학술논문
Roles of mitochondria-generated reactive oxygen species on X-ray-induced apoptosis in a human hepatocellular carcinoma cell line, HLE.
Document Type
Article
Author
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.
Source
Subject
*REACTIVE oxygen species
*MITOCHONDRIAL physiology
*PHYSIOLOGICAL effects of x-rays
*APOPTOSIS
*LIVER cancer
*CELL lines
*SUPEROXIDE dismutase
*PHYSIOLOGICAL oxidation
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Language
ISSN
1071-5762
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. [ABSTRACT FROM AUTHOR]