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缺血再灌注损伤时大鼠肾脏中抗氧化酶的表达

Expression of antioxidant enzymes in rat kidney during ischemia-reperfusion injury.

作者信息

Singh I, Gulati S, Orak J K, Singh A K

机构信息

Department of Pediatrics, Medical University of South Carolina, Charleston 29425.

出版信息

Mol Cell Biochem. 1993 Aug 25;125(2):97-104. doi: 10.1007/BF00936438.

Abstract

The effect of ischemia-reperfusion on activity, protein and m-RNA levels of catalase, copper-zinc and manganese containing superoxide dismutases and glutathione peroxidase, the enzymes that are involved in free radical detoxification was studied in rat kidney. Ischemia alone did not alter either the activities or protein levels of superoxide dismutase and glutathione peroxidase. However, catalase activity was found to be inhibited to 82% of control. The inhibition of catalase was due to the inactivation of the enzyme as there was no significant change in enzyme protein level. Reperfusion following ischemia, however, led to a significant decrease in both the activities as well as the protein levels of all the antioxidant enzymes. The observed overall decrease in total superoxide dismutase activity was the net effect of a decrease in copper-zinc superoxide dismutase while manganese superoxide dismutase activity was found to be increased following reperfusion. This observed increase manganese superoxide dismutase activity was the result of its increased protein level. The mRNA levels for catalase, superoxide dismutases, and glutathione peroxidase were observed to be increased (100-145% of controls) following ischemia; reperfusion of ischemic kidneys, however, resulted in a significant decrease in the levels of mRNAs coding for all the enzymes except manganese superoxide dismutase which remained high. These results suggest that in tissue, the down regulation of the antioxidant enzyme system could be responsible for the pathophysiology of ischemia-reperfusion injury.

摘要

在大鼠肾脏中研究了缺血再灌注对过氧化氢酶、含铜锌和锰的超氧化物歧化酶以及谷胱甘肽过氧化物酶(这些参与自由基解毒的酶)的活性、蛋白质和mRNA水平的影响。单独缺血并未改变超氧化物歧化酶和谷胱甘肽过氧化物酶的活性或蛋白质水平。然而,发现过氧化氢酶活性被抑制至对照的82%。过氧化氢酶的抑制是由于酶的失活,因为酶蛋白水平没有显著变化。然而,缺血后的再灌注导致所有抗氧化酶的活性以及蛋白质水平均显著下降。观察到的总超氧化物歧化酶活性的总体下降是铜锌超氧化物歧化酶活性下降的净效应,而锰超氧化物歧化酶活性在再灌注后被发现增加。观察到的锰超氧化物歧化酶活性增加是其蛋白质水平增加的结果。缺血后,过氧化氢酶、超氧化物歧化酶和谷胱甘肽过氧化物酶的mRNA水平被观察到增加(为对照的100 - 145%);然而,缺血肾脏的再灌注导致除锰超氧化物歧化酶(其仍保持高水平)外所有酶的编码mRNA水平显著下降。这些结果表明,在组织中,抗氧化酶系统的下调可能是缺血再灌注损伤病理生理学的原因。

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