Pharmacobiochemical Laboratory, Comenius University School of Medicine, Bratislava, Slovakia.
J Cell Mol Med. 2010 Nov;14(11):2667-74. doi: 10.1111/j.1582-4934.2009.00879.x.
Brain energy disorders can be present in aged men and animals. To this respect, the mitochondrial and free radical theory of aging postulates that age-associated brain energy disorders are caused by an imbalance between pro- and anti-oxidants that can result in oxidative stress. Our study was designed to investigate brain energy metabolism and the activity of endogenous antioxidants during their lifespan in male Wistar rats. In vivo brain bioenergetics were measured using ³¹P nuclear magnetic resonance (NMR) spectroscopy and in vitro by polarographic analysis of mitochondrial oxidative phosphorylation. When compared to the young controls, a significant decrease of age-dependent mitochondrial respiration and adenosine-3-phosphate (ATP) production measured in vitro correlated with significant reduction of forward creatine kinase reaction (kfor) and with an increase in phosphocreatine (PCr)/ATP, PCr/Pi and PME/ATP ratio measured in vivo. The levels of enzymatic antioxidants catalase, GPx and GST significantly decreased in the brain tissue as well as in the peripheral blood of aged rats. We suppose that mitochondrial dysfunction and oxidative inactivation of endogenous enzymes may participate in age-related disorders of brain energy metabolism.
脑能量代谢障碍可发生于老年人群和动物。从这个角度来看,衰老的线粒体和自由基理论认为,与年龄相关的脑能量代谢障碍是由抗氧化剂和自由基之间的失衡引起的,这种失衡可能导致氧化应激。我们的研究旨在研究雄性 Wistar 大鼠在其整个生命周期中的脑能量代谢和内源性抗氧化剂的活性。体内脑生物能量学使用 ³¹P 磁共振波谱(NMR)进行测量,体外通过测量线粒体氧化磷酸化的极谱分析进行测量。与年轻对照组相比,体外测量的与年龄相关的线粒体呼吸和三磷酸腺苷(ATP)生成的显著下降与体内正向肌酸激酶反应(kfor)的显著降低以及磷酸肌酸(PCr)/ATP、PCr/Pi 和 PME/ATP 比值的增加相关。在老年大鼠的脑组织和外周血液中,酶抗氧化剂过氧化氢酶、谷胱甘肽过氧化物酶和谷胱甘肽转移酶的水平显著降低。我们推测,线粒体功能障碍和内源性酶的氧化失活可能参与了与年龄相关的脑能量代谢障碍。