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缺血缺氧和巴比妥类麻醉对线粒体磷脂自由基氧化的影响。

Effect of ischemic anoxia and barbiturate anesthesia on free radical oxidation of mitochondrial phospholipids.

作者信息

Majewska M D, Strosznajder J, Lazarewicz J

出版信息

Brain Res. 1978 Dec 15;158(2):423-34. doi: 10.1016/0006-8993(78)90685-6.

Abstract

The mitochondrial fraction obtained from brains of animals submitted to ischemia shows a decrease of phospholipid level, especially plasmalogens in the fraction of ethanolamine phospholipids and choline phospholipids. There appears simultaneously an increase of free radical oxidation processes of unsaturated fatty acids from these phospholipids. The peroxidation processes of mitochondrial lipids are stimulated by calcium ions and, to a smaller extent, by magnesium ions. Barbiturate anesthesia inhibits the peroxidation of fatty acids and increases the antioxidant abilities of the nervous tissue. Nembutal added in vitro remains without effect on the above processes. The effect of acetylcholine and the antioxidant ability of nervous tissue under barbiturate anesthesia with respect to ischemia are discussed.

摘要

从经历缺血的动物大脑中获得的线粒体部分显示磷脂水平降低,尤其是乙醇胺磷脂和胆碱磷脂部分中的缩醛磷脂。同时,这些磷脂中不饱和脂肪酸的自由基氧化过程增加。线粒体脂质的过氧化过程受到钙离子的刺激,在较小程度上也受到镁离子的刺激。巴比妥类麻醉抑制脂肪酸的过氧化,并增强神经组织的抗氧化能力。体外添加戊巴比妥对上述过程没有影响。讨论了乙酰胆碱的作用以及巴比妥类麻醉下神经组织对缺血的抗氧化能力。

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