Roles of Mitochondrial Reactive Oxygen Spesies in Suppression of Apoptosis Induced by X-irradiation

用正常人MnSOD和无线粒体靶向信号（MTS）的MnSOD瞬时转染人细胞。线粒体活性氧（ROS），脂质过氧化和细胞凋亡作为一个功能的时间后，18.8戈伊照射。结果表明，X射线照射后2h，线粒体活性氧水平升高，并达到最大值。真正的MnSOD，但不是MnSOD缺乏MTS，保护线粒体ROS，脂质过氧化和细胞凋亡。此外，线粒体ROS的水平一直被发现总是与线粒体中真正的MnSOD的水平相关。这些结果表明，只有当MnSOD位于线粒体是有效的保护对细胞损伤的X射线辐射和线粒体是X射线诱导的细胞氧化损伤的关键部位。

Human ells was transiently transfected with normal human MnSOD and MnSOD without a mitochondrial targeting signal (MTS). Mitochondrial reactive oxygen species (ROS), lipid peroxidation, and apoptosis were examined as a function of time following 18.8 Gy X-ray irradiation. The results showed that the level of mitochondrial ROS increased and reached a maximum level 2 h after X-ray irradiation. Authentic MnSOD, but not MnSOD lacking MTS, protected against mitochondrial ROS, lipid peroxidation, and apoptosis. In addition, the levels of mitochondrial ROS were consistently found to always correlate with the levels of authentic MnSOD in mitochondria. These results suggest that only when MnSOD is located in mitochondria is it efficient in protecting against cellular injuries by X-ray irradiation and that mitochondria are the critical sites of X-ray-induced cellular oxidative injuries.