| Project/Area Number |
06671517
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
TANIGUCHI Yoshihisa Sch.of Medicine, Kyoto University Assistant Professor, 医学研究科, 助手 (20243016)
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| Co-Investigator(Kenkyū-buntansha) |
MORI Kenjiro Sch.of Medicine, Kyoto University Professor, 医学研究科, 教授 (20025620)
ARAI Toshiviki Sch.of Medicine, Kyoto University Associate Professor, 医学研究科, 助教授 (80175950)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1995: ¥700,000 (Direct Cost: ¥700,000)
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| Keywords | Oxidative Stress / gene expression / thioredoxin / 酸素ストレス |
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| Research Abstract |
Hemorrhage and operational procedures induce transient hypoperfusion in organs with followed re-perfusion, and anesthetized patients are usually administered with higher concentration oxygen than atmosphere. These conditions serve the generation of ROI.Oxidative stress induces defensive reactions dealing with ROIs or ROI-induced damages. These involve induction of enzymes with radical scavenging and repair activities such as superoxide dismutase, catalase, gultathion hydrogenase, and thioredoxin. We analyzed the induction of these genes in patients who were under general anesthesia and were inspired with higher concentration of oxygen. We analyzed the mRNA levels of the genes in Jurkat cell or human normal lymphocytes using Northern blotting in vitro against the oxidative agents. We could not recognized the change of the levels of the mRNA of superoxide dismutase, catalase and gultathion hydrogenase genes against these oxidative agents. However, the expression of thioredoxin gene was induced against these agents. We cloned the thioredoxin gene from human genomic library, and introduced the promoter region with various deleted lengths from the transcription initiation site into the CAT reporter gene. We found a region from -976 to -890 which was required the response for the induction of the gene against oxidative agents. Since the region had no homologous sequence with known sequence elements of DNA binding proteins, thioredoxin gene may use a new element for the gene induction against oxidative stress.
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