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 biomacromolecule 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.

砷污染是对水生生态系统的普遍威胁。长期暴露于砷对水生生物大脑的影响尚不清楚。本研究旨在评估砷引起的鲤鱼脑损伤（鲤属）和二价锌离子（Zn ²⁺）的改善作用。）可以从氧化应激（OxS），紧密连接（TJ），细胞凋亡和自噬等方面进行补充。砷暴露（2.83 mg / L）30天后，确定了对大脑的氧化损伤，如抗氧化剂系统抑制（过氧化氢酶-超氧化物歧化酶系统和谷胱甘肽系统）和生物大分子过氧化水平升高（丙二醛和8-羟基脱氧鸟苷）所示。 ）。此外，我们还发现血脑屏障（紧密连接减少）和神经传导（AChE耗竭）受损提示大脑功能受损。从机制上讲，凋亡和自噬细胞死亡是由典型的形态学指示的，包括核分裂和自噬，并伴有关键的生物指标（Bcl-2，胱天蛋白酶和自噬相关基因家族蛋白）。相反，锌的共同给药如上述生物指示剂的回收所表明，含砷²⁺（1 mg / L）可有效减轻这种损害。这项研究为砷引起的脑毒性提供了新的见解，并建议锌制剂在砷的水生污染中的应用。