Arsenite induce neurotoxicity of common carp: Involvement of blood brain barrier, apoptosis and autophagy, and subsequently relieved by zinc (II) supplementation

Arsenic pollution is a common threat to aquatic ecosystems. The effects of chronic exposure to arsenite on the brains of aquatic organisms are unknown. This study was designed to evaluate arsenic-induced brain damage in common carp (Cyprinus carpio) and the ameliorating effects of divalent zinc ion (Zn2+) supplementation from the aspects of oxidative stress (OxS), tight junction (TJ), apoptosis and autophagy. After arsenite exposure (2.83 mg/L) for 30 days, oxidative damage to the brain was determined, as indicated by inhibited antioxidants system (catalase-superoxide dismutase system, and glutathione system) and elevated levels of biomacmmolecule peroxidation (malondialdehyde and 8-hydroxydeoxyguanosine). Moreover, we also found functional damage to the brain as suggested by injuries to the blood-brain barrier (decreases in tight junction) and nerve conduction (depletion of AChE). Mechanisticly, apoptotic and autophagic cell death were indicated by typical morphologies including karyopyknosis and autophagosome, accompanying by key bio-indicators (Bcl-2, caspase and autophagy related gene family proteins). In contrast, the coadministration of Zn2+ (1 mg/L) with arsenite effectively alleviated this damage as suggested by the recovery of the aforementioned bioindicators. This study provides new insight into the brain toxicity caused by arsenite and suggests the application of zinc preparations in the aquatic pollution of arsenic.

Automated summary

This study investigated the brain damage caused by arsenite exposure in common carp and the protective effects of zinc ion supplementation. Results showed that zinc ion coadministration effectively alleviated oxidative damage, tight junction injuries, nerve conduction depletion, and apoptotic and autophagic cell death induced by arsenite in the brain.