Host: The Japan Radiation Research Society
Co-host: City of Kitakyushu, University of Occupational and Environmental Health, Japan
Ionizing radiation produces short-lived radicals through hydrolysis of water molecules. Recently, it is suggested that radiation causes disturbance of intracellular oxidation control system in mitochondria. Because elevated intracellular oxidative stress is involved in various delayed effects, we examined delayed production of ROS in normal human cells exposed to gamma-rays. Involvement of delayed dysfunction of mitochondria was also investigated. Immortalized normal human diploid cells were used in this study. The amount of reactive oxygen species (ROS) was determined using aminophenyl fluorescein (APF) reagent. Levels of superoxide localized within mitochondria were measured by MitoSox Red reagent. Mitochondria were visualized by staining with MitoTracher reagent, and structural change was examined under fluorescence microscope. While transient increase in the ROS level was detected immediately after irradiation, it returned to the control level within a few hours. Then, the second increase became obvious 2 to 3 days after irradiation, which was accompanied by the increased level of mitochondrial superoxide. Interestingly, delayed morphological change was observed in mitochondria, suggesting that delayed dysfunction of mitochondria causes delayed oxidative stress.
