| Project/Area Number |
22221004
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| Research Category |
Grant-in-Aid for Scientific Research (S)
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| Allocation Type | Single-year Grants |
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| Research Field |
Risk sciences of radiation/Chemicals
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| Research Institution | Kyushu University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
SAKUMI Kunihiko 九州大学, 生体防御医学研究所, 准教授 (50211933)
TSUCHIMOTO Daisuke 九州大学, 生体防御医学研究所, 助教 (70363348)
OKA Sugako 九州大学, 生体防御医学研究所, 学術研究員 (80467894)
SHENG Zijing 九州大学, ヌクレオチドプール研究センター, 助教 (90467895)
AKIMOTO Yoriko 九州大学, 生体防御医学研究所, 非常勤研究員 (50613254)
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| Co-Investigator(Renkei-kenkyūsha) |
OHYAGI Yasumasa 九州大学, 医学研究院, 教授 (30301336)
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| Project Period (FY) |
2010-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥217,100,000 (Direct Cost: ¥167,000,000、Indirect Cost: ¥50,100,000)
Fiscal Year 2014: ¥38,740,000 (Direct Cost: ¥29,800,000、Indirect Cost: ¥8,940,000)
Fiscal Year 2013: ¥45,630,000 (Direct Cost: ¥35,100,000、Indirect Cost: ¥10,530,000)
Fiscal Year 2012: ¥43,680,000 (Direct Cost: ¥33,600,000、Indirect Cost: ¥10,080,000)
Fiscal Year 2011: ¥44,460,000 (Direct Cost: ¥34,200,000、Indirect Cost: ¥10,260,000)
Fiscal Year 2010: ¥44,590,000 (Direct Cost: ¥34,300,000、Indirect Cost: ¥10,290,000)
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| Keywords | 活性酸素 / 放射線 / DNA / RNA / 突然変異 / バイスタンダー効果 / 細胞死 / 神経変性 / 酸化的損傷 / ヌクレオチドプール / 細胞増殖阻害 / 自然突然変異 / アルツハイマー病 / 環境ストレス / 化学物質 / 病態モデル / 酸化ヌクレオチド / 脱アミノ化ヌクレオチド / DNA修復 / 環境スレス |
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| Outline of Final Research Achievements |
We elucidated the importance of nucleotide pools as the targets of radiation and environmental stress as well as the biological significance of the quality control mechanisms for the nucleotide pools. Under the breakdown of nucleotide pool homeostasis, damaged nucleotides are incorporated into nuclear and mitochondrial genomes, and thus inducing mutagenesis, which results in carcinogenesis or congenital abnormalities. Damaged bases accumulated in genomes are efficiently removed by DNA repair mechanisms, however, persistent DNA repair induces programmed cell death. The cell death can contribute to suppression of carcinogenesis, while in brain or neural tissues the cell death rather causes neurodegeneration, such as Alzheimer's disease or retinal degeneration. Moreover, we revealed that damaged nucleosides released from the damaged cells act on adjacent cells, thus causing various bystander effects.
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| Assessment Rating |
Verification Result (Rating)
A
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Assessment Rating |
Result (Rating)
A: Progress in the research is steadily towards the initial goal. Expected research results are expected.
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