Significance of necrosis DNA fragmentation under oxidative stress and immune response
| Project/Area Number |
24590587
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Immunology
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| Research Institution | Tokyo University of Science |
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Principal Investigator |
MIZUTA RYUSHIN 東京理科大学, 生命医科学研究所, 准教授 (50297628)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2014: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2012: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | ネクローシス / DNA断片化 / 酸化ストレス / 自己免疫疾患 / SLE / アポトーシス / ＤＮＡ断片化 / アセトアミノフェン / ＴＵＮＥＬ |
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| Outline of Final Research Achievements |
Using specific inhibitors, we revealed that Acrolein, a low molecular-weight aldehyde produced under oxidative stress, is an exacerbation factor of acetaminophen-induced liver failure in mouse. From the analysis of DNase γ gene knock-out mouse, we also found that DNase γ cooperates with DNase I in inhibiting the liver failure by accelerating DNA degradation and sequestration/removal of dead cells.
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Report
(4 results)
Research Products
(15 results)
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[Journal Article] Acrolein, a highly toxic aldehyde generated under oxidative stress in vivo, aggravates the mouse liver damage after acetaminophen overdose.2014
Author(s)
Arai, T., Koyama, R., Yuasa, M., Kitamura, D., Mizuta, R.
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Journal Title
BIOMEDICAL RESEARCH-TOKYO
Volume: ３５
Pages: 389-395
NAID
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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