| Project/Area Number |
63480145
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Experimental pathology
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| Research Institution | Sapporo Medical University |
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Principal Investigator |
MORI Michio Sapporo Medical College, Dept. Pathol., Professor, 医学部, 教授 (00045288)
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| Co-Investigator(Kenkyū-buntansha) |
HATTORI Atsuo Sapporo Medical College, Dept. Pathol., Instructor, 医学部, 助手 (90208538)
ENOMOTO Katsuhiko Sapporo Medical College, Dept. Pathol., Associate Professor, 医学部, 助教授 (20151988)
伝法 公麿 札幌医科大学, 医学部, 助教授 (00045444)
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| Project Period (FY) |
1988 – 1990
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| Project Status |
Completed (Fiscal Year 1990)
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| Budget Amount *help |
¥4,600,000 (Direct Cost: ¥4,600,000)
Fiscal Year 1990: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1989: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1988: ¥3,200,000 (Direct Cost: ¥3,200,000)
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| Keywords | Hereditary hepatitis / Liver cell injury / Fulminant hepatitis / Chronic hepatitis / Liver cancer / Animal model / 肝癌発生機構 / LECラット / 肝癌 / 遺伝性肝障害 / 肝障害 / リボゾ-ムRNA / 薬物代謝酵素 / ガラクトサミン肝障害 / lipid peroxidation / polyploidy |
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| Research Abstract |
The LEC strain of rats, which spontaneously develop acute hepatitis associated with jaundice, chronic hepatitis and finally hepatocellular carcinomas, was found and established recently at the Center for Experimental Plants and Animals, Hokkaido University, Sapporo.
We have extensively studied the pathogenesis of spontaneous hepatitis in the LEC rat and found that the hepatitis is controlled by a single autosomal recessive gene. No infectious agents were detected. Abnormally high ploid nuclei were found in the hepatocyte of the LEC rat, but no direct relation between such an abnormality in the ploidy and the development of hepatitis was found. Experimental studies have shown that the LEC rat is highly sensitive to the hepatotoxic effect of D-galactosamine. Biochemical studies revealed that the S-adenosylmethionine synthetase activity in the liver of LEC rat is low at birth and decreased to a half level on the time of the onset of hepatitis, suggesting that the decrease in this enzyme have a key role for the development of spontaneous hepatitis and high sensitivity of the LEC rat to D-galactosamine hepatotoxicity.
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