Nishikawa T, Takahashi J A, Fujibayashi Y, Fujisawa H, Zhu B, Nishimura Y, Ohnishi K, Higuchi K, Hashimoto N, Hosokawa M
Department of Neurosurgery, Faculty of Medicine, Kyoto University, Japan.
Neurosci Lett. 1998 Sep 25;254(2):69-72. doi: 10.1016/s0304-3940(98)00646-6.
In order to characterize the early stage of mitochondrial dysfunction, we investigated the redox state and oxidative phosphorylation of the brain mitochondria from 2-month-old Senescence-accelerated mouse (SAM)P8 and SAMR1 mice; SAMP8 mice exhibit various signs of age-associated neurodegeneration and rapid mitochondrial dysfunction, although SAMR1 mice do not. The redox state was estimated as the reduction rate of Cu-pyruvaldehyde-bis (N4-methylthiosemicarbazone) (Cu-PTSM), the reduction of which is closely related to the electron leakage from the mitochondrial electron transport system in the brain, using electron spin resonance spectrometry (ESRS). The oxidative phosphorylation was measured polarographically. The SAMP8 mouse brain mitochondria demonstrated higher redox state and a higher activity of mitochondrial respiration with lower respiration control ratio than the mitochondria of SAMR1 mouse brains. This indicates that an inefficient hyperactive state can exist in the mitochondrial electron transport system before the age-associated mitochondrial dysfunction develops.
为了表征线粒体功能障碍的早期阶段，我们研究了2月龄衰老加速小鼠（SAM）P8和SAMR1小鼠脑线粒体的氧化还原状态和氧化磷酸化；SAMP8小鼠表现出各种与年龄相关的神经退行性变迹象和快速的线粒体功能障碍，而SAMR1小鼠则没有。使用电子自旋共振光谱法（ESRS），将氧化还原状态估计为铜-丙酮醛-双（N4-甲基硫代半卡巴腙）（Cu-PTSM）的还原率，其还原与脑线粒体电子传递系统的电子泄漏密切相关。通过极谱法测量氧化磷酸化。与SAMR1小鼠脑线粒体相比，SAMP8小鼠脑线粒体表现出更高的氧化还原状态和更高的线粒体呼吸活性，呼吸控制率更低。这表明在与年龄相关的线粒体功能障碍发展之前，线粒体电子传递系统中可能存在低效的高活性状态。
