Department of Oncology, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.
Free Radic Res. 2012 Aug;46(8):1029-43. doi: 10.3109/10715762.2012.698012. Epub 2012 Jun 25.
HLE, a human hepatocellular carcinoma cell line 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. Our results showed that the level of mitochondrial ROS increased and reached a maximum level 2 hours 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.
HLE 是人肝癌细胞系，用正常的人 MnSOD 和没有线粒体靶向信号（MTS）的 MnSOD 进行瞬时转染。研究了在 18.8Gy X 射线照射后，线粒体活性氧（ROS）、脂质过氧化和细胞凋亡随时间的变化。结果表明，线粒体 ROS 水平在 X 射线照射后 2 小时增加并达到最大值。真正的 MnSOD，但不是没有 MTS 的 MnSOD，能抵抗线粒体 ROS、脂质过氧化和细胞凋亡。此外，线粒体 ROS 的水平始终与线粒体中真正的 MnSOD 水平相关。这些结果表明，只有当 MnSOD 位于线粒体中时，它才能有效地防止 X 射线照射引起的细胞损伤，而线粒体是 X 射线诱导的细胞氧化损伤的关键部位。
