| Project/Area Number |
04670312
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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 |
Hygiene
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| Research Institution | Miyazaki Medical College |
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Principal Investigator |
TAKENAKA Hitoshi Miyazaki Medical College, Department of Hygiene, Senior Research Associate, 医学部, 助手 (10179658)
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| Co-Investigator(Kenkyū-buntansha) |
HAMADA Minoru Miyazaki Medical College, Department of Hygiene, Professor, 医学部, 教授 (90039529)
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| Project Period (FY) |
1992 – 1993
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| Project Status |
Completed (Fiscal Year 1993)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1993: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1992: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | Ischemia / Reperfusion / Heart / Sarcoplasmic reticulum / Stress Protein / Liver / Mitochondria / a-Tocopherol / 再灌流 / alpha-トコフェロール / 虚血再潅流 / 細胞壊死 / 酸化的リン酸化 / ビタミンE |
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| Research Abstract |
Several polypeptides associated with isolated cardiac sarcoplasmic reticulum appeared and disappeared during and after global ischemia and subsequent reperfusion. There were several polypeptides in the region of 90-98 kDa. 97 kDa-polypeptide changed its content from about 8.8% to 9.9% after ischemia and to 7.7% after reperfusion. Polypeptide ranging 65-70 kDa markedly increased after ischemia and further after reperfusion. Doublet bands at about 97kDa were reacted with anti-HSP 70 gene family antibody. The smaller band in the above doublet was also reacted with anti-GRP 94 antibody. Polypeptides at 67, 43, and 29 kDa present in control and ischemic heart disappeared after reperfusion. It was indicate that various stress were synthesized degraded during ischemia and reperfusion.
Partial ischemia/reperfusion model of rat liver was used to analyze the relationship between plasmic glucose and insulin levels and to examine the effect of administration of a-tocopherol(a-Toc)prior to ischemia/repefusion injury of mitochondrial functions. Plasmic glucose was elevated after reperfusion in both of the control and a-Toc group, whereas plasmic insulin was increased only in reperfused control. a-Toc content in mitochondria decreased by ischemia. Activated mitochondrial functions in non-ischemic lobes was likely to compensate inhibited mitochondrial functions in ischemic lobes. Mitochondrial yield was decreased only in reperfused control group. Cytochrome c oxidase activity was lowered by ischemia and restored by reperfusion. Ischmia/reperfusion injury takes place in a step before the complex III.Lipid peroxides in plasma and mitochondria were elevated by reperfusion in ischemic lobes but not in non-ischemic lobes. These results indicated that lipid peroxidatiion contribute to ischemia/reperfusion injury and that ischemic injury and reperfusion injury could occur parallelly but not sequentially.
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