Document Detail

Synergistic effect of vitamin E and selenium in the chemoprevention of mammary carcinogenesis in rats.
MedLine Citation:
PMID:  6413056     Owner:  NLM     Status:  MEDLINE    
The present study showed that vitamin E, although ineffective by itself, was able to potentiate the ability of selenium to inhibit the development of mammary tumors induced by dimethylbenz(a)anthracene (DMBA) in rats. Animals were maintained on a high-polyunsaturated fat (20% corn oil) diet in order to increase the degree of oxidant stress; additional selenium and/or vitamin E were present at a concentration of 2.5 and 1000 mg/kg of diet, respectively. It should be noted that rats tolerated these levels of supplementation very well with no obvious undesirable effect. Furthermore, our results indicated that vitamin E facilitated the anticarcinogenic action of selenium only when it was present during the proliferative phase. We then proceeded to examine whether DMBA administration would lead to any persistent damage in tissue peroxidation or changes in activities of enzymes associated with peroxide metabolism. It was found that DMBA resulted in an acute but modest increase in lipid peroxidation at 24 hr after carcinogen treatment. This perturbation was only of a transient nature. By comparing the response in a target tissue (mammary fat pad) and a non-target tissue (liver), it can be inferred that DMBA may have a differential effect on the degree of oxidant stress. The antagonistic effect of selenium and vitamin E in suppressing lipid peroxidation was then evaluated. Several conclusions can be drawn regarding the antioxidant potency of these agents in conjunction with their efficacies in cancer prevention. First, although vitamin E is a more effective antioxidant than selenium, it is apparent that systemic suppression of lipid peroxidation by vitamin E subsequent to a carcinogenic insult is not sufficient to inhibit tumor formation. Vitamin E supplementation increases significantly the microsomal hydroperoxidase activity. At the present time, it is unclear what role, if any, this enzyme plays in the synergistic effect of vitamin E and selenium in the inhibition of tumorigenesis. Secondly, the anticarcinogenic action of high levels of selenium is not related to its biochemical function in the regulation of the selenium-dependent glutathione peroxidase. The explanation for this is that the enzyme is already operating at near maximal capacity under normal physiological conditions. Additional selenium will not further increase its activity, since the enzyme protein becomes the limiting factor. Finally, vitamin E may be able to provide a more favorable climate against oxidant stress, thereby potentiating the action of selenium via some other mechanism.
P M Horvath; C Ip
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Cancer research     Volume:  43     ISSN:  0008-5472     ISO Abbreviation:  Cancer Res.     Publication Date:  1983 Nov 
Date Detail:
Created Date:  1983-11-23     Completed Date:  1983-11-23     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  2984705R     Medline TA:  Cancer Res     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  5335-41     Citation Subset:  IM    
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MeSH Terms
Adipose Tissue / metabolism
Drug Synergism
Lipid Peroxides / metabolism
Liver / metabolism
Mammary Neoplasms, Experimental / physiopathology,  prevention & control*
Rats, Inbred Strains
Selenium / therapeutic use*
Vitamin E / therapeutic use*
Grant Support
Reg. No./Substance:
0/Lipid Peroxides; 1406-18-4/Vitamin E; 57-97-6/9,10-Dimethyl-1,2-benzanthracene; 7782-49-2/Selenium

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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