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Decrease in biliary excretion of copper in Long-Evans cinnamon (LEC) rats causing spontaneous hepatitis due to a
1Department of Public Health, Sapporo Medical College, Japan.
Research Communications in Chemical Pathology and Pharmacology
|July 1, 1993
Summary
New mutant LEC rats show impaired copper excretion into bile, leading to hepatic copper accumulation and liver dysfunction. This suggests a genetic defect affecting biliary copper transport and spontaneous hepatitis in these rats.
Area of Science:
- Hepatology
- Toxicology
- Genetics
Background:
- The Long-Evans Cinnamon (LEC) rat is a mutant model exhibiting spontaneous hepatitis and hepatic copper accumulation.
- Understanding the mechanism of copper excretion is crucial for liver disease research.
Purpose of the Study:
- To investigate the role of biliary copper excretion in hepatic copper overload in LEC rats.
- To compare copper metabolism and excretion between LEC rats and control Fischer rats.
Main Methods:
- Intravenous copper chloride infusion in LEC and Fischer rats.
- Measurement of biliary copper concentrations before and after infusion.
- Excretion of horseradish peroxidase along with copper to assess biliary transport.
Main Results:
- LEC rats exhibited significantly lower basal and post-infusion biliary copper levels compared to Fischer rats.
- Copper excretion in LEC rats was markedly reduced, leading to hepatic accumulation.
- Impaired excretion of co-infused horseradish peroxidase in LEC rats indicated compromised biliary transport.
Conclusions:
- The study concludes that impaired biliary copper excretion is the primary cause of hepatic copper accumulation in LEC rats.
- This defect in copper excretion is linked to the hepatobiliary dysfunction and spontaneous hepatitis observed in this model.
- The findings highlight a potential genetic basis for copper transport defects in liver disease.