| Co-Investigator(Kenkyū-buntansha) |
KURASAKI Masaaki Hokkaido Univ., Fac.of Environ.Earth Sci., Inst., 大学院・地球環境科学研究院, 助手 (80161727)
HOSOKAWA Toshiyuki Hokkaido Univ., Center of Res.Develop.Higher Edu., Associate Prof., 高等教育機能開発総合センター, 助教授 (00157025)
FUJITA Hiroyoshi Hokkaido Univ., Grad.School of Med., Prof., 大学院・医学研究科, 教授 (60142931)
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| Budget Amount *help |
¥15,100,000 (Direct Cost: ¥15,100,000)
Fiscal Year 2005: ¥4,700,000 (Direct Cost: ¥4,700,000)
Fiscal Year 2004: ¥5,400,000 (Direct Cost: ¥5,400,000)
Fiscal Year 2003: ¥5,000,000 (Direct Cost: ¥5,000,000)
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| Research Abstract |
In the present study, we intended to clarify a metabolism of trace metals, which affected central nervous system activity. With various cultured cells, we examined changes of a metallochaperone of copper, CCS, Cu,Zn-SOD, which received copper from CCS, and Ctr1, which was copper transporter in a copper lack and too much states. In a copper lack state, the quantity of protein of CCS and Cu,Zn-SOD increased. On the other hand, in a state having too much copper, the quantity of protein of CCS and Cu,Zn-SOD showed a significant fall. Furthermore, I made an animal having too much a zinc intake. In a state having too much zinc, a copper absorption obstruction in an intestinal tract was occurred. It was suggested that the copper in intestinal tract cell decreased, and a copper transporter protein ATP7A decreased as well.
When it added copper chelate in a cultured cell of a nerve cell origin, it became clear that arachidonic acid metabolism changed in a cell. A fall of Cu,Zn-SOD activity by copper lack caused rises of NO and active oxygen species as the cause and affected arachidonic acid metabolism in a cell.
We examined metal binding ability of metallothionein-3 (MT-3), which specifically emerged to a central nervous system. It became clear that copper-binding affinity of MT-3 is very much higher in comparison with other metallothioneins.
With a visual observation method of neurotransmission, we clarified influence of tributyltin on the neurotransmission. As a result, tributyltin obstructed the long-term potentiation, which was related to learning and memory.
Furthermore, I put the metal-binding protein, which caused the central nervous disorder and examination of obstacle outbreak mechanism of active oxygen species.
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