This Article Order Full text via Infotrieve Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Tatematsu, M. Articles by Farber, E. Search for Related Content PubMed PubMed Citation Articles by Tatematsu, M. Articles by Farber, E.

American Journal of Pathology, Vol 114, 418-430, Copyright © 1984 by American Society for Investigative Pathology

REGULAR ARTICLES

Studies on the proliferation and fate of oval cells in the liver of rats treated with 2-acetylaminofluorene and partial hepatectomy

M Tatematsu, RH Ho, T Kaku, JK Ekem and E Farber

The kinetics of oval cell proliferation in the liver and their fate were studied by combined autoradiography and immunohistochemical staining for epidermal prekeratin and epoxide hydrolase (EH). The oval cell proliferation was induced in rats by exposure to dietary 2- acetylaminofluorene (2-AAF) for 2 weeks with the midway performance of partial hepatectomy (PH). The labeling with 3H-thymidine [3H-TdR] was done in different groups of rats by two procedures: continuous exposure for 1 week with the aid of a minipump and brief exposure by the administration of a single dose. The livers of groups of animals were examined from 1 to 10 weeks after PH. Oval cells and duct epithelium showed positive staining for prekeratin and negative for EH, whereas hepatocytes showed the reverse pattern of staining. A critical finding was the observation that the exposure to the 2-AAF inhibited virtually completely the labeling of hepatocytes with [3H]-TdR in the caudate lobe and incompletely in the right lobe without interfering with the labeling of the oval cells in either lobe. This made it possible to study the fate of the oval cells vis-a-vis hepatocytes. This qualitative-quantitative study of oval cells and hepatocytes clearly indicates that oval cells under these experimental conditions do not become hepatocytes within 10 weeks. Over 80% of oval cells disappear within this period, and the remainder persist as such. These results indicate that under one set of experimental conditions related to hepatocarcino-genesis in the rat, no evidence for the conversion of oval cells to hepatocytes was obtained.

This article has been cited by other articles:

				Y N Kallis, M R Alison, and S J Forbes Bone marrow stem cells and liver disease Gut, May 1, 2007; 56(5): 716 - 724. [Full Text] [PDF]

				K. M. Braun, A. W. Thompson, and E. P. Sandgren Hepatic Microenvironment Affects Oval Cell Localization in Albumin-Urokinase-Type Plasminogen Activator Transgenic Mice Am. J. Pathol., January 1, 2003; 162(1): 195 - 202. [Abstract] [Full Text] [PDF]

				E. J. Croager, P. G.J. Smith, and G. C.T. Yeoh Ethanol interactions with a choline-deficient, ethionine-supplemented feeding regime potentiate pre-neoplastic cellular alterations in rat liver Carcinogenesis, October 1, 2002; 23(10): 1685 - 1694. [Abstract] [Full Text] [PDF]

				K. M. Braun and E. P. Sandgren Cellular Origin of Regenerating Parenchyma in a Mouse Model of Severe Hepatic Injury Am. J. Pathol., August 1, 2000; 157(2): 561 - 569. [Abstract] [Full Text] [PDF]