Skip Navigation



ToxSci Advance Access published online on February 23, 2005
Toxicological Sciences, doi:10.1093/toxsci/kfi128
This Article
Right arrow Advance Access manuscript (PDF) Freely available
Right arrow All Versions of this Article:
85/1/507    most recent
kfi128v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Bursch, W.
Right arrow Articles by Schulte-Hermann, R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bursch, W.
Right arrow Articles by Schulte-Hermann, R.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Toxicological Sciences © The Author 2005. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org
Received July 20, 2004
Accepted February 14, 2005

Carcinogenicity

No increase of apoptosis in regressing mouse liver after withdrawal of growth stimuli or food restriction

Wilfried Bursch 1*, Ute Wastl 1, Karin Hufnagl 1, and Rolf Schulte-Hermann 1

1 Medizinische Universität Wien, Univ. Klinik für Innere Medizin I Abtl. Institut für Krebsforschung, Borschkegasse 8a, A-1090 Wien

* To whom correspondence should be addressed.
Wilfried Bursch, E-mail: wilfried.bursch{at}meduniwien.ac.at


  Abstract

In short-term in vivo experiments, liver growth and regression in mice with high (C3H/He), intermediate (B6C3F1) or low (C57BL/6J) susceptibility to hepatocarcinogenesis was compared. Liver growth was induced by dietary administration of phenobarbital (PB; 750 ppm) or nafenopin (NAF; 500 ppm). The following results were obtained:

1. PB or NAF treatment for 7 days produced moderate increases of liver DNA (15% or 25-28%, resp.) along with pronounced hypertrophy. Liver growth was strongest in C3H/He mice.

2. Cessation of PB or NAF treatment led to a rapid regression of liver hypertrophy. However, the enhanced hepatic DNA content persisted for at least 2 weeks in all mouse strains.

3. Apoptosis was not increased at any time after cessation of treatment in all strains.

4. Food restriction to 60% of the ad libitum intake did neither amplify regression of liver hyperplasia nor the occurrence of apoptosis.

In conclusion, the highly susceptible C3H/He mice exhibited the strongest liver growth response to PB. No strain difference in the occurrence of apoptosis was detected. Mouse hepatocytes in liver regressing after mitogen withdrawal do not enter apoptosis as readily as rat hepatocytes.

Keywords: Phenobarbital; Nafenopin; C3H/He; B6C3F1; C57Bl/6J; liver weight; protein content; DNA content; DNA synthesis; apoptosis.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.