De Leo M E, Borrello S, Passantino M, Palazzotti B, Mordente A, Daniele A, Filippini V, Galeotti T, Masullo C
Institute of General Pathology, Catholic University, School of Medicine, Rome, Italy.
Neurosci Lett. 1998 Jul 10;250(3):173-6. doi: 10.1016/s0304-3940(98)00469-8.
Substantial evidence supports the hypothesis that oxygen free radicals are involved in various neurodegenerative disorders. To assess the presence of oxidative stress in Alzheimer's disease (AD) we examined the activity of the enzyme copper-zinc superoxide dismutase (CuZnSOD) in red blood cells, the levels of the mitochondrial inducible enzyme manganese superoxide dismutase (MnSOD) mRNA in lymphocytes, and the total radical-trapping antioxidant capacity (TRAP) in plasma of AD patients and in a group of age-matched non-demented controls. We found that CuZnSOD activity (P < 0.01 vs. controls) was significantly increased as well as the MnSOD mRNA levels while the total antioxidant status (P < 0.001 vs. controls) was decreased in AD patients. These findings support the role of oxidative alterations in the pathogenetic mechanism underlying AD neurodegeneration.
大量证据支持氧自由基参与各种神经退行性疾病的假说。为评估阿尔茨海默病（AD）中氧化应激的存在情况，我们检测了AD患者及一组年龄匹配的非痴呆对照者红细胞中铜锌超氧化物歧化酶（CuZnSOD）的活性、淋巴细胞中线粒体诱导酶锰超氧化物歧化酶（MnSOD）mRNA的水平以及血浆中的总自由基捕获抗氧化能力（TRAP）。我们发现，AD患者的CuZnSOD活性（与对照组相比，P < 0.01）显著升高，MnSOD mRNA水平也升高，而总抗氧化状态（与对照组相比，P < 0.001）降低。这些发现支持了氧化改变在AD神经退行性变潜在发病机制中的作用。
