Department of Biochemistry and Biotechnology, Precarpathian National University named after Vassyl Stefanyk, Ivano-Frankivsk 76025, Ukraine.
Chemosphere. 2011 Oct;85(6):983-9. doi: 10.1016/j.chemosphere.2011.06.078. Epub 2011 Jul 20.
Cobalt is an essential element, but at high concentrations it is toxic. In addition to its well-known function as an integral part of cobalamin (vitamin B₁₂), cobalt has recently been shown to be a mimetic of hypoxia and a stimulator of the production of reactive oxygen species. The present study investigated the responses of goldfish, Carassius auratus, to 96 h exposure to 50, 100 or 150 mg L⁻¹ Co²⁺ in aquarium water (administered as CoCl₂). The concentrations of cobalt in aquaria did not change during fish exposure. Exposure to cobalt resulted in increased levels of lipid peroxides in brain (a 111% increase after exposure to 150 mg L⁻¹ Co²⁺) and liver (30-66% increases after exposure to 50-150 mg L⁻¹ Co²⁺), whereas the content of protein carbonyls rose only in kidney (by 112%) after exposure to 150 mg L⁻¹ cobalt. Low molecular mass thiols were depleted by 24-41% in brain in response to cobalt treatment. The activities of primary antioxidant enzymes, superoxide dismutase (SOD) and catalase, were substantially suppressed in brain and liver as a result of Co²⁺ exposure, whereas in kidney catalase activity was unchanged and SOD activity increased. The activities of glutathione-related enzymes, glutathione peroxidase and glutathione-S-transferase, did not change as a result of cobalt exposure, but glutathione reductase activity increased by ∼40% and ∼70% in brain and kidney, respectively. Taken together, these data show that exposure of fish to Co²⁺ ions results in the development of oxidative stress and the activation of defense systems in different goldfish tissues.
钴是一种必需元素，但浓度过高时会有毒性。除了作为钴胺素（维生素 B₁₂）的组成部分的已知功能外，钴最近还被证明是缺氧的模拟物和活性氧物质产生的刺激物。本研究调查了金鱼（Carassius auratus）在水族箱水中暴露于 50、100 或 150 mg L⁻¹ Co²⁺ 96 h 时的反应（以 CoCl₂的形式给药）。在鱼类暴露期间，水族箱中的钴浓度没有变化。暴露于钴会导致大脑（暴露于 150 mg L⁻¹ Co²⁺后增加 111%）和肝脏（暴露于 50-150 mg L⁻¹ Co²⁺后增加 30-66%）中的脂质过氧化物水平升高，而蛋白质羰基的含量仅在肾脏中升高（在 150 mg L⁻¹钴暴露后增加 112%）。低分子质量硫醇在大脑中因钴处理而减少了 24-41%。超氧化物歧化酶（SOD）和过氧化氢酶等主要抗氧化酶的活性由于 Co²⁺暴露而在大脑和肝脏中受到实质性抑制，而在肾脏中过氧化氢酶活性保持不变，SOD 活性增加。谷胱甘肽相关酶，如谷胱甘肽过氧化物酶和谷胱甘肽-S-转移酶，的活性并未因钴暴露而改变，但谷胱甘肽还原酶的活性分别增加了约 40%和 70%。总的来说，这些数据表明，鱼类暴露于 Co²⁺离子会导致氧化应激的发展和不同金鱼组织中防御系统的激活。
