Study on functional food constituents which can regulate programed cell death.
| Project/Area Number |
17500537
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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 |
Eating habits, studies on eating habits
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| Research Institution | Hyogo University of Teacher Education |
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Principal Investigator |
MASUZAWA Yasuo Hyogo University of Teacher Education, Graduate School of Education, Professor (30119622)
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| Co-Investigator(Kenkyū-buntansha) |
KISHIDA Etsu Hyogo Univaeity of Teacher Education, Graduate School of Education, Associate Professor (70214773)
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| Project Period (FY) |
2005 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,750,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥150,000)
Fiscal Year 2007: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2006: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2005: ¥2,600,000 (Direct Cost: ¥2,600,000)
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| Keywords | apoptosis / necrosis / inhibition / TNF / antioxidant / docosahexaenoic acid / Vitamine E / methyl mercury |
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| Research Abstract |
1. Preincubation of L929 cells with various polyunsaturated fatty acids enriched the corresponding fatty acids in phospholipids, and some fatty acids attenuated cell death induced by TNF. The order of effective PUFA activity was DHA>DPA(n-3)? EPA>AA = 20:3(n-6)? 22:4(n-6). DNA laddering was not detected, and cells were coincidently stained with both annexin V-FITC and propidium iodide, indicating that the death mode was necrotic. Combined with our previous data (J. Nutr. 130: 1095-1101, 2000), DHA-enriched membranes can protect cell against TNF irrespective of death modes and that membranous DHA may abrogate the death signaling common to necrosis and apoptosis.
2. Various antioxidants such as N-acetyl cystein (NAC), 2-mercaptoetnanol (2-ME) reduced the apoptotic cell perventages induced by TNF in dose dependent fashion. Water-solible antioxidants increased cellular glutathion level, but inhibitory activity of antioxidants against TNF-induced apoptosis did not correlate with the glutathion-increasing activity. It was indicated that cellular glutathion level shows only little effect on cellular sensitivity to apoptotic stimulation by TNF, and that antioxidants can inhibit TNF-induced apoptosis by directly scavenging reactive oxygen species, constructing a part of apoptotic signals of TNF.
3. The effect of fatty acid supplementation on death of PC12 cells induced by methyl mercury. Different from apoptosis or necrosis induced by THF, supplementation of DHA or arachidonic acids in cell culture accelerate methyl mercury-induced cell death. This indicates that methyl mercury induces cell death.
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Report
(4 results)
Research Products
(9 results)
