Laboratory of Bioenergetics, Department of Life Sciences, University of Liège, Sart Tilman, Belgium.
Toxicol Mech Methods. 2004;14(1-2):97-101. doi: 10.1080/15376520490257455.
The aim of this study was to investigate the effects of in vivo and in vitro anoxia and reoxygenation on the oxidative phosphorylation of brain mitochondria and to study the protective effects of Ginkgo biloba extract (EGb 761). Cerebral ischemia and reperfusion induced slight decreases in respiration rates and in the efficiency of oxidative phosphorylation. Total protection of mitochondrial function was observed after chronic pretreatment of rat with EGb 761. On the contrary, in vitro anoxia and reoxygenation of isolated brain mitochondria during respiratory assay promoted important alteration in respiration rates (around -50%) and in the oxidative phosphorylation yield (-44%). Partial protection was observed after anoxia and reoxygenation in the presence of EGb 761. Such a difference between in vivo and in vitro results could be explained by an intracellular antioxidant pool that could protect mitochondria in vivo.
本研究旨在探讨体内和体外缺氧及复氧对脑线粒体氧化磷酸化的影响，并研究银杏叶提取物（EGb761）的保护作用。脑缺血再灌注引起呼吸速率和氧化磷酸化效率轻微下降。用 EGb761 对大鼠进行慢性预处理后，观察到线粒体功能的完全保护。相反，在呼吸测定中，分离的脑线粒体的体外缺氧和复氧导致呼吸速率（约-50%）和氧化磷酸化产率（-44%）发生重要变化。在 EGb761 存在的情况下，缺氧和复氧后观察到部分保护。这种体内和体外结果之间的差异可以用一种可以在体内保护线粒体的细胞内抗氧化剂池来解释。
