1990 Fiscal Year Final Research Report Summary
Pathogenesis of Hereditary Hepatitis in LEC Rats
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 |
Research Field |
Experimental pathology
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Research Institution | Sapporo Medical University |
Principal Investigator |
MORI Michio Sapporo Medical College, Dept. Pathol., Professor, 医学部, 教授 (00045288)
|
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)
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Project Period (FY) |
1988 – 1990
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Keywords | Hereditary hepatitis / Liver cell injury / Fulminant hepatitis / Chronic hepatitis / Liver cancer / Animal model / 肝癌発生機構 |
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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