Skip Navigation

This Article
Right arrow Full Text (PDF)
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 arrow Search for citing articles in:
ISI Web of Science (31)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Walaszek, Z.
Right arrow Articles by Webb, T. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Walaszek, Z.
Right arrow Articles by Webb, T. E.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 1984 Oxford University Press

other

Inhibition of 7,12-dimethylbenzanthracene-induced rat mammary tumorigenesis by 2,5-di-O-acetyl-D-glucaro-1, 4:6,3-dilactone, an in vivo ß-glucuronidase inhibitor

Zbigniew Walaszek, Malgorzata Hanausek-Walaszek and Thomas E. Webb

Department of Physiological Chemistry and The Comprehensive Cancer Center, The Ohio State University Columbus, OH 43210, USA

2,5-Di-O-acetyl-D-glucaro-1,4:6,3-dilactone (DAGDL) is a slow release form of D-glucaro-1,4-lactone (GL), a non-toxic natural inhibitor of ß-glucuronidase. When administered orally to female rats in conjunction with a carcinogenic dose of 7,12-dimethylbenzanthracene (DMBA), this compound caused a 70% reduction in the number of rats with mammary tumors and 72% reduction in the number of mammary tumors per rat. Co-administration also reduces the induction by DMBA of a 60 kd oncofetal protein, previously shown to be associated with carcinogenesis and tumorigenesis. DAGDL administration depressed ß-glucuronidase activity both in the absence and presence of concurrent treatment with DMBA and also markedly reduced binding of DMBA to organ DNA. The anti-carcinogenic effect of DAGDL appears to be independent of route of administration of DMBA. It is proposed that inhibition of ß-glucuronidase increases the proportion of DMBA which is sequestered and excreted as the glucuronide and therefore unavailable for activation to the proximal carcinogen.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 J. Nutr.Home page
J. W. Lampe, S. S. Li, J. D. Potter, and I. B. King
Serum {beta}-Glucuronidase Activity Is Inversely Associated with Plant-Food Intakes in Humans
J. Nutr., June 1, 2002; 132(6): 1341 - 1344.
[Abstract] [Full Text] [PDF]

Home page
 Hum Exp ToxicolHome page
C. Sacco and E.J. Calabrese
Selective Inhibition of Gastrointestinal {beta}-Glucuronidase by Poly(vinylbenzyl D-glucaro(1,4)lactonate). Part 2. Poly(vinylbenzyl D-Glucaro(1,4) lactonate) In vitro Inhibition Studies
Human and Experimental Toxicology, January 1, 1994; 13(11): 759 - 763.
[Abstract] [PDF]


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.