Chair and Department of Human Anatomy, Medical University of Lublin, 20-090, Lublin, Poland.
Department of Biochemistry and Toxicology, Faculty of Animal Sciences and Bioeconomy, University of Life Sciences in Lublin, 20-950, Lublin, Poland.
J Trace Elem Med Biol. 2021 Sep;67:126777. doi: 10.1016/j.jtemb.2021.126777. Epub 2021 May 8.
Copper has an important role in nervous system function, as a cofactor of many enzymes and in the synthesis of neurotransmitters. Both the dose and the chemical form of copper can determine the impact of this element on metabolism, the neurological system and the immune system.
The aim of the study was to determine whether and in what form the addition of copper changes the level of amyloid beta and acetylcholinesterase level in selected rat tissues.
Thirty, healthy, male, albino Wistar rats aged 7 weeks were randomly divided into 3 groups. Three experimental treatments were used to evaluate the effects of different levels and sources of Cu (6.5 mg kg of diet) in the diet: Cu - rats fed a diet without Cu supplementation; Cu - rats fed a diet with CuCO (6.5 mg kg of diet) during two months of feeding; Cu - rats fed a diet with Cu nanoparticles (6.5 mg kg of diet) during two months of feeding. In blood serum and tissue homogenates there rated the indicators proving the potential neurodegenerative effect and epigenetic DNA damage induced by chemical form of copper or lack of additional copper supplementation in diet were determined. There were analysed: level of acetylcholinesterase, β-amyloid, low-density lipoprotein receptor-related protein 1, apyrimidinic endonuclease, thymidine glycosidase, alkylpurine-DNA-N-glycosylase and glycosylated acetylcholinesterase.
Irrespective of the form of copper added, it was found to increase acetylcholinesterase level in the brain, spleen and liver, as well as in the blood plasma of the rats. Copper in the form of CuCO was found to increase acetylcholinesterase level in the kidneys. The addition of both forms of copper caused a marked increase in the plasma concentration of β-amyloid in comparison with the diet with no added Cu. The addition of both forms of copper caused a marked increase in the plasma concentration of β-amyloid in comparison with the diet with no added Cu.
A lack of added Cu in the diet of rats reduces the concentration of amyloid-β in the blood, whereas administration of copper, in the form of either CuNPs or CuCO, increases the level of this peptide in the blood. The use of copper in the form of CuNPs in the diet of rats does not increase the level of β-amyloid more than the use of the carbonate form of this element. The use of CuNPs or CuCO in the diet of rats increases acetylcholinesterase level in the brain, spleen, liver, and blood. CuNPs in the diet of rats were not found to increase acetylcholinesterase level to a greater extent than Cu carbonate.
铜在神经系统功能中起着重要作用,它是许多酶的辅助因子,也是神经递质合成的辅助因子。铜的剂量和化学形式都可以决定这种元素对新陈代谢、神经系统和免疫系统的影响。
本研究旨在确定添加铜的形式和剂量是否会改变选定大鼠组织中淀粉样β和乙酰胆碱酯酶的水平。
30 只 7 周龄健康雄性白化 Wistar 大鼠随机分为 3 组。使用 3 种不同的实验处理方法来评估饮食中不同水平和来源的 Cu(饮食中 6.5mg/kg)对大鼠的影响:Cu-大鼠不补充铜的饮食;Cu-大鼠在两个月的喂养期间用 CuCO(饮食中 6.5mg/kg)喂养;Cu-大鼠在两个月的喂养期间用 Cu 纳米粒子(饮食中 6.5mg/kg)喂养。在血清和组织匀浆中,评估了证明化学形式的铜或缺乏额外的铜补充在饮食中具有潜在神经退行性作用和表观遗传 DNA 损伤的指标。分析了乙酰胆碱酯酶、β-淀粉样蛋白、低密度脂蛋白受体相关蛋白 1、嘧啶糖苷内切酶、胸苷糖苷酶、烷基嘌呤-DNA-N-糖基化酶和糖基化乙酰胆碱酯酶的水平。
无论添加的铜的形式如何,都发现它能增加大脑、脾脏和肝脏以及大鼠血浆中的乙酰胆碱酯酶水平。CuCO 的形式被发现能增加肾脏中的乙酰胆碱酯酶水平。与未添加 Cu 的饮食相比,两种形式的铜都能显著增加血浆中β-淀粉样蛋白的浓度。
大鼠饮食中缺乏添加的 Cu 会降低血液中β-淀粉样蛋白的浓度,而以 CuNPs 或 CuCO 的形式添加铜会增加血液中这种肽的水平。在大鼠饮食中使用 CuNPs 形式的铜不会比使用该元素的碳酸盐形式增加β-淀粉样蛋白的水平。在大鼠饮食中使用 CuNPs 或 CuCO 会增加大脑、脾脏、肝脏和血液中的乙酰胆碱酯酶水平。在大鼠饮食中没有发现 CuNPs 比 Cu 碳酸盐更能增加乙酰胆碱酯酶的水平。