Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
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 ISI Web of Science
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 arrow Search for citing articles in:
ISI Web of Science (3)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Lin, X.
Right arrow Articles by Campbell, T. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lin, X.
Right arrow Articles by Campbell, T. C.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Carcinogenesis, Vol. 20, No. 9, 1793-1799, September 1999
© 1999 Oxford University Press

Carcinogenesis

The promotion effect of anorectic drugs on aflatoxin B1-induced hepatic preneoplastic foci

Xu Lin2,3, David A. Levitsky, John M. King1 and T. Colin Campbell

Division of Nutritional Sciences and
1 Department of Pathology, Veterinary Medicine College, Cornell University, Ithaca, NY 14853, USA

The ability of three extensively used anorectic drugs, namely fenfluramine (FN), fluoxetine (FX) and amphetamine (AM), to alter the development of aflatoxin B1 (AFB1)-induced {gamma}-glutamyl-positive (GGT+) preneoplastic liver foci was investigated in 135 male weanling F344 rats. Following AFB1 administration, 15 rats were killed, while the rest were divided into four groups and fed diets containing either FN, FX, AM or control diet, with half of the animals in each group subsequently being killed at 4 weeks and half at 10 weeks. All three anorectic drugs as expected suppressed initial food intake, growth rate, body weight gain and food efficiency. They also tended to suppress body fat mass and to decrease plasma levels of T3 and T4. FN significantly (P < 0.05) increased GGT+ foci number/cm2 and number/cm3, while FX significantly increased GGT+ foci number/cm2 and the volume fraction of foci. Histopathological staining also revealed that FN- and FX-treated animals had more serious morphological alterations in their liver tissue. In contrast, foci development was, if anything, suppressed by AM feeding. These results indicate that serotoninergic drugs (FN and FX), as opposed to dopaminergic drugs (AM), may have tumor promoter activity, at least for liver tissue.

Abbreviations: AFB1, aflatoxin B1; AM, amphetamine; BAT, brown adipose tissue; DIT, diet-induced thermogenesis; FN, fenfluramine; FX, fluoxetine; GGT, {gamma}-glutamyltranspeptidase; GGT+, {gamma}-glutamyl-positive; H&E, hematoxylin and eosin; T3, triiodothryonine; T4, thyroxine.

2 Present address: Box 2619, Duke University Medical Center, Durham, NC 27710, USA

3 To whom correspondence should be addressed at: DUMC—2619/MSRB, Durham, NC 27710, USA Email: lin00026{at}mc.duke.edu


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.