2002 Fiscal Year Final Research Report Summary
Therapeutic strategies of redox modification for renal failure
| Project/Area Number |
13670789
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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 |
Pediatrics
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| Research Institution | Fukui Medical University |
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Principal Investigator |
TSUKAHARA Hirokazu Fukui Medical University, Faculty of Medicine, Assistant Professor, 医学部附属病院, 講師 (90207340)
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| Co-Investigator(Kenkyū-buntansha) |
HATA Ikue Fukui Medical University, Faculty of Medicine, Research Associate, 医学部, 助手 (50251997)
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| Project Period (FY) |
2001 – 2002
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| Keywords | Renal failure / Redox modification / Oxidative stress / Reactive oxygen species / Reactive nitrogen species / Gas biology |
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| Research Abstract |
Renal failure is a syndrome characterized by an abrupt, in most cases, reversible kidney dysfunction, or a progressive, in most cases, irreversible kidney dysfunction. The spectrum of inciting factors is broad, and the pathophysiology of renal failure includes endothelial, glomerular and tubular dysfunction, which vary in severity and time of appearance. The present project was designed to examine the contribution of oxidative and nitrosative stress to the renal damage in vivo and in vitro situations. The results obtained with this project are the following.
(1) We have demonstrated using the rat model of acute renal failure that L-Nil (inducible NO synthase inhibitor), lecithinized SOD, and ebselen (scavenger of peroxynitrite) treatments improve renal function due to their suppression of peroxynitrite production or its scavenging, consequently preventing lipid peroxidation and oxidative DNA damage.
(2) We have found that the methylenetetrahy drofolate reductase (MTHFR) TT genotype may b
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e associated with early development and progression of childhood segmental glomerulosclerosis.
(3) We examined whether advanced glycosylation end product (AGE) production and oxidative stress are augmented in young patients with type 1 diabetes at early clinical stages of the disease. The results have indicated that accumulation of AGEs, whose formation is closely linked to oxidative stress, and resultant endothelial dysfunction may start early in the course of type 1 diabetes.
(4) We examined the effect of NO on the adhesion of human microvascular endothelial cells using the ECIS technique. The results have suggested that NO modulates cell-matrix and/or cell-cell adhesion in endothelial cells and that this molecule might modify microvascular permeability in human tissues and organs.
(5) We have reviewed basic chemical aspects of the oxidation and disproportionation of NO, and also established the formulas for reliably predicting NO_2 or N_2O formation in any set of NO (with O_2) and in any time. Less
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Research Products
(15 results)
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[Publications] Tsukahara H, Sekine K, Uchiyama M, Kawakami H, Hata I, Todoroki Y, Hiraoka M, Kaji M, Yorifuji T, Momoi T, Yoshihara K, Beppu M, Mayumi M: "Formation of advanced glycosylation end products and oxidative stress in young patients with type 1 diabetes"Pedaitr Res. (in press). (2003)
Description
「研究成果報告書概要(欧文)」より
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[Publications] Tsukahara H, Shibata R, Ohta N, Y, Sato S, Hiraoka M, Ito S, Nishima S, Mayumi M: "Increased pentosidine, an advanced glycation endproduct, in urine from children with acute exacerbation of atopic dermatitis and its relation with oxidative stress"Metabolism. (in press). (2003)
Description
「研究成果報告書概要(欧文)」より
