| Project/Area Number |
09670227
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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 |
Experimental pathology
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| Research Institution | OKAYAMA UNIVERSITY |
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Principal Investigator |
KAWABATA Teruyuki Okayama University Medical School, Lecturer, 医学部, 講師 (60201448)
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| Co-Investigator(Kenkyū-buntansha) |
MIZUNO Masashi Kobe University, Chemical Science and Engineering, Assistant Professor, 大学院・自然科学研究科, 助教授 (00212233)
OKADA Shigeru Okayama University Medical School, Professor, 医学部, 教授 (20033201)
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| Project Period (FY) |
1997 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 1999: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1998: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1997: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | inflammation / carcinogenesis / iron / nitric oxide |
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| Research Abstract |
We studied changes of iron metabolism on inflammation and the role of iron concerning with nitric oxide generation. We prepared iron-loaded rats fed with 2.5% carbonyl iron and induced inflammation by a single I.p. injection of lipopolysaccharide (LPS) into the rats. The iron overload was checked with histochemical and biochemical studies. In this model, serum AST and ALT did not increase significantly and were not different between iron-loaded and control rats. Serum iron decreased transiently after LPS injection and the decrease was less intensive in iron-loaded rats than control. Inducible nitric oxide synthase (iNOS) was induced at an early stage on several organs and disappeared until 24 and 48 hours. However, serum nitrogen oxides (NOx) and nitrosyl hemoglobin (NO-Hb) were kept high even after the disappearance of iNOS. We did not find the significant differences of several free radical damage such as protein oxidation, but the necrotic foci and the death rate appeared different between iron-loaded and control rats. In vitro study of the effect of nitric oxide on aconitase, which is a family protein of iron-regulatory protein-1 (IRP-1), nitric oxide inactivated the aconitase under atmosphere, but could not detect thyl radical which has been reported. In model iron-complex of hydroxylipoic acid and hydroxylipoamide, we did not detect thyl radical. The chemical mechanism of nitric oxide on aconitase inactivation was still unclear. It may need another methodological approach.
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