@article{oai:repo.qst.go.jp:00048533,
 author = {Indo, Hiroko and Inanami, Osamu and Koumura, Tomoko and Suenaga, Shigeaki and Yen, Hsiu-Chuan and Kakinuma, Shizuko and Matsumoto, Kenichiro and Nakanishi, Ikuo and St, Clair William and K., St Clair Daret and Matsui, Hirofumi and Cornette, Richard and Gusev, Oleg and Okuda, Takashi and Nakagawa, Yasuhito and Ozawa, Toshihiko and Majima, Hideyuki and 柿沼 志津子 and 松本 謙一郎 and 中西 郁夫 and 松井 裕史 and 小澤 俊彦 and 馬嶋 秀行},
 issue = {8},
 journal = {Free Radical Research},
 month = {Jun},
 note = {HLE, a human hepatocellular carcinoma cell line was transiently transfected with normal human MnSOD and MnSOD without a mitochondrial target 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.},
 pages = {1029--1043},
 title = {Roles of Mitochondria-Generated Reactive Oxygen Species on X-ray-Induced Apoptosis in a Human Hepatocellular Carcinoma Cell Line, HLE},
 volume = {46},
 year = {2012}
}