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      Induction of Aldose Reductase Gene Expression in LEC Rats during the Development of the Hereditary Hepatitis and Hepatoma

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          We examined age‐related changes in the protein and the mRNA expression of aldose reductase in livers of Long‐Evans with a cinnamon‐like color (LEC) rats, which develop hereditary hepatitis and hepatoma with aging, using Long‐Evans with an agouti color rats as controls. The levels of the protein and mRNA of aldose reductase increased after 20 weeks, at the stage of acute hepatitis, and were maintained at 60 weeks of age, while those of aldehyde reductase seemed to be constant at all ages. The expression of aldose reductase was marked in cancerous lesions in hepatoma‐bearing LEC rat liver compared to uninvolved surrounding tissues. These results indicated that elevation of aldose reductase accompanied hepatocarcinogenesis and may be related to the acquisition of immortality of the cancer cells through detoxifying cytotoxic aldehyde compounds.

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          Most cited references 25

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          Single-step method of RNA isolation by acid guanidinium thiocyanate-phenol-chloroform extraction.

          A new method of total RNA isolation by a single extraction with an acid guanidinium thiocyanate-phenol-chloroform mixture is described. The method provides a pure preparation of undegraded RNA in high yield and can be completed within 4 h. It is particularly useful for processing large numbers of samples and for isolation of RNA from minute quantities of cells or tissue samples.
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            Spontaneous hepatic copper accumulation in Long-Evans Cinnamon rats with hereditary hepatitis. A model of Wilson's disease.

             Y. Li,  S. Sato,  Y. Kojima (1991)
            Long-Evans Cinnamon (LEC) rats, an inbred strain of a mutant rat isolated from Long-Evans rats, develop hereditary hepatitis. To elucidate the role of copper metabolism in the development of the hepatitis in LEC rats, we examined the copper concentration in the tissues and serum levels of copper and ceruloplasmin. Copper concentration in the liver of LEC rats was over 40 times that of normal Long-Evans Agouti (LEA) rats, while the serum ceruloplasmin and copper concentrations in LEC rats decreased significantly. The hepatocytes of LEC rats show steatosis in cytoplasm and pleomorphism of mitochondria, resembling the histologic features of the liver in Wilson's disease. These findings suggest that the hereditary hepatitis in LEC rats is closely associated with copper toxicity, and may be dealing with a rat form of Wilson's disease. Thus the LEC rats will provide a unique and useful animal model for clarifying the mechanism and for developing treatment strategies for Wilson's disease and other abnormal copper metabolism in humans.
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              The LEC rat has a deletion in the copper transporting ATPase gene homologous to the Wilson disease gene.

              The Long-Evans Cinnamon (LEC) rat shows similarity to Wilson disease in many clinical and biochemical features. We have cloned cDNAs for the rat gene (Atp7b) homologous to the human Wilson disease gene (ATP7B) and have used them to identify a partial deletion in the Atp7b gene in the LEC rat. The deletion removes at least 900 bp of the coding region at the 3' end, includes the crucial ATP binding domain and extends downstream of the gene. Our results provide convincing evidence for defining the LEC rat as an animal model for Wilson disease. This model will be important for studying liver pathophysiology, for developing therapy for Wilson disease and for studying the pathway of copper transport and its possible interaction with other heavy metals.

                Author and article information

                Jpn J Cancer Res
                Jpn. J. Cancer Res
                Japanese Journal of Cancer Research : Gann
                Blackwell Publishing Ltd (Oxford, UK )
                April 1996
                : 87
                : 4 ( doiID: 10.1111/cas.1996.87.issue-4 )
                : 337-341
                [ 1 ]Department of Biochemistry, Osaka University Medical School, 2‐2 Yamadaoka, Suita, Osaka 565
                [ 2 ]Dako Japan, Nishinotouin‐higashiiru, Shijo‐dori, Shimogyo‐ku, Kyoto 600
                [ 3 ]Department of Pathology, Osaka University Medical School, 2‐2 Yamadaoka, Suita, Osaka 565
                Author notes
                [* ]To whom requests for reprints should be addressed.
                Page count
                References: 28, Pages: 5
                Custom metadata
                April 1996
                Converter:WILEY_ML3GV2_TO_NLMPMC version:4.6.9 mode:remove_FC converted:04.11.2015


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