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锌对蛋白质缺乏大鼠肝脏氧化应激酶的保护作用。

Protective effects of zinc on oxidative stress enzymes in liver of protein-deficient rats.

作者信息

Sidhu Pardeep, Garg M L, Dhawan D K

机构信息

Institute of Physiology and Experimental Pathophysiology, Friedrich-Alexander University, Erlangen, Germany.

出版信息

Drug Chem Toxicol. 2005;28(2):211-30. doi: 10.1081/dct-52551.

Abstract

Persons afflicted with protein malnutrition are generally deficient in a variety of essential micronutrients like zinc, copper, iron, and selenium, which in turn affects number of metabolic processes in the body. To evaluate the protective effects of zinc on the enzymes involved in oxidative stress induced in liver of protein-deficient rats, the current study was designed. Zinc sulfate at a dose level of 227 mg/L zinc in drinking water was administered to female Sprague-Dawley normal control as well as protein-deficient rats for a total duration of 8 weeks. The effects of zinc treatment in conditions of protein deficiency were studied on rat liver antioxidant enzymes, which included catalase, glutathione peroxidase (GPx), glutathione reductase (GR), superoxide dismutase (SOD), glutathione reduced (GSH), and glutathione-S-transferase (GST). Protein deficiency in normal rats resulted in a significant increase in hepatic activities of catalase, glutathione peroxidase, glutathione reductase, and glutathione-S-transferase and the levels of lipid peroxidation. A significant inhibition in the levels of reduced glutathione and the enzyme activity of superoxide dismutase has been observed after protein deficiency in normal rats. Interestingly, Zn treatment to protein-deficient animals lowered already raised activity catalase, glutathione peroxidase, and glutathione-S-transferase and levels of lipid peroxidation to significant levels when compared to protein-deficient animals. Also, Zn treatment to the protein-deficient animals resulted in a significant elevation in the levels of GSH and SOD activity as compared to their respective controls, thereby indicating its effectiveness in regulating their levels in adverse conditions. It has also been observed that concentrations of zinc, copper, iron, and selenium were found to be decreased significantly in protein-deficient animals. However, the levels of these elements came back to within normal limits when zinc was administrated to protein-deficient rats. This study concludes that zinc has the potential to regulate the activities of oxidative stress enzymes as well as essential hepatic elements.

摘要

患有蛋白质营养不良的人通常缺乏多种必需的微量营养素,如锌、铜、铁和硒,这反过来又会影响体内的许多代谢过程。为了评估锌对蛋白质缺乏大鼠肝脏中诱导的氧化应激相关酶的保护作用,设计了本研究。将饮用水中锌剂量水平为227mg/L的硫酸锌给予雌性斯普拉格-道利正常对照大鼠以及蛋白质缺乏大鼠,持续8周。研究了蛋白质缺乏条件下锌处理对大鼠肝脏抗氧化酶的影响,这些酶包括过氧化氢酶、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)。正常大鼠的蛋白质缺乏导致过氧化氢酶、谷胱甘肽过氧化物酶、谷胱甘肽还原酶和谷胱甘肽-S-转移酶的肝脏活性以及脂质过氧化水平显著增加。正常大鼠蛋白质缺乏后,观察到还原型谷胱甘肽水平和超氧化物歧化酶的酶活性受到显著抑制。有趣的是,与蛋白质缺乏动物相比,对蛋白质缺乏动物进行锌处理可使已经升高的过氧化氢酶、谷胱甘肽过氧化物酶和谷胱甘肽-S-转移酶活性以及脂质过氧化水平显著降低。此外,与各自的对照组相比,对蛋白质缺乏动物进行锌处理导致GSH水平和SOD活性显著升高,从而表明其在不利条件下调节其水平的有效性。还观察到,蛋白质缺乏动物体内锌、铜、铁和硒的浓度显著降低。然而,当给蛋白质缺乏大鼠施用锌时,这些元素的水平恢复到正常范围内。本研究得出结论,锌具有调节氧化应激酶活性以及肝脏必需元素的潜力。

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