2002 Fiscal Year Final Research Report Summary
The study of regulation mechanisms on vitamin A metabolism by retinoid dehydrogenases and those physiological roles
| Project/Area Number |
13660134
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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 |
食品科学・栄養科学
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| Research Institution | Tokyo University of Agriculture |
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Principal Investigator |
MASUSHIGE Shoichi Tokyo University of Agriculture, Faculty of Applied Bioscience, Department of Bioscience, Professor, 応用生物科学部, 教授 (70078153)
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| Co-Investigator(Kenkyū-buntansha) |
KATO Haruno Tokyo University of Agriculture, Department of Bioscience, Assistant, 応用生物科学部, 助手
KIDA Satoshi Tokyo University of Agriculture, Department of Bioscience, Associate Professor, 応用生物科学部, 助教授 (80301547)
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| Project Period (FY) |
2001 – 2002
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| Keywords | retinoic aid / vitamin A / RolDH / RalDH / emotional behavior / estrogen / nuclear receptor / behavior al analysis |
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| Research Abstract |
It is well known that retinoic acid (RA) is an active metabolite of vitamin A, and has numerous biological functions via RAR and RXR. However the regulation mechanism of RA homeostasis in vivo is not clearly elucidated. In this study, we Attempted to clarify how RA metabolism was regulated by expression level of retinoid-dehydrogenase genes according with Retinoid status. RA is generated from retinol by the action of two kinds of enzyme. One is the retinol-dehydrogenase (RolDH) family, and the other is retinal-dehydrogenase (RalDH) family. Each family has several isozymes which are designated as RolDH1 -4 or RalDH1-3 respectively. Weaning male rats (Wistar strain) were fed on a retinoid free diet for 35-40 days. Retinoid depleted were sacrificed without treatment, and liver, lung, brain and testis were removed. Others were orally given 100 ug of atRA or 9cRA, or 1 mg of Rol per head. At the several time intervals after administration of retinoids animals were sacrificed, the organs were also removed, then total RNA was extracted from each tissue, and mRNA levels of RolDHs and RalDHs were analyzed by northern blot method. The results obtained showed that the expression of each isozyme gene was organ-specifically regulated in accordance with retinoid status. In addition, we cloned a novel retinol-dehydrogenase gene, and characterized it.
And then, we attempted to clarify some new function of retinoid signal transduction on the emotional behavior of mouse, by using of open field test, elevated zero maze test, and social dominance tube task after administration of atRA or estrogen. The results showed that those lipid soluble ligands have some effect on mouse behavior, increased anxiety and became aggressive. Moreover we found that mRNA level of serotonin transporter in brain was changed with dose of ligand, atRA, estrogen, or agonist of them.
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