Liver disease is characterized by fatty liver,
hepatitis, fibrosis and cirrhosis and is a major cause of
illness and death worldwide. The prevalence of liver
diseases highlights the need for animal models for
research on the mechanism of disease pathogenesis and
efficient and cost-effective treatments. Here we show
that a senescence-accelerated mouse strain (SAMP8
mice), displays severe liver pathology, which is not seen
in senescence-resistant mice (SAMR1). The livers of
SAMP8 mice show fatty degeneration, hepatocyte death,
fibrosis, cirrhotic changes, inflammatory mononuclear
cell infiltration and sporadic neoplastic changes. SAMP8
mice also show abnormal liver function tests:
significantly increased levels of alanine aminotransferase
(ALT) and aspartate aminotransferase (AST).
Furthermore, titers of murine leukemia virus are higher
in livers of SAMP8 than in those of SAMR1 mice. Our
observations suggest that SAMP8 mouse strain is a
valuable animal model for the study of liver diseases.
The possible mechanisms of liver damage in SAMP8
mice are also discussed