Villalobos M A, De La Cruz J P, Carrasco T, Smith-Agreda J M, Sánchez de la Cuesta F
Department of Anatomy, School of Medicine, University of Málaga, Spain.
Brain Res Bull. 1994;33(3):313-8. doi: 10.1016/0361-9230(94)90199-6.
The antioxidant effect of alpha-tocopherol was assessed in a model of ischemia-reperfusion in the rat brain. In this model, permanent ischemia of the cortical branches of the middle cerebral artery was combined with bilateral occlusion of the common carotid arteries for 1 h and restoration of circulation for a period of 2 h. Lipid peroxidation and mitochondrial reduction of tetraphenyl tetrazolium (TPT) were determined in both untreated and d-alpha-tocopherol treated rats. Ferrous sulfate and ascorbic acid (FeAs) were used to induce lipid peroxidation via the formation of hydroxyl anions. Malondialdehyde (MDA) increased in the ischemia-reperfusion areas (+101%), but FeAs-induced MDA did not vary in the area of permanent ischemia. Brain tissue undergoing ischemia-reperfusion was about 50% less sensitive to the antioxidant effect of ascorbic acid. The reduction of TPT showed 52% mitochondrial damage in the area of ischemia-reperfusion, whereas mitochondrial activity in the area of permanent ischemia was 177 times lower as compared to controls. d-alpha-tocopherol caused a 40% inhibition of MDA production and 16.5% and 21.5% decrease in mitochondrial activity in the areas of ischemia-reperfusion and permanent ischemia, respectively.
在大鼠脑缺血再灌注模型中评估了α-生育酚的抗氧化作用。在该模型中，大脑中动脉皮质支的永久性缺血与双侧颈总动脉闭塞1小时并恢复循环2小时相结合。在未处理和d-α-生育酚处理的大鼠中均测定了脂质过氧化和四苯基四氮唑（TPT）的线粒体还原。硫酸亚铁和抗坏血酸（FeAs）用于通过羟基阴离子的形成诱导脂质过氧化。缺血再灌注区域丙二醛（MDA）增加（+101%），但FeAs诱导的MDA在永久性缺血区域没有变化。经历缺血再灌注的脑组织对抗坏血酸抗氧化作用的敏感性降低约50%。TPT的还原显示缺血再灌注区域线粒体损伤52%，而永久性缺血区域的线粒体活性与对照组相比降低了177倍。d-α-生育酚分别使缺血再灌注区域和永久性缺血区域的MDA产生抑制40%，线粒体活性降低16.5%和21.5%。
