2007 Fiscal Year Final Research Report Summary
The Mechanism of Cell Death during Hypoxia
| Project/Area Number |
18590628
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Legal medicine
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| Research Institution | Chiba University |
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Principal Investigator |
IWASE Hirotaro Chiba University, Graduate School of Medicine, Dept. of Legal Medicine, Professor (30272420)
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| Project Period (FY) |
2006 – 2007
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| Keywords | hypoxia / lipid peroxidation / active oxygen / forensic medicine / cell death |
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| Research Abstract |
Many reseaithers indicate that lipid peroxidation and other oxidants occur in dell damage during ischemia-reperfusion. However it is still not clear that whether oxidants occur during ischemia or reperfusion phase. In this study, mouse emdryonic fibroblasts (MEFs) were used for experiment, to see how and when the oxidants occur during ischemia (reperfusion, or hypoxia and reoxygenation.). Some antioxidants or inhibitors of electron transfer system were treated for the cells to see the mechanism of lipid peroxidation. We used fluorescent dyes to detect the lipid peroxidation and dell damage. As a result, cell death occurs from ischemia pahase, and 63.9% cells were dead after reperfusion. Cell death was inhibited by KCN. Cell death during ischemia was inhibited by antimycinAor myxothiazol, and that during reperfusion was not inhibited by them. Lipid peroxidation was detected during ischemia and not during reperfusion, and it was inhibited by KCN and was not by antimacin A, myxotiazol or rotenone. From these results it was indicated that lipid peroxidation did not cccur during reperfusion but did during ischemia, and KCN could inhibit cell death and lipid peroxidation during ischemia.
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