Wang Yu, Zhao Hongjing, Liu Yachen, Guo Menghao, Tian Ye, Huang Puyi, Xing Mingwei
College of Wildlife and Protected Area, Northeast Forestry University, Harbin, 150040, Heilongjiang, PR China.
College of Wildlife and Protected Area, Northeast Forestry University, Harbin, 150040, Heilongjiang, PR China.
Aquat Toxicol. 2021 Mar;232:105765. doi: 10.1016/j.aquatox.2021.105765. Epub 2021 Jan 25.
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 (Zn) 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 Zn (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常见威胁。长期接触亚砷酸盐对水生生物大脑的影响尚不清楚。本研究旨在从氧化应激（OxS）、紧密连接（TJ）、细胞凋亡和自噬等方面评估亚砷酸盐对鲤鱼（Cyprinus carpio）大脑的损伤以及补充二价锌离子（Zn）的改善作用。在亚砷酸盐暴露（2.83 mg/L）30天后，确定了大脑的氧化损伤，表现为抗氧化系统（过氧化氢酶-超氧化物歧化酶系统和谷胱甘肽系统）受到抑制以及生物大分子过氧化水平（丙二醛和8-羟基脱氧鸟苷）升高。此外，我们还发现了大脑的功能损伤，表现为血脑屏障受损（紧密连接减少）和神经传导受损（乙酰胆碱酯酶耗竭）。从机制上讲，典型的形态学特征（包括核固缩和自噬体）以及关键生物指标（Bcl-2、半胱天冬酶和自噬相关基因家族蛋白）表明存在凋亡和自噬性细胞死亡。相比之下，锌（1 mg/L）与亚砷酸盐共同给药有效地减轻了这种损伤，上述生物指标的恢复表明了这一点。本研究为亚砷酸盐引起的脑毒性提供了新的见解，并建议在砷的水污染中应用锌制剂。
