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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: Evidence was obtained that in combination glucarate may play an adjuvant role, with the retinoid as the effector, and ineffective sub-optimal dosages of glucarate and 13-cis-retinoic acid interacted synergistically to inhibit the growth in vitro of the MCF-7 human breast cancer cells.
13 citations
TL;DR: 9-Hydroxyellipticine (9-hydroxy-5,11-dimethyl-6-H-pyrido[4,3b]carbazole), a potent inhibitor of monooxygenases, strongly inhibits the initiation of skin tumors by 7,12-dim methylbenz[a]anthracene (DMBA) in male NMRI Swiss mice.
13 citations
TL;DR: Isoflavone intake significantly inhibited the development of premenopausal and postmenopausal mammary tumors in normal rats and ovariectomized rats compared with control group.
Abstract: To determine the associations between isoflavone (49.72% genistin, 5.32% daidzin, 34.54% glycitin) and breast cancer risk, 150 rats were given 5 mg 7,12-dimethylbenz(a)anthracene and half of them were ovariectomized. Then normal rats and ovariectomized rats were divided into 5 groups: control group, isoflavone high (HI), middle (MI), or low (LI) dose group consuming 100, 500, or 1000 mg isoflavones/kg diet, estrogen group (2.5 mg stilboestrol/kg diet). After 24 weeks, tumor incidences were 73% in control group, 7% in HI, 7% in MI, 27% in LI, and 80% in estrogen group for normal rats; 60% in control group, 13% in HI, 7% in MI, 13% in LI, and 73% in estrogen group for ovariectomized rats. Isoflavone treatment decreased tumor incidence and mean tumor number per rat and increased mean latent period compared with those in control group and estrogen group group significantly (p<0.05). The mRNA and protein expression of estrogen receptor β were significantly higher in isoflavone treatment groups than those in control group group. Moreover, isoflavone treatment significantly decreased 8-hydroxydeoxyguanosine content and increased superoxide dismutase level in normal rats and decreased malondialdehyde concentrations in ovariectomized rats compared with control group. In conclusions, isoflavone intake significantly inhibited the development of premenopausal and postmenopausal mammary tumors.
13 citations
TL;DR: None of the three applied doses induced aneuploidy under conditions leading to an increase in tumors and/or chromosomal damage in keratinocyte cultures derived from HRA/Skh mice after single in vivo applications of DMBA.
Abstract: Micronucleus induction, chromosomal damage and aneuploidy were evaluated in whole skin keratinocyte cultures derived from HRA/Skh mice after single in vivo applications of 0.256, 2.56 and 25.6 μg (1, 10 and 100 nmoles) of the carcinogen, 7,12-dimethylbenz[ a ]anthracene (DMBA). These genotoxicity end-points were compared with papilloma and carcinoma occurrence at the same dose levels of carcinogen. While the lower 2 doses of DMBA significantly increased the incidence of micronuclei and other chromosomal anomalies in keratinocytes, the two highest doses resulted in a significantly increased papilloma yield (0.297 and 3.895 papillomas/mouse) and incidence (24.3 and 100%). Carcinomas appeared only at the highest dose (0.125 carcinomas/mouse; 5% incidence). Neither papillomas nor carcinomas occurred in solvent-treated control mice. None of the three applied doses induced aneuploidy under conditions leading to an increase in tumors and/or chromosomal damage.
13 citations
TL;DR: The results of the present study suggest that the chemopreventive effect of coumarin is probably due to its anti-lipid peroxidative potential and modulating effect on carcinogen detoxification agents in favor of the excretion of ultimate carcinogenic metabolites of DMBA during DMBA-induced hamster buccal pouch carcinogenesis.
Abstract: The aim of the present study was to investigate the chemopreventive effect of coumarin against 7, 12-dimethylbenz[a]anthracene (DMBA)-induced hamster buccal pouch carcinogenesis by monitoring tumor incidence and histopathological changes as well as by analyzing the status of biochemical markers (lipid peroxidation, enzymatic and non-enzymatic antioxidants, phase I and phase II detoxification enzymes). Oral squamous cell carcinomas were induced in the buccal pouch of Syrian golden hamsters by painting with 0.5% DMBA in liquid paraffin three times a week for 14 weeks. We noted 100% tumor formation with marked abnormalities in the biomarkers status in hamsters treated with DMBA alone. Oral administration of coumarin at a dose of 100 mg/kg body weight (bw) to DMBA treated hamsters completely prevented the tumor formation as well as restored the staus of biochemical variables. The results of the present study thus suggest that the chemopreventive effect of coumarin is probably due to its anti-lipid peroxidative potential and modulating effect on carcinogen detoxification agents in favor of the excretion of ultimate carcinogenic metabolites of DMBA during DMBA-induced hamster buccal pouch carcinogenesis.
13 citations