Institute of Physiology and Experimental Pathophysiology, Friedrich-Alexander University, Erlangen, 91054, Germany.
Toxicol Mech Methods. 2005;15(6):411-7. doi: 10.1080/15376520500195715.
This study was designed to determine the oxidative stress induced by nickel sulfate in the liver in the protein-deficient rats. Nickel sulfate in the dose of 800 mg/L in drinking water was administrated to Sprauge Dawley (SD) rats as well as protein-deficient rats for a total duration of 8 weeks. The effects of nickel treatment and protein deficiency separately and in combination were studied on rat liver antioxidant defense system enzymes like catalase, glutathione peroxidase (GPX), glutathione reductase (GR), superoxide dismutase (SOD), reduced glutathione (GSH), and glutathione-S-transferase (GST), as well as on lipid peroxidation (LPO). The investigations revealed a significant increase in the activity of enzymes, which include catalase, Gpx, GR and GST, and in the levels with LPO following nickel treatment in combination with protein deficiency. On the contrary, feeding to control rats resulted in a significant depression in the levels of SOD and GSH. However, nickel treatment to normal rats caused a significant increase in the activity of enzymes catalase and GST and in the levels of LPO, whereas the levels of GSH get significantly depressed. Further, nickel treatment to protein-deficient rats did not cause any additional alteration in the status of liver antioxidants as were observed in conditions of protein deficiency.
本研究旨在确定硫酸镍在蛋白质缺乏大鼠肝脏中诱导的氧化应激。在饮用水中添加 800mg/L 的硫酸镍,分别对 Sprauge Dawley(SD)大鼠和蛋白质缺乏大鼠进行为期 8 周的处理。研究了镍处理和蛋白质缺乏单独和联合作用对大鼠肝脏抗氧化防御系统酶(如过氧化氢酶、谷胱甘肽过氧化物酶(GPX)、谷胱甘肽还原酶(GR)、超氧化物歧化酶(SOD)、还原型谷胱甘肽(GSH)和谷胱甘肽-S-转移酶(GST))以及脂质过氧化(LPO)的影响。研究发现,在镍处理与蛋白质缺乏联合作用下,酶(包括过氧化氢酶、Gpx、GR 和 GST)的活性以及 LPO 水平显著增加。相反,给予对照大鼠饲料导致 SOD 和 GSH 水平显著降低。然而,镍处理正常大鼠导致过氧化氢酶和 GST 的酶活性以及 LPO 水平显著增加,而 GSH 水平显著降低。此外,在蛋白质缺乏的情况下,镍处理蛋白质缺乏大鼠并没有导致肝脏抗氧化剂状态发生任何额外的改变。