FREE-RADICALS IN CEREBRAL ISCHEMIA
FREE-RADICALS IN CEREBRAL ISCHEMIA
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DOI：
10.1161/01.str.9.5.445
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发表时间：
1978-01-01
期刊：
影响因子：
8.3
通讯作者：
RANSOHOFF, J
中科院分区：
文献类型：
--
作者：
FLAMM, ES;DEMOPOULOS, HB;RANSOHOFF, J
在猫中，研究了脑缺血可能在中枢神经系统膜成分内引发一系列病理性自由基反应的可能性。正常存在的电子传递自由基需要足够的分子氧才能有序地传递电子和质子。组织氧气的减少解除了对电子传递自由基的控制，并允许它们在细胞膜(如线粒体)之间启动病理性的自由基反应。病理性的自由基反应导致多种产物，每种产物的浓度可能太小，不能在早期检测到它们。通过病理性自由基反应消耗的一种主要抗氧化剂的减少，可以跟踪时间进程。测定大鼠大脑中动脉闭塞后缺血区和对照组脑组织中抗坏血酸含量。可检测到的抗坏血酸含量逐渐减少，从1小时的25%下降到24小时的65%。这种正常存在的抗氧化剂和自由基清除剂的减少可能表明消耗了抗坏血酸，以试图抑制发生在细胞膜成分中的病理性自由基反应。
The possibility that cerebral ischemia may initiate a series of pathological free radical reactions within the membrane components of the CNS was investigated in the cat. The normally occurring electron transport radicals require adequate molecular O2 for orderly transport of electrons and protons. A decrease in tissue O2 removes the controls over the electron transport radicals, and allows them to initiate pathologic radical reactions among cell membranes such as mitochondria. Pathologic radical reactions result in multiple products, each of which may be present in too small a concentration to permit their detection at early time periods. It is possible to follow the time course, by the decrease of a major antioxidant as it is consumed by the pathologic radical reactions. Ascorbic acid was measured in ischemic and control brain following middle cerebral artery occlusion. There was a progressive decrease in the amount of detectable ascorbic acid ranging from 25% at 1 h to 65% at 24 h after occlusion. The reduction of this normally occurring antioxidant and free radical scavenger may indicate consumption of ascorbic acid in an attempt to quench pathological free radical reactions occurring within cytomembrane components.