@misc{oai:repo.qst.go.jp:00065443,
 author = {犬童, 寛子 and 鶴岡, 千鶴 and 柿沼, 志津子 and 鈴木, 雅雄 and 松本, 謙一郎 and 中西, 郁夫 and Yen, Hsiu-Chuan and 松井, 裕史 and 小澤, 俊彦 and 馬嶋, 秀行 and 犬童 寛子 and 鶴岡 千鶴 and 柿沼 志津子 and 鈴木 雅雄 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},
 month = {Mar},
 note = {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., 第32回Cytoprotection研究会},
 title = {ρ0 Cells Are Susceptible to X-Irradiation},
 year = {2014}
}