Cardoso Sandra Morais, Proença M Teresa, Santos Sancha, Santana Isabel, Oliveira Catarina R
Faculty of Medicine, Center for Neuroscience of Coimbra, University of Coimbra, 3004 517, Portugal.
Neurobiol Aging. 2004 Jan;25(1):105-10. doi: 10.1016/s0197-4580(03)00033-2.
Cytochrome c oxidase (COX) activity reportedly is reduced in Alzheimer's disease (AD) brain and platelets. The reasons for the defect in either tissue are unknown, but its presence in a non-degenerating tissue suggests it is not simply a consequence of neurodegeneration. We now offer confirmation of the AD platelet COX defect. Compared to age-matched controls, in mitochondria isolated from AD platelets there was a 15% decrease in COX activity despite the fact that COX subunits were present at normal levels. Platelet ATP levels were diminished in AD (from 11.33 +/- 0.52 to 9.11 +/- 0.72 nmol/mg), while reactive oxygen species (ROS) were increased (from 97.03 +/- 25.9 to 338.3 +/- 100 K/mg). Platelet membrane fluidity, Vitamin E, and cholesterol content were similar between groups. We conclude that COX catalytic activity is indeed diminished in AD platelet mitochondria, does not result from altered membrane fluidity, and is associated with ROS overproduction and ATP under-production.
据报道,细胞色素c氧化酶(COX)活性在阿尔茨海默病(AD)患者的大脑和血小板中降低。两种组织中这种缺陷的原因尚不清楚,但它在非退化组织中的存在表明这不仅仅是神经退行性变的结果。我们现在证实了AD患者血小板COX缺陷。与年龄匹配的对照组相比,从AD患者血小板中分离出的线粒体中,COX活性降低了15%,尽管COX亚基的水平正常。AD患者血小板中的ATP水平降低(从11.33±0.52降至9.11±0.72 nmol/mg),而活性氧(ROS)增加(从97.03±25.9升至338.3±100 K/mg)。两组之间血小板膜流动性、维生素E和胆固醇含量相似。我们得出结论,AD患者血小板线粒体中的COX催化活性确实降低,不是由膜流动性改变引起的,并且与ROS过量产生和ATP产生不足有关。