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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: The therapeutic property of D-Pinitol might be due to its strong antioxidant and remarkable induction in phase II and significant modulation in phase I drug metabolizing enzymes and prominent influence in the proteins of apoptotic, anti-apoptotic and tumor suppressors which ultimately end up with the consideration in the treatment of genotoxin mediated carcinogenesis.

17 citations

Journal ArticleDOI
TL;DR: The results of the present study confirm that OCs, such as dieldrin and CD, play a role in modifying PAH-induced carcinogenesis in fish.
Abstract: The present study examined whether modified xenobiotic transport, resulting from chlordecone (CD) or dieldrin pretreatment, would alter polycyclic aromatic hydrocarbon (PAH) or organochlorine (OC) target organ doses and subsequent tumor organo-specificity or incidence rates in rainbow trout. Additionally, the potential for exposure to dieldrin or CD, following PAH exposure, to enhance tumor incidence was assessed. Evaluation of CD pretreatment effects on [ 14 C]CD disposition in trout was conducted following two ip (0-15 mg/kg) and two dietary (0-0.4 mg/kg/d) pretreatment regimes. To assess the influence of OC pretreatment on cancer induced by the PAH 7,12-dimethyl-benz[a]anthracene (DMBA), juvenile trout were fed control, CD (0.1, 0.4 mg/kg/d), or dieldrin (0.1, 0.3 mg/kg/d) diets for 9 wk, received a waterborne [ 3 H]DMBA exposure (1 mg/L, 20 h), and resumed control, CD, or dieldrin diets for 33 wk. [ 3 H]DMBA disposition and hepatic [ 3 H]DMBA binding were examined immediately and 24 h after exposure. Hepatic and stomach tumor incidences were determined 33 wk after DMBA exposure. CD pretreatment did not influence [ 14 ]CD or [ 3 H]DMBA hepatic concentrations, hepatic [ 3 H]DMBA DNA binding, or hepatic/stomach tumor incidence. It did, however, elevate bile [ 14 C]CD and [ 3 H]DMBA concentrations. Postinititation exposure to CD weakly enhanced DMBA-induced hepatic tumor incidence at the low but not the high CD dose. Dieldrin pretreatment did not influence stomach [ 3 H]DMBA equivalents or stomach tumor incidence but did cause an elevation in biliary and hepatic concentrations of [ 3 H]DMBA equivalents. [ 3 H]DMBA binding to liver DNA was significantly increased and hepatic tumor incidence was elevated by dieldrin pretreatment. Dieldrin treatment following DMBA initiation did not enhance hepatic or stomach tumor incidence. Eco-epidemiology studies, to date, have reported correlations between the co-occurrence of PAHs and OCs and elevated tumor incidence in feral fish, but cause-and-effect relationships have been difficult to establish. The results of the present study confirm that OCs, such as dieldrin and CD, play a role in modifying PA H-induced carcinogenesis in fish.

17 citations

Journal Article
TL;DR: The derivatives of 7,12-dimethylbenz(a)anthracene produced in the different cultures were indistinguishable by thin-layer chromatography and by high-pressure liquid chromatography but differed in their relative proportions.
Abstract: Cultured mouse macrophages and tracheal and lung tissue each produced the same ethyl acetate-soluble derivatives of 7,12-dimethylbenz(a)anthracene (DMBA). The derivatives produced in the different cultures were indistinguishable by thin-layer chromatography and by high-pressure liquid chromatography but differed in their relative proportions. The greatest difference was seen between lungs and macrophages. The predominant metabolite produced by lungs was 8,9-dihydro-8,9-dihydroxy-7,12-dimethylbenz(a)anthracene, while macrophages produced equal quantities of both 8,9-dihydro-8,9-dihydroxy-7,12-dimethylbenz(a)anthracene and a second uncharacterized derivative, Metabolite B, at low DMBA doses ( 0.05 µg/ml medium). Macrophages released the majority of the ethyl acetate-soluble metabolites that they produced into the surrounding medium. With the exception of 8,9-dihydro-8,9-dihydroxy-7,12-dimethylbenz(a)anthracene, these derivatives were accumulated within tracheal and lung tissue when these organs were cocultivated with macrophages in the presence of DMBA.

16 citations

Journal Article
TL;DR: The results of animal experiments may serve as a basis for application of gene expression investigations as a screening method in humans because DMBA is a typical environmental carcinogen.
Abstract: Dimethylbenz[a]anthracene is a pluripotent carcinogenic chemical, which acts as an initiator by causing point mutations in certain oncogenes and tumor suppressor genes. Changes in their expression may be another possible area of investigation the carcinogenic effect of DMBA. Elevated expression of oncogenes was previously has been shown after treatment with carcinogenic compounds. In the present study, expression of c-myc, c-Ha-ras and p53 24 hours after a single dose treatment of DMBA in the spleen and in the liver of Long-Evans rats was investigated. Control animals were injected with the solvent corn oil only. We could not find any significant change on the transcriptional level of the investigated oncogenes in the liver. In the spleen, the overexpression of Ha-ras was 2-fold and c-myc was 3-fold higher in the DMBA-treated rats than in the corresponding control group. Since DMBA is a typical environmental carcinogen, the results of animal experiments may serve as a basis for application of gene expression investigations as a screening method in humans.

16 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20236
202215
202121
202018
201912
201823