| Project/Area Number |
07457065
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 | Hokkaido University |
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Principal Investigator |
MORIUCHI Tetsuya Cancer Inst.Div.Cell Biol., Hokkaido University Professor, 医学部, 教授 (20174394)
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| Co-Investigator(Kenkyū-buntansha) |
OKADA Futoshi Cancer Inst.Div.Cell Biol., Hokkaido University Instructor, 医学部, 助手 (00250423)
HAMADA Junichi Cancer Inst.Div.Cell Biol., Hokkaido University Assist.Prof, 医学部, 講師 (50192703)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥7,500,000 (Direct Cost: ¥7,500,000)
Fiscal Year 1996: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 1995: ¥5,800,000 (Direct Cost: ¥5,800,000)
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| Keywords | LEC rat / p53 / glutathione peroxidase / hepatitis / グルタチオン・ベルオキシダーゼ |
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| Research Abstract |
The Long-Evans Cinnamon (LEC) rat is a mutant strain in which hepatitis and liver cancer spontaneously develop at extremely high rates. We observed marked reduction in the activity of cellular glutathione peroxidase (GSH-Px) in the liver of LEC rats and p53 knockout mice. To determine whether GSH-Px promoter is activated by p53, liciferase assay was performed. Activation of GSH-Px promoter was found in both cell llines expressing wild-type p53 and mutant p53, indicating that GSH-Px promoter is activated by N-terminal activation domain of p53. To investigate the role of selenium-dependent GSH-Px in the development of hereditary hepatitis, we compared incidences and grades of acute hepatitis between the LEC rats fed with seleniumm-supplemented diet and selenium-deficient diet. We found that selenium-deficient status and resultant GSH-Px deficiency does not promote hepatitis but rather have an inhibitory effect on the development of hepatitis in LEC rats.
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