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镍对增强蛋白质缺乏大鼠肝毒性无效。

Ineffectiveness of nickel in augmenting the hepatotoxicity in protein deficient rats.

作者信息

Sidhu P, Garg M L, Morgenstern P, Vogt J, Butz T, Dhawan D K

机构信息

Institute of Physiology and Experimental Pathophysiology, Friedrich-Alexander University, Erlangen-91054, Germany.

出版信息

Nutr Hosp. 2005 Nov-Dec;20(6):378-85.

Abstract

This study was designed to determine the toxic effects of nickel sulfate on the biochemical and elemental profile of liver in protein deficient rats. Nickel sulfate in the dose of 800mg/l in drinking water was administrated to Sprauge Dawley (S.D) normal control as well as protein deficient rats for a total duration of eight weeks. The effects of nickel treatment and protein deficiency when given separately and in combination were studied on rat liver marker enzymes like Alkaline phosphatase (ALP),Glutamate oxaloacetate transaminase (GOT), Glutamate pyruvate transaminase (GPT) and also on the status of essential elements in rat liver. Protein deficient, Ni treated as well as combined protein deficient and nickel treated rats showed significant reductions in the body weight and hepatic protein contents as compared to normal control rats. Hepatic alkaline phosphatase activity and alanine aminotransferase showed a significant elevation in rats subjected to protein deficiency, nickel treatment and combined protein deficiency and nickel treatment. As regards to hepatic levels of aspartate aminotransferase a significant elevation was observed in protein deficient and nickel treated protein deficient animals. Nickel administration to normal and protein deficient rats has resulted in a significant increase in concentrations of nickel, phosphorus and sulfur in liver tissue. The concentration of zinc and copper in liver tissue decreased significantly in protein deficient, nickel treated and nickel treated protein deficient animals. Tissue iron concentrations were found to be decreased in protein deficient animals, but the concentrations of iron got elevated significantly in nickel treated and nickel treated protein deficient animals. It has been observed that selenium got decreased significantly in protein deficient, nickel treated and nickel treated protein deficient animals when compared to normal animals. The elevation of selenium in nickel treated protein deficient animals was also significantly higher when compared to protein deficient animals.

摘要

本研究旨在确定硫酸镍对蛋白质缺乏大鼠肝脏生化和元素特征的毒性作用。将饮用水中剂量为800mg/l的硫酸镍给予Sprauge Dawley(S.D)正常对照大鼠以及蛋白质缺乏大鼠,为期八周。分别研究了镍处理和蛋白质缺乏单独及联合作用对大鼠肝脏标志物酶如碱性磷酸酶(ALP)、谷氨酸草酰乙酸转氨酶(GOT)、谷氨酸丙酮酸转氨酶(GPT)的影响,以及对大鼠肝脏中必需元素状态的影响。与正常对照大鼠相比,蛋白质缺乏、镍处理以及蛋白质缺乏与镍联合处理的大鼠体重和肝脏蛋白质含量均显著降低。蛋白质缺乏、镍处理以及蛋白质缺乏与镍联合处理的大鼠肝脏碱性磷酸酶活性和丙氨酸转氨酶显著升高。至于肝脏天冬氨酸转氨酶水平,在蛋白质缺乏和镍处理的蛋白质缺乏动物中观察到显著升高。给正常和蛋白质缺乏大鼠施用镍导致肝脏组织中镍、磷和硫的浓度显著增加。在蛋白质缺乏、镍处理以及镍处理的蛋白质缺乏动物中,肝脏组织中锌和铜的浓度显著降低。在蛋白质缺乏动物中发现组织铁浓度降低,但在镍处理以及镍处理的蛋白质缺乏动物中,铁的浓度显著升高。据观察,与正常动物相比,蛋白质缺乏、镍处理以及镍处理的蛋白质缺乏动物中的硒显著降低。与蛋白质缺乏动物相比,镍处理的蛋白质缺乏动物中硒的升高也显著更高。

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