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3 "Copper"
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Original Articles
The Effect of Copper on 3'-Methyl-4-dimethylaminoazobenzene Induced hepatic Carcinogenesis.
Jung Sook Moon, Young Nyun Park, Chan Il Park
Korean J Pathol. 1992;26(4):360-371.
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AbstractAbstract PDF
To elucidate the effect of copper on the 3'-methyl-4-dimethylaminoazobenzene(3'-MeDAB) induced hepatic carcinogenesis, Sprague-Dawley rats were divided into 4 groups according to 3'-MeDAB and copper administration: I. noraml control, II. copper only, III. 3'-MeDAB only, IV. 3'-MeDAB plus copper. The animals of groups III and IV were fed experimental diet containing 0.06% 3'-MeDAB. Copper was administrated intraperitoneally in a dose of 0.5 mg, twice a weak. Animals were sacrificed at different intervals. Liver weight, hepatic copper content and gross and microscopical changes of the liver were examined and the cell kinetics of various lesions in the hepatic carcinogenesis was studied by applying the immunohistochemical method for bromodeoxyuridine(BrdU). The hepatic copper content was significantly increased in animals given copper but returned to the normal value after cessation of adminstration. 3'-MeDAB administration caused oval cell proliferation and produced hyperplastic nodules, cholangiofibrosis and carcinoma of the liver. Simultaneous administration of copper did not alter the incidence of 3'-MeDAB induced lesions, except for carcinoma. The liver weight and the size of hepatic nodules and masses were smaller in group IV than in group III. The liver weight as well as the nodularity and the mass formation continued to increase affect cessation of 3'-MeDAB administration. Copper did not affect the BrdU labelling indices of the hepatic lesions induced by 3'-MeDAB. The oval cell proliferation and the BrdU labelling indices of the oval cell and the hyperplastic nodule were decreased, but the incidence of cholangiofibrosis and its BrdU labelling index were still elevated after cessation of 3'MeDAB administration. These findings indicate that copper could delay the developement of 3'-MeDAB induced hepatic lesions, but not suppress, since copper does not stay long enough to accumulate in the rat liver, and that copper could not affect the proliferation of 3'-MeDAB induced hepatic lesions once developed.
The Effect of Common Bile Duct Ligation on Liver Morphology and Coper Metabolism in Rat.
Kyoung Sook Kim, Chanil Park, Jang Whan Cho, In Joon Choi, Yoo Bock Lee
Korean J Pathol. 1990;24(4):402-411.
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To clarity the effect of biliary obliteration on copper metabolism of rat liver and on the hepatic morphology, 0.5% cuppuric sulfate was administered intraperitoneally for 42 days following ligation of the common bile duct (CBD) of Sprague-Dawley rats. The blood copper concentration, the hepatic copper content and the accumulation patterns of copper and copper binding protein in the liver were examined and compared with those of the simple CBD ligation group and the simple copper over loaded group. CBD ligation induced marked proliferation of bile ductular structures which, after expanding the portal tracts, invaded and divided the hepatic lobules. There was, however, no excess fibosis beyond what needed to support the new ductules. The blood copper concentration and the hepatic copper content were increased by copper overload with or without CBD ligation, particularly incases with CBD ligation. Liver cell necrosis did not occur by the overloaded copper alone in rats. The hepatic copper and copper binding protein were accumulated at periportal liver cells in the group of coppe overload after CBD ligatio, whereas they began to appear at perivenular hepatocytes in the simple copper overloaded group. In conclusion, it is suggested that CBD ligation does not induce excess fibrosis or liver cirrhosis in rat as far as during our experimental period, but affect significantly on copper metabolism by intrahepatic redistribution of the copper and the copper binding proteins.
Case Report
Wilson's Disease: Report of a Case with Comprehensive Review of the Previously Reported Cases in Korean Literature.
Mi Kyung Lee, Chan Il Park
Korean J Pathol. 1987;21(4):278-284.
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We reported a case of Wilson's disease, which was histologically confirmed by liver biopsy in a 15 year-old boy and made a comprehensive analysis on the sum of 22 cases reported in Korean literature. Although Wilson's disease is still rare, it should be included in the differential diagnosis of chronic liver diseases particularly in children of 5 to 15 years old. For the clinical diagnosis of Wilson's disease, changes in serum ceruloplasmin, plasma copper and urine copper values are most important as well as Kayser-Fleischer ring and family hestory. The serum level of GOT, when elevated, were always higher than GPT. This atypical transaminase profile may be a clue for diagnosis of hepatic diseases by a metabolic derangement. Among various histologic changes of the liver in Wilson's disease, what have diagnostic importance are anisonucleosis, nuclear glycogenosis and Mallory body, all of which may appear in any stages of the disease. In 3 cases only neurologic symptoms such as dysarthria and athetosis were found. Hemolytic anemia was another rare complication.

J Pathol Transl Med : Journal of Pathology and Translational Medicine