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RECORD NUMBER: 6 OF 15

OLS Field Name OLS Field Data
Main Title Effects of Selenium on 7,12-Dimethylbenz(a)anthracene-Induced Mammary Carcinogenesis and DNA Adduct Formation.
Author Ip, C. ; Daniel, F. B. ;
CORP Author Health Effects Research Lab., Research Triangle Park, NC. ;Roswell Park Memorial Inst., Buffalo, NY.
Year Published 1985
Report Number EPA/600/J-85/155;
Stock Number PB86-101011
Additional Subjects Carcinogenesis ; Selenium ; Toxicology ; Deoxyribonucleic acids ; Metabolism ; Liver ; Enzymes ; Substitutes ; Malignant neoplasms ; Public health ; Human nutrition ; Laboratory animals ; Rats ; Chemical analysis ; Reprints ; Environmental health ; Benzanthracene/dimethyl
Holdings
Library Call Number Additional Info Location Last
Modified
Checkout
Status
NTIS  PB86-101011 Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy. 06/21/1988
Collation 7p
Abstract
The purpose of the present investigation was to determine the effects of dietary selenium deficiency or excess on 7,12-dimethylbenz(a)anthracene (DMBA)-induced mammary neoplasia in rats and to delineate whether selenium-mediated modification of mammary carcinogenesis was associated with changes in carcinogen: DNA adduct formation and activities of liver microsomal enzymes that are involved in xenobiotic metabolism. Results of this experiment indicated that selenium deficiency enhanced mammary carcinogenesis only when this nutritional condition was maintained in the postinitiation phase. Likewise, an excess of selenium intake inhibited neoplastic development only when this regimen was continued after DMBA administration. In either case, deficient or excess selenium at the time of carcinogenic insult failed to produce a significant effect on subsequent tumor yield, if selenium intake was returned to normal during the proliferative phase of tumor growth. Based on the results of these studies, it is suggested that selenium-mediated modification of mammary tumorigenesis is not exerted via alterations in carcinogenic initiation (i.e., metabolism or DNA adduct formation).