Chan P H, Chu L, Fishman R A
Department of Neurology, School of Medicine, University of California, San Francisco 94143.
Brain Res. 1988 Jan 26;439(1-2):388-90. doi: 10.1016/0006-8993(88)91500-4.
Effects of complete ischemia on levels of antioxidative enzymes including copper-zinc (CuZn) superoxide dismutase (SOD), manganese (Mn)-SOD, and glutathione peroxidase (GSH-Px) were studied in rat brain regions at 30 and 60 min following decapitation. CuZn-SOD activities were significantly decreased in cerebral cortex and hippocampus at both time points whereas the enzyme activities were decreased at 60 min in cerebellum and caudate areas. The reduction of Mn-SOD activities followed the same pattern of CuZn-SOD in various brain regions. However, GSH-Px activities in these brain regions were not affected by decapitation ischemia. These data suggest that the reduction of CuZn-SOD and Mn-SOD activities during ischemia, in conjunction with the significant decrease in the contents of alpha-tocopherol and other endogenous antioxidants, may compromise the brain's ability to defend against the toxic effects of superoxide radicals formed by ischemia and by subsequent reoxygenation.
在断头后30分钟和60分钟，研究了完全缺血对大鼠脑区抗氧化酶水平的影响，这些抗氧化酶包括铜锌（CuZn）超氧化物歧化酶（SOD）、锰（Mn）-SOD和谷胱甘肽过氧化物酶（GSH-Px）。在两个时间点，大脑皮层和海马体中的CuZn-SOD活性均显著降低，而小脑和尾状核区域的酶活性在60分钟时降低。在各个脑区，Mn-SOD活性的降低与CuZn-SOD的模式相同。然而，这些脑区的GSH-Px活性不受断头缺血的影响。这些数据表明，缺血期间CuZn-SOD和Mn-SOD活性的降低，连同α-生育酚和其他内源性抗氧化剂含量的显著下降，可能会损害大脑抵御缺血及随后再给氧形成的超氧自由基毒性作用的能力。
