| Project/Area Number |
02454490
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
医学一般
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| Research Institution | Hokkaido University |
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Principal Investigator |
KOYAMA Tomiyasu Hokkaido University, Research Institute of Electronic Sciences, Professor, 電子科学研究所, 教授 (50001681)
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| Co-Investigator(Kenkyū-buntansha) |
ARAISO Tsunehisa Hokkaido University, Research Institute of Electronic Sciences, Associate Profes, 電子科学研究所, 助教授 (30151145)
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| Project Period (FY) |
1990 – 1992
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| Project Status |
Completed (Fiscal Year 1992)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 1992: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1991: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1990: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | biomembrane / dynamic microstructure / time-resolved fluorometer / intramolecular oscillation / Ischemia combined with reperfusion / peroxidation / hydration of lipid layer / phospholipase / coenzyme / sarcoplasmic reticulum / ATPase / 過労 / 筋小胞体 / Ca^<2+>-ATPase / 心筋虚血・再潅流 / 心筋ミトコンドリア膜 / 脂質分子の揺動角 / 脂質過酸化 / アドリアマイシン |
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| Research Abstract |
Dynamic microstructure and its effects to cellular function were studied with a nanosecond time-resolved fluorometer. (1). Measurements of membrane viscosity (n) and wobbling angle of phospholipids (0) of plasma and mitochondrial membranes isolated from bullfrog suggested that the complex requirements of biomembranes of organelles performing different functions appear to be met by the particular dynamic microstructure of the biomembranes (1,2 ). (2). n increased and 0 decreased in rabbit heart subjected to ischemia combined with reperfusion. These changes will limit transmembrane movements of biomaterials. None of these parameters was changed in rats exposed only to ischemia (5,9). (3). Isolated cardiac mitochondria were exposed to peroxidizing conditions or adriamycin. n increased and 0 decreased, accompanied with strong decreases in the DPH fluorescence intensity and life time. The hydration of phospholipid layers of mitochondria occurs as a consequence of lipid peroxidation and also
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by adriamycin (3). (4). A quinoyl compound, idebenone pretreatment, suppressed the peroxidation- induced changes in the dynamic microstructure. Protection of phospholipids against peroxidation by antioxidative substances is effective in keeping nearly normal physical properties in the dynamic microstructure of cardiac mitochondrial membranes (4). (5). Phospholipids in cardiac mitochondria strongly decreased after a prolonged swim due to an activity increase in phospholipase A_2. The dynamic microstructure, however, showed no changes despite the remarkable decrease in phospholipids. This was probably because cholesterol was lost from mitochondrial membranes concurrently with phospholipids and the ratio of cholesterol to phospholipids did not change (7). Preadministration of a coenzyme, CoQ_<10> suppressed the exercise-induced decrease in mitochondrial phospholipids (8). (6). Lipid titration of sarcoplasmic reticulum with phospholipids having shorter acyl chains produced a lipid exchange by 70 % and caused an increase in the intramolecular oscillation of Ca-ATPase (6,11). Also a titration with an arachidonoyl phospholipid caused an increase in the intramolecular oscillation accompanied with a reduction in ATPase activity (10). The conformation and the suitable intramolecular oscillation of the ATPase are maintained with the adequate physical properties of surrounding phospholipids and the conformation changes in ATPase which permit an increase in intramolecular oscillation cause a decrease in the ATPase activity. Less
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