量研学術機関リポジトリ「QST-Repository」は、国立研究開発法人 量子科学技術研究開発機構に所属する職員等が生み出した学術成果（学会誌発表論文、学会発表、研究開発報告書、特許等）を集積しインターネット上で広く公開するサービスです。 Welcome to QST-Repository where we accumulates and discloses the academic research results(Journal Publications, Conference presentation, Research and Development Report, Patent, etc.) of the members of National Institutes for Quantum and Radiological Science and Technology.
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Oxidative stress has been focused as cause of many diseases with chronic symptoms. In such diseases, mitochondria have been paid attention as the trigger of diseases. Mitochondria DNA (mtDNA) have 13 genes, which encode parts of electron transport chain (ETC). Previously we have reported evidence of reactive oxygen species (ROS) generation by mitochondria in cells with impaired electron transport chain and mitochondrial DNA damage. Inhibitors for ETC, or mitochondrial DNA damages generate more ROS from mitochondria (Indo et al. Mitochondrion 2007). Cells without mitochondrial DNA, ρ0 cells produce more ROS, lipid peroxidation, and pronounced more apoptosis at condition without uridine and pyruvate. ρ0 cells decrease in the red/green fluorescence intensity ratio, i.e., mitochondrial depolarization. The higher sensitivity to X-rays against ρ0 cells, higher rate of chromosomal aberration and larger amount of DNA double strand breaks indicated that pronounced radiation sensitive compared to the parental cells. Moreover ρ0 cells indicated less activity of manganese superoxide dismutase (MnSOD). These results indicate that ρ0 cells are radiation sensitive at the nuclear effects besides their mitochondria mediated apoptosis, and these results suggest mitochondria are the primary sites of X-irradiation-induced cellular injuries.
ρ0 Cells Are Susceptible to X-Irradiation
