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铜介导的大鼠肝脏氧化应激

Copper-mediated oxidative stress in rat liver.

作者信息

Ozcelik Dervis, Ozaras Resat, Gurel Zafer, Uzun Hafize, Aydin Seval

机构信息

Department of Biophysics, Cerrahpasa Medical Faculty, University of Istanbul, Istanbul, Turkey.

出版信息

Biol Trace Elem Res. 2003 Winter;96(1-3):209-15. doi: 10.1385/BTER:96:1-3:209.

DOI:10.1385/BTER:96:1-3:209
PMID:14716100
Abstract

Copper is an essential trace element with various biological functions. Excess copper, however, is extremely toxic, leading to many pathological conditions that are consistent with oxidative damage to membranes and molecules. Exposure to high levels of copper results in various changes in the tissues. In liver, hypertrophy of hepatocytes, hepatitis, hepatocellular necrosis, and hepatocellular death are the results. Lipid peroxidation causes dysfunction in the cell membrane, decreased fluidity, inactivation of receptors and enzymes, and changes ion permeability. In this study, we aimed to determine the effect of copper on oxidative and antioxidative substances in plasma and liver tissue in a rat model. Sixteen male Sprague-Dawley rats were divided into two groups: Group 1 rats included control rats given tap water. Group 2 rats were given water containing copper in a dose of 100 microg/mL. All rats were sacrificed at 4 wk under ether anesthesia. Plasma and liver superoxide dismutase (SOD) activities, plasma and liver MDA (malondialdehyde) levels, and liver glutathione (GSH) levels were studied. Plasma and liver SOD activities were found to be higher in group 2 than those in group 1. Although plasma MDA levels were higher in group 2, MDA levels in liver tissues were comparable. Liver tissue glutathione levels were lower in group 2. It was concluded that although copper is needed in trace amounts, an excess amount is toxic for the organism. It increases lipid peroxidation and depletes GSH reserves, which makes the organism more vulnerable to other oxidative challenges.

摘要

铜是一种具有多种生物学功能的必需微量元素。然而,过量的铜具有极强的毒性,会导致许多与膜和分子氧化损伤一致的病理状况。接触高浓度的铜会导致组织发生各种变化。在肝脏中,会出现肝细胞肥大、肝炎、肝细胞坏死和肝细胞死亡。脂质过氧化会导致细胞膜功能障碍、流动性降低、受体和酶失活以及离子通透性改变。在本研究中,我们旨在确定铜对大鼠模型血浆和肝组织中氧化和抗氧化物质的影响。16只雄性Sprague-Dawley大鼠被分为两组:第1组大鼠为饮用自来水的对照大鼠。第2组大鼠饮用含100微克/毫升铜的水。所有大鼠在乙醚麻醉下于4周时处死。研究了血浆和肝脏超氧化物歧化酶(SOD)活性、血浆和肝脏丙二醛(MDA)水平以及肝脏谷胱甘肽(GSH)水平。发现第2组的血浆和肝脏SOD活性高于第1组。虽然第2组的血浆MDA水平较高,但肝脏组织中的MDA水平相当。第2组肝脏组织的谷胱甘肽水平较低。得出的结论是,虽然铜是微量必需的,但过量的铜对生物体有毒。它会增加脂质过氧化并消耗GSH储备,这使得生物体更容易受到其他氧化应激的影响。

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