1987 Fiscal Year Final Research Report Summary
Biochemical Process of Ischemic Injury of Liver and Protection against the Injury.
| Project/Area Number |
61480130
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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 |
Pathological medical chemistry
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| Research Institution | Faculty of Medicine, Osaka University |
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Principal Investigator |
TAGAWA Kunio Faculty of Medicine, Osaka University, 医学部, 教授 (40028296)
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| Co-Investigator(Kenkyū-buntansha) |
KUROSAWA Kazuhei Faculty of Medicine, Osaka University, 医学部, 助手 (70178127)
KAMIIKE Wataru Faculty of Medicine, Osaka University, 医学部, 助手 (40152847)
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| Project Period (FY) |
1986 – 1987
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| Keywords | Ischemic liver / Cellular Calcium / Mitochondria / Cytoskelton system / Myosin / 遊離ATP |
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| Research Abstract |
1. Anoxic incubation of isolated rat liver mitochondria caused disruption of the proton barrier of the inner membrane which subsequently led to loss of oxidative phosphorylation. This mitochondrial dysfunction under anoxia was involved depletion of intramitochondrial ATP, dissociation of the CaATP^<2-> complex to liberate free Ca^+, activation of phospholipase A_2 by the free Ca^<2+> released and disruption of the proton barrier of the inner membrane.
2. The flow rate of bile is closely correlated with the cellular level of ATP. However, after prolonged hypothermic anoxia, reoxygenation restored the cellular level of ATP but not the rate of bile excretion. Most of the metabolic enzyme systems in hepatocytes were well preserved after hypothermic incubation, like the cellular level of ATP. Incubation of isolated liver in medium containing Ca^<2+> caused serious damage to the system for bile excretion without affecting the cellular level of ATP. These data indicated that Ca^<2+> influx during ischemia resulted in decreased bile formation.
3. There are two forms of ATP in rat heart; one is detectable by ^<31>P-NMR spectroscopy and the oter is not. From the characteristics of the ^<31>P-NMR, the former seems to be free ATP in the cytosol, and the latter to be protein-bound and mitochondrial ATP. During ischemia, the free ATP in the cytosol seemd to be depleted mopre rapidly than the other form of ATP.
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