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Related Experiment Videos

Copper and hepatic function.

C A Owen

    Ciba Foundation Symposium
    |January 1, 1980
    PubMed
    Summary

    Bedlington terriers accumulate excessive liver copper due to impaired bile excretion, mimicking human copper diseases. This leads to cirrhosis, ascites, and jaundice, despite initial lack of inflammation.

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    Area of Science:

    • Veterinary Pathology
    • Genetics
    • Toxicology

    Background:

    • Impaired hepatic copper excretion causes copper accumulation in the liver.
    • This occurs in cholestasis, primary biliary cirrhosis, and inherited copper diseases.
    • Bedlington terriers exhibit a genetic defect leading to severe hepatic copper accumulation.

    Purpose of the Study:

    • To investigate the pathogenesis of copper accumulation in Bedlington terriers.
    • To compare the canine condition with human copper storage diseases.
    • To characterize the histological and biochemical changes associated with canine copper toxicosis.

    Main Methods:

    • Observation of Bedlington terriers from six months to eight years of age.
    • Quantification of hepatic copper concentrations using X-ray emission spectroscopy.
    • Histopathological examination of liver tissues.
    • Comparison with mongrel dogs and human copper diseases.

    Main Results:

    • Bedlington terriers show progressive hepatic copper accumulation, peaking by 5-8 years.
    • Copper concentrations can exceed 10,000 microgram/g dry weight, far above normal levels.
    • Early stages show minimal inflammation/fibrosis, with copper localized in lysosomes.
    • Later stages develop hepatic cirrhosis, ascites, and jaundice.

    Conclusions:

    • Bedlington terriers serve as a valuable model for inherited copper toxicosis.
    • The canine condition shares similarities with Wilson's disease despite histological differences.
    • Understanding this model can provide insights into human copper metabolism disorders.

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