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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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TL;DR: It is shown that ovarian progesterone, acting either directly or in synergism with prolactin, is necessary for the growth of chemically-induced mammary tumors during lactation, as most growing tumors regressed after cessation of hormone treatment.
Abstract: Summary The endocrine factors affecting postpartum growth of mammary tumors were studied in Sprague-Dawley female rats bearing 7,12-dimethylbenz(a)anthracene-induced mammary tumors. The majority of tumors were classified as mammary adenocarcinomas, but a few mammary fibroadenomas and “mixed” tumors were also observed. All rats developed tumors during pregnancy and all tumors grew rapidly until parturition. Ovariectomy performed on Day 2 of lactation abolished the stimulatory effect of suckling on tumor growth in rats nursing 6 pups. While the daily administration of 1 mg progesterone/day to ovariectomized lactators resulted in growth of only a few tumors, daily administration of 6 mg progesterone stimulated growth of nearly 50% of the tumors during the postpartum period. Administration of either bovine or ovine prolactin to non-nursed, tumor-bearing rats for 25 days postpartum stimulated tumor maintenance and growth to varying degrees, depending upon the dose. The stimulatory action of prolactin on tumor growth was abolished by ovariectomy performed on Day 2 postpartum. Tumor growth was dependent on the continuance of the hormone treatment, as most growing tumors regressed after cessation of hormone treatment. These data indicate that ovarian progesterone, acting either directly or in synergism with prolactin, is necessary for the growth of chemically-induced mammary tumors during lactation.
23 citations
TL;DR: Calcium glucarate and N-(4-hydroxyphenyl)retinamide were evaluated individually and in combination in the diet as preventative chemical agents, by using the induction of rat mammary tumors by 7,12-dimethylbenz[a]anthracene as the test system.
Abstract: Calcium glucarate and N-(4-hydroxyphenyl)retinamide were evaluated individually and in combination in the diet as preventative chemical agents, by using the induction of rat mammary tumors by 7,12-dimethylbenz[a]anthracene as the test system. When tested separately over 18 weeks, optimal doses of calcium glucarate (128 mmol/kg of diet) or N-(4-hydroxyphenyl)retinamide (1.5 mmol/kg of diet) administered daily inhibited tumor incidence by 50% or 57% and tumor multiplicity by 50% or 65%, respectively. Suboptimal doses of calcium glucarate (32 mmol/kg) and of N-(4-hydroxyphenyl)retinamide (0.75 mmol/kg) inhibited tumor incidence by 15% and 5% but had no inhibitory effect on tumor multiplicity. In contrast, the combination of calcium glucarate (32 mmol/kg) and N-(4-hydroxyphenyl)retinamide (0.75 mmol/kg) inhibited tumor incidence and tumor multiplicity by 50%. Similar synergism was observed with the combination of calcium glucarate (64 mmol/kg) and N-(4-hydroxyphenyl)retinamide (0.75 mmol/kg), the inhibition being 55-60%. HPLC analysis of the bile of female rats injected intraperitoneally with a single dose of the retinamide [60 mg/kg (body weight)] showed that the excretion of the retinamide and its glucuronide were markedly suppressed by pretreatment with an oral dose of calcium glucarate [4.5 mmol/kg (body weight)].
23 citations
23 citations
TL;DR: These findings not only demonstrate that the epithelial P450 enzymes play important roles in the clearance of DMBA, but also suggest that P 450 enzymes in both mammary epithelial and stromal cells contribute to carcinogen-mediated DNA damage.
23 citations
Journal Article•
TL;DR: Results indicate that, in contrast to its effects with other carcinogens in other tissues, ellagic acid is not a potent inhibitor of DMBA metabolism, DNA-binding and carcinogenicity with rat mammary tissue.
Abstract: Naturally-occurring components of the human food supply have recently received attention as possible agents for cancer chemoprevention. The plant phenol ellagic acid has been reported to be an effective inhibitor of carcinogen metabolism and certain chemically-induced tumors. Therefore, we evaluated the efficacy of ellagic acid in inhibiting DMBA metabolism, DNA-binding and the initiation of DMBA-induced carcinogenesis in rat mammary tissue. Mammary epithelial cell aggregates were isolated from rats fed control and ellagic acid (0.4 and 0.8%) containing diets. When incubated with DMBA, aggregates from ellagic acid-fed rats exhibited a significant but modest inhibition of DMBA metabolism and DNA-binding. An inhibition of DMBA-DNA binding and DMBA metabolism in secondary cultures of mammary epithelial cells also was detected only when ellagic acid was added at 150 molar excess compared to DMBA. The feeding of ellagic acid (0.8%) to rats for 28 days prior to the administration of DMBA resulted in a 21% reduction in mammary tumor incidence at 21 weeks which was, however, not statistically significant. Together, these results indicate that, in contrast to its effects with other carcinogens in other tissues, ellagic acid is not a potent inhibitor of DMBA metabolism, DNA-binding and carcinogenicity with rat mammary tissue.
22 citations