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| Research article summary (published 29 Jun 2006): |
Dietary supplementation of resveratrol suppresses colonic tumour incidence in 1,2-dimethylhydrazine-treated rats by modulating biotransforming enzymes and aberrant crypt foci development.
Full Abstract
Diet-induced changes in the activities of bacterial enzymes are known to play a role in colon cancer development. Resveratrol has been implicated as a protective agent in carcinogenesis. In the present study, the effect of resveratrol on the activities of faecal and colonic biotransforming enzymes such as beta-glucuronidase, beta-glucosidase, beta-galactosidase, mucinase, nitroreductase and faecal sulfatase activity was assessed. The total number of aberrant crypt foci and their distribution in the proximal, medial and distal colon were observed in 1,2-dimethylhydrazine (DMH)-induced rats (group 3) and other treatment groups (groups 4-6). DMH (0.02 g/kg body weight) was given subcutaneously once a week for 15 consecutive weeks, and the experiment was terminated at 30 weeks. DMH-treated rats showed elevated levels of cancer-associated bacterial enzyme activities, whereas on resveratrol supplementation in three different regimens, rats showed lowered activities. Resveratrol supplementation throughout the experimental period (group 6) exerted a more pronounced effect (P < 0.01) by modulating the development of aberrant crypt foci and the activities of bacterial enzymes than did the other treatment regimens (groups 4 and 5). Thus, the present results demonstrate the inhibitory effect of resveratrol on DMH-induced colon carcinogenesis in rats.
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Author information
Author/s: Sengottuvelan, Murugan (M); Nalini, Namasivayam (N);
Affiliation: Department of Biochemistry and Biotechnology, Annamalai University, Annamalainagar - 608 002, Tamilnadu, India.
Journal and publication information
Publication Type: Journal Article; Research Support, Non-U.S. Gov't
Journal: The British journal of nutrition (Br J Nutr), published in England. (Language: eng)
Reference: 2006-Jul; vol 96 (issue 1) : pp 145-53
Dates: Created 2006/07/27; Completed 2006/08/22; Revised 2006/11/15;
PMID: 16870003, status: MEDLINE (last retrieval date: 12/26/2008)
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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