Department of Food and Nutrition, Kyung Hee University, 1, Hoegi-dong, Dongdaemun-gu, Seoul 130-701, Republic of Korea.
Food Chem Toxicol. 2011 Sep;49(9):2459-63. doi: 10.1016/j.fct.2011.04.037. Epub 2011 May 12.
Antimycin A (AMA), which inhibits complex III of the electron transport system, has been used as a reactive oxygen species (ROS) generator in biological systems. We investigated the effects of AMA on various parameters related to mitochondrial function in osteoblastic MC3T3-E1 cells. Here, we show that AMA-induced cell death was accompanied by the loss of ATP, complex I and IV activities, and mitochondrial membrane potential. Moreover, AMA stimulated oxidative stress and induced cytochrome c release from mitochondria in osteoblasts. Our data support AMA-induced death in osteoblasts via a mitochondria-dependent pathway. These biochemical changes in mitochondria were effectively prevented upon pre-treatment with ROS scavengers, indicating that ROS plays a critical role as an upstream controller in the AMA-induced cell dysfunction.
抗霉素 A（AMA）抑制电子传递系统的复合物 III，已被用作生物系统中活性氧（ROS）的产生剂。我们研究了 AMA 对成骨细胞 MC3T3-E1 细胞中与线粒体功能相关的各种参数的影响。在这里，我们表明 AMA 诱导的细胞死亡伴随着 ATP、复合物 I 和 IV 活性以及线粒体膜电位的丧失。此外，AMA 刺激成骨细胞中的氧化应激并诱导细胞色素 c 从线粒体释放。我们的数据支持 AMA 通过线粒体依赖性途径诱导成骨细胞死亡。在用 ROS 清除剂进行预处理时，有效地预防了线粒体中的这些生化变化，表明 ROS 作为 AMA 诱导的细胞功能障碍的上游控制器起着关键作用。
