| Project/Area Number |
16K15571
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Radiation science
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| Research Institution | Tokyo Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
桑原 義和 東北医科薬科大学, 医学部, 准教授 (00392225)
鈴木 正敏 東北大学, 災害復興新生研究機構, 助教 (60515823)
富田 和男 鹿児島大学, 医歯学域歯学系, 助教 (60347094)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | がん細胞 / 放射線療法 / 化学療法 / 交叉耐性 / ミトコンドリア / ミトコンドリア欠失細胞 / 分割照射 / エピジェネティクス / 放射線耐性 / 代謝 |
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| Outline of Final Research Achievements |
We analyzed the role of mitochondria (mt) on the phenotype expression of CRR cells that continue to proliferate under fractionated irradiation of 2 Gy/day x-rays. Reactive oxygen species (ROS) derived from mt was detected in the parent cells after acute irradiation with 10 Gy, but was not detected in CRR cells, and the mitDNA copy number and ATP amount were decreased. Using ethidium bromide, mtDNA deleted ρ0 cells could be established from parental ells but was impossible from CRR cells. Only one ρ0 cells could be established from HepG2-CRR to which maintenance irradiation paused. Expression of the antioxidant enzyme group in ρ0 cells showed no specific tendency compared to the parental cells but was rather sensitive to H202. It was suggested that the influx of H 2O2 is accelerated by the decrease in cell membrane potential of ρ0 cells.
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