AVM exposure. By using an in vitro cell culture system, we observed similar downregulations of antioxidative genes when hepatopancreas cells were treated with ML385, a CncC specific inhibitor. Moreover, rapid phosphorylation of the JNK protein was observed in hepatopancreas cells upon AVM exposure. When JNK was inhibited, cells were more vulnerable to AVM and AVM-induced robust expression of the CncC gene was blocked.