细胞色素c对大鼠脑体外脂质过氧化物形成的影响。
Effect of cytochrome c on formation of lipid peroxides in rat brain in vitro.
作者信息
Hattori T, Nishimura Y, Sakai N, Yamada H, Kawai K, Nozawa Y
机构信息
Department of Neurosurgery, Gifu University School of Medicine, Japan.
出版信息
Free Radic Res Commun. 1987;4(1):41-9. doi: 10.3109/10715768709088087.
Antioxidant activity of exogenous cytochrome c was investigated in vitro using the whole brain homogenate, mitochondrial fraction and postmitochondrial supernatant containing microsomes prepared from rat brains. Increments in the amount of lipid peroxides were observed in each fraction when incubated at 30 degrees C, while the addition of cytochrome c (200 mM) effectively suppressed the production of peroxides. This depressive effect of cytochrome c was more prominent in the supernatant than in the mitochondrial fraction. Although the peroxidation was enhanced markedly by the addition of NADPH (2 mM), particularly in the mitochondrial fraction, cytochrome c was able to prevent its acceleration. This inhibitory mechanism might be explained by the fact that cytochrome c deprived superoxide radicals of electrons generated in ischemic insult. The results of the present study suggest that exogenous cytochrome c has free radical scavenging or antioxidant activity, which might be responsible in part for its cerebral protective action during ischemia.
使用从大鼠大脑制备的全脑匀浆、线粒体组分和含有微粒体的线粒体后上清液，在体外研究了外源性细胞色素c的抗氧化活性。当在30℃孵育时，在每个组分中均观察到脂质过氧化物量的增加，而添加细胞色素c（200 mM）可有效抑制过氧化物的产生。细胞色素c的这种抑制作用在上清液中比在线粒体组分中更明显。尽管添加NADPH（2 mM）可显著增强过氧化作用，尤其是在线粒体组分中，但细胞色素c能够阻止其加速。这种抑制机制可能是由于细胞色素c夺取了缺血性损伤中产生的超氧自由基的电子。本研究结果表明，外源性细胞色素c具有自由基清除或抗氧化活性，这可能部分解释了其在缺血期间的脑保护作用。
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