Morin Christophe, Zini Roland, Tillement Jean-Paul
Département de Pharmacologie, Faculté de Médecine de Paris XII, 8 rue du Général Sarrail, F-94010, Créteil, France.
Biochem Biophys Res Commun. 2003 Aug 1;307(3):477-82. doi: 10.1016/s0006-291x(03)01203-8.
Rat brain mitochondria were successively submitted to anoxia and reoxygenation. The main mitochondrial functions were assessed at different reoxygenation times. Although the respiratory control ratio decreased, the activity for each one of the enzymes participating in the respiratory chain was not affected. However, during reoxygenation, mitochondrial membrane lipoperoxidation quickly increased and was proportional to the decrease seen in membrane fluidity. Under the same conditions, cytochrome c and cardiolipin were released from mitochondria and their rate of release increased with reoxygenation time. The release of cytochrome c and cardiolipin was followed by the collapse of the membrane potential and it was not inhibited by cyclosporin A. Addition of the antioxidant alpha-tocopherol abolished all these reoxygenation-induced changes. These data indicate that, in this model, reoxygenation promotes the uncoupling of respiratory chain, and cytochrome c and cardiolipin releases. These events are not related to the membrane potential collapse but to an oxidative stress.
将大鼠脑线粒体依次进行缺氧和复氧处理。在不同的复氧时间评估主要的线粒体功能。尽管呼吸控制率下降，但参与呼吸链的每种酶的活性并未受到影响。然而，在复氧过程中，线粒体膜脂质过氧化迅速增加，且与膜流动性的降低成正比。在相同条件下，细胞色素c和心磷脂从线粒体中释放出来，其释放速率随复氧时间的增加而增加。细胞色素c和心磷脂的释放之后是膜电位的崩溃，并且不受环孢素A的抑制。添加抗氧化剂α-生育酚消除了所有这些复氧诱导的变化。这些数据表明，在该模型中，复氧促进呼吸链解偶联以及细胞色素c和心磷脂的释放。这些事件与膜电位崩溃无关，而是与氧化应激有关。
