The Effect of Ethanol on 3'-Methyl-4-dimethylaminoazobenzene Induced Carcinogenesis in Rat Liver.
- Author:
Chan Il PARK
;
Ho Guen KIM
;
So Young JIN
;
Woo Ick YANG
;
Yoo Bock LEE
- Publication Type:Original Article
- Keywords:
Hepatocarcinogenesis;
3'-Methyl-4-dimethylaminoazobenzene;
Ethanol;
Oval cell;
Cholangiofibrosis
- MeSH:
Male;
Humans;
Rats;
Animals;
Incidence
- From:Korean Journal of Pathology
1991;25(1):21-29
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
This study is aimed to elucidate the biological nature of the precancerous lesions and to evaluate whether the ethanol alters 3'-Methyl-4-dimethylaminoazobenzene (3'-Me-DAB) induced experimental hepatocarcinogenesis. A total of 108 Sprague-Dawley male rats were used for the experiment and divided into 6 groups according to 3'-Me-DAB and ethanol administration. Administration of the drugs were carried out daily by nasogastric tube insertion and the animals were sacrificed at different interval. A part of right lateral lobe was prepared for the histological examination. Cell kinetics of the immunohistochemical method for bromodeoxyuridine (BrdU). The administration of 3'-Me-DAB induced oval cell proliferation, hyperplastic nodule, cholangiofibrosis and carcinoma in the liver. The mean labelling indices, the percentages of BrdU labelled cells, of hepatocytes were increased by administration of 3'-Me-DAB, only to reverse after cessation of the drug (2.58 vs 0.61). The labelling indices of the oval cells were also affected by the administration and cessation of 3'-Me-DAB (11.41 vs 4.48). In contrast, the cholangiofibrosis did not decrease but were still increasing following cessation of 3'-Me-DAB administration (4.37 vs 5.17 and 8.25 vs 11.29). These finding that the hyperplastic nodule and particularly the cholangiofibrosis have an autonomous proliferative potential and are definite precancerous lesions in the experimental hepatocarcinogenesis. Short term administration of ethanol decreased the incidence of development of the precancerous lesions, but did not affect the labelling indices in all the pathologic lesions of hepatocarcinogenesis.
