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实验性诱导心肌梗死中的脂质过氧化与清除机制

Lipid peroxidation and scavenger mechanism in experimentally induced heart infarcts.

作者信息

Röth E, Török B, Zsoldos T, Matkovics B

出版信息

Basic Res Cardiol. 1985 Sep-Oct;80(5):530-6. doi: 10.1007/BF01907916.

Abstract

Dog experiments were performed to describe the time course of lipid peroxidation after various ischemic influences of the heart measured by formation of malondialdehyde (MDA), and the scavenger action determined by reduced glutathione (GSH) content and superoxide dismutase (SOD) activity. Experimental groups consisted of control dogs having intact hearts and dogs with acute ramus descendens anterior ligature (LAD) having ischemic areas through 15, 30, 45 minutes and 1, 2, 3, 24 hours. Heart tissue for biochemical assays was excised from both the ischemic areas and from nonischemic left ventricle. The acute ischemia caused characteristic alterations in the biochemical parameters: MDA level gradually increased with its peak value being found at the end of 3 hours ligature. GSH levels decreased moderately, whereas SOD levels reduced sharply. As increased MDA formation indicates breakdown of the polyunsaturated fatty acids (PUFA) in the membranes and decreased GSH and SOD levels indicate impairment of the natural scavengering, the observed changes clearly outline the extent of disintegration of membrane structure and function.

摘要

进行犬类实验,以描述通过丙二醛(MDA)形成来测量心脏在各种缺血影响后脂质过氧化的时间进程,以及通过还原型谷胱甘肽(GSH)含量和超氧化物歧化酶(SOD)活性确定的清除作用。实验组包括心脏完好的对照犬以及急性结扎前降支(LAD)的犬,后者在15、30、45分钟以及1、2、3、24小时后出现缺血区域。用于生化分析的心脏组织取自缺血区域和非缺血的左心室。急性缺血导致生化参数出现特征性变化:MDA水平逐渐升高,在结扎3小时结束时达到峰值。GSH水平适度下降,而SOD水平急剧下降。由于MDA形成增加表明膜中多不饱和脂肪酸(PUFA)分解,GSH和SOD水平下降表明天然清除功能受损,观察到的变化清楚地勾勒出膜结构和功能的解体程度。

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