School of Medicine and Applied Radiological Science Research Institute, Jeju National University, Jeju-si 690-756, Republic of Korea.
Food Chem Toxicol. 2010 Mar;48(3):922-7. doi: 10.1016/j.fct.2010.01.001. Epub 2010 Jan 12.
This study investigated the cytoprotective effect of butin, a flavonoid, on hydrogen peroxide (H(2)O(2))-induced mitochondrial dysfunction. Electron spin resonance (ESR) spectrometry revealed butin's significant scavenging effects on superoxide radicals and hydroxyl radicals. When H(2)O(2) was used to induce an increase in mitochondrial reactive oxygen species (ROS) in Chinese hamster lung fibroblast (V79-4) cells, butin treatment decreased high level of ROS. Butin also attenuated intracellular Ca(2+) levels that have been induced by H(2)O(2). Furthermore, butin recovered ATP levels and succinate dehydrogenase activity that had been decreased by H(2)O(2) treatment. We conclude these results suggest butin decreased mitochondrial ROS accumulation, balanced intracellular Ca(2+) levels, and improved mitochondrial energy production, thus recovering mitochondrial function.
本研究探讨了黄酮类化合物布替那对过氧化氢（H2O2）诱导的线粒体功能障碍的细胞保护作用。电子自旋共振（ESR）谱表明布替那对超氧自由基和羟自由基有显著的清除作用。当用 H2O2 诱导中国仓鼠肺成纤维细胞（V79-4 细胞）中线粒体活性氧（ROS）增加时，布替那处理可降低高水平的 ROS。布替那还可减轻 H2O2 诱导的细胞内 Ca2+水平升高。此外，布替那还恢复了 H2O2 处理降低的 ATP 水平和琥珀酸脱氢酶活性。我们的结论是，这些结果表明布替那可减少线粒体 ROS 积累，平衡细胞内 Ca2+水平，改善线粒体能量产生，从而恢复线粒体功能。
