2003 Fiscal Year Final Research Report Summary
Mechanism of myocardial tissue damage in patients with diabetes, chronic renal failure and hemodialysis
| Project/Area Number |
14570171
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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 |
Human pathology
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| Research Institution | Fukuoka University |
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Principal Investigator |
SAKATA Noriyuki Fukuoka University, School of Medicine, Professor, 医学部, 教授 (20134273)
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| Co-Investigator(Kenkyū-buntansha) |
UESUGI Noriko Fukuoka Univ., School of Medicine, Research Assistant, 医学部, 助手 (70279264)
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| Project Period (FY) |
2002 – 2003
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| Keywords | Chronic renal failure / Diabetes mellitus / Myocardial tissue / Myofilament / Glycoxidation / Hydroxyl radical |
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| Research Abstract |
The present study was done to clanfy the role of glycoxidation stress on the damage of cardiac muscle and arterial tissue in patients with diabetes, chronic renal failure and hemodialysis. The level of pentosidine, a glycoxidation product, was significantly increased in the matrix proteins of arterial tissues and myofilament protein of myocardium of the patients with hemodialysis and chronic renal failure as compared to controls. The calcium-binding activity arid pentosidine level of collagen, a matrix protein, was time-dependently increased with in vitro incubation of glucose. In arterial tissues, the glycoxidative modification of matrix protein may be closely related to medial calcification in patients with diabetes and chronic renal failure. The level of urea hydrogen peroxide (UHP) was significantly higher in cardiac tissues of patients with chronic renal failure and hemodialysis than in those of controls. In vitro incubation of cardiac tissues with ribose formed pentosidine in dose dependent manner of urea or serum ultrafiltrate of patients with hemodialysis. The presence of urea, dose-dependently increased the generation of UHP in these incubation systems. Blocking experiment with catalase, SOD and mannitol showed that pentosidine formation was significantly enhanced by hydroxyl radical generated from UHP via Fenton reaction. Thus, glycoxidative modification of these proteins may be enhanced by the formation of UHP via Fenton reaction and may contribute to cardiac and arterial dysfunction in patients with chronic renal failure and hemodialysis.
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