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7,12-Dimethylbenz[a]anthracene
About: 7,12-Dimethylbenz[a]anthracene is a research topic. Over the lifetime, 1717 publications have been published within this topic receiving 40892 citations.
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18 citations
Journal Article•
TL;DR: The induction and subsequent growth of mammary carcinomas in female Sprague-Dawley rats is significantly enhanced by dividing oral exposures to 7,12-dimethylbenz(a)anthracene into 5 weekly doses, and it is slightly depressed by 5 doses given every other day, as compared with single doses.
Abstract: The induction and subsequent growth of mammary carcinomas in female Sprague-Dawley rats is significantly enhanced by dividing oral exposures to 7,12-dimethylbenz(a)anthracene into 5 weekly doses, and it is slightly depressed by 5 doses given every other day, as compared with single doses.
18 citations
TL;DR: The amounts of all three types of metabolites formed are much reduced by the presence of oestradiol and it is likely that the steroid acts by reducing the amounts of epoxide intermediates formed rather than by inhibiting the various reactions concerned in their further metabolism.
18 citations
TL;DR: It is concluded that the total administered dose of DMBA is a more important determinant of immunotoxicity than the length of exposure.
18 citations
TL;DR: The binding of 7,12-dimethylbenz[a]anthracene to DNA in intact cultured mouse embryo cells is not qualitatively influenced by concentration over a forty-fold dose range, suggesting limitations in the use of microsomal systems as models for target tissue activation.
Abstract: The nature of the metabolites of 7,12-dimethylbenz[a]anthracene (DMBA) binding to DNA in the presence of Aroclor-induced rat liver microsomes is not affected by the presence or absence of magnesium ions, but is dependent on the concentration of the hydrocarbon. At high concentrations of DMBA, the primary route of metabolic activation is through the K-region oxide while, at low concentrations of DMBA, activation is through other routes. A small proportion of these latter products elute from Sephadex LH-20 columns with mouse embryo cell [14C]DMBA-DNA adducts which are known to arise through reaction of the bay region diol-epoxide of DMBA with cellular DNA. In contrast to the dose-dependence of activation of DMBA by microsomes, the binding of this carcinogen to DNA in intact cultured mouse embryo cells is not qualitatively influenced by concentration over a forty-fold dose range. These findings suggest limitations in the use of microsomal systems as models for target tissue activation.
18 citations