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Enhancement by ethyl alcohol of experimental hepatocarcinogenesis induced by N ‐nitrosomorpholine
Author(s) -
Tatsuta Masaharu,
Iishi Hiroyasu,
Baba Miyako,
Yano Hiroyuki,
Iseki Kazushige,
Uehara Hiroyuki,
Nakaizumi Akihiko
Publication year - 1997
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19970611)71:6<1045::aid-ijc21>3.0.co;2-b
Subject(s) - ornithine decarboxylase , endocrinology , medicine , glutathione , alcohol , glutathione s transferase , ethanol , saline , enzyme , chemistry , biology , biochemistry
The effects of ethyl alcohol (EtOH) during or after treatment with N ‐nitrosomorpholine (NNM) on hepatocarcinogenesis, ornithine decarboxylase (ODC) activity and the labeling index of the liver were investigated in male Sprague‐Dawley rats. Rats were given drinking water containing NNM for 8 weeks and received i.p. injections of 1 g EtOH/kg body weight every other day during or after treatment with NNM. Pre‐neoplastic and neoplastic lesions staining positively for glutathione‐S‐transferase, placental type (GST‐P), were examined immunohistochemically. At the end of experiment at week 16, administration of EtOH after NNM treatment had no significant effect on the number and size of GST‐P‐positive hepatic lesions, whereas administration of EtOH during NNM treatment significantly increased the number and percentage area but not the mean area of GST‐P‐positive hepatic lesions. EtOH caused significant increases in the ODC activity of the liver and in the labeling indices of enzyme‐altered lesions and the adjacent hepatocytes after the cessation of EtOH administration but not during EtOH treatment. Our findings indicate that EtOH enhances hepatocarcinogenesis and suggest that this effect may be closely related to the increases in ODC activity and cell proliferation in enzyme‐altered lesions and the adjacent liver after EtOH treatment. Int. J. Cancer 71: 1045‐1048, 1997. © 1997 Wiley‐Liss Inc.