Roles of mitochondria-generated reactive oxygen species on X-ray-induced apoptosis in a human hepatocellular carcinoma cell line, HLE |
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| Authors: | Indo Hiroko P Inanami Osamu Koumura Tomoko Suenaga Shigeaki Yen Hsiu-Chuan Kakinuma Shizuko Matsumoto Ken-Ichiro Nakanishi Ikuo St Clair William St Clair Daret K Matsui Hirofumi Cornette Richard Gusev Oleg Okuda Takashi Nakagawa Yasuhito Ozawa Toshihiko Majima Hideyuki J |
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| Affiliation: | Department of Oncology, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan. |
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| Abstract: | 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. |
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