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自由基对胞质肌酸激酶活性的影响以及抗氧化酶和巯基化合物的保护作用。

Effects of free radicals on cytosolic creatine kinase activities and protection by antioxidant enzymes and sulfhydryl compounds.

作者信息

Genet S, Kale R K, Baquer N Z

机构信息

Hormone and Drug Research Laboratory, School of Life Sciences, Jawaharlal Nehru University, New Delhi, India.

出版信息

Mol Cell Biochem. 2000 Jul;210(1-2):23-8. doi: 10.1023/a:1007071617480.

Abstract

The main purpose of this study was to investigate the effect of free radicals and experimental diabetes on cytosolic creatine kinase activity in rat heart, muscle and brain. Hydrogen peroxide decreased creatine kinase activity in a dose dependent manner which was reversed by catalase. Xanthine/xanthine oxidase, which produces superoxide anion, lowered the creatine kinase activity in the same manner whose effect was protected by superoxide dismutase. N-acetylcysteine and dithiothreitol also significantly ameliorated the effect of Xanthine/xanthine oxidase and hydrogen peroxide. Experimental diabetes of twenty-one days (induced by alloxan), also caused a similar decrease in the activity of creatine kinase. This led us to the conclusion that the decrease in creatine kinase activity during diabetes could be due to the production of reactive oxygen species. The free radical effect could be on the sulfhydryl groups of the enzyme at the active sites, since addition of sulfhydryl groups like N-acetylcysteine and dithiothreitol showed a significant reversal effect.

摘要

本研究的主要目的是探讨自由基和实验性糖尿病对大鼠心脏、肌肉和脑组织中胞质肌酸激酶活性的影响。过氧化氢以剂量依赖性方式降低肌酸激酶活性,而过氧化氢酶可使其逆转。产生超氧阴离子的黄嘌呤/黄嘌呤氧化酶以相同方式降低肌酸激酶活性,其作用可被超氧化物歧化酶保护。N-乙酰半胱氨酸和二硫苏糖醇也显著改善了黄嘌呤/黄嘌呤氧化酶和过氧化氢的作用。21天的实验性糖尿病(由四氧嘧啶诱导)也导致肌酸激酶活性出现类似下降。这使我们得出结论,糖尿病期间肌酸激酶活性降低可能是由于活性氧的产生。自由基的作用可能是针对酶活性位点的巯基,因为添加如N-乙酰半胱氨酸和二硫苏糖醇等巯基显示出显著的逆转作用。

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