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.

Acid lability of the hydrocarbon-deoxyribonucleoside linkages in 7,12-dimethylbenz[a]anthracene-modified deoxyribonucleic acid.

Abstract: DNA containing bound radioactive 7,12-dimethylbenz[a]anthracene was isolated from mouse fetal cell cultures exposed to this carcinogen. The carcinogen-deoxyriboside adducts within the DNA were found to be sensitive to acid-catalyzed hydrolysis. Adducts derived from reaction of a syn-dihydrodiol epoxide with deoxyadenosine residues in DNA were the most sensitive to acid and were hydrolyzed to yield a 1,2,3,4-tetrahydrotetraol of 7,12-dimethylbenz[a]anthracene under mild conditions. The structure of this tetraol was established by synthesis and mass spectrometry. Although definitive structures cannot be assigned at present to the nucleic acid adducts of this potent carcinogen, the present findings confirm and extend earlier work assigning partial structures to the major adducts.

Regression of progestin-accelerated 7,12-dimethylbenz[a]anthracene-induced mammary tumors in Sprague-Dawley rats by p53 reactivation and induction of massive apoptosis: a pilot study.

Abstract: p53 Reactivation and induction of massive apoptosis (PRIMA-1) is a small-molecule compound that reactivates mutant p53, restoring its normal tumor suppressor function. PRIMA-1 effectively suppresses the growth of homogeneous p53-deficient tumor xenografts in immunosuppressed mice; however, the ability of PRIMA-1 to suppress the growth of mammary tumors in rodents and other species is not well characterized. Here, we examined the ability of PRIMA-1 to suppress the growth of 7,12-dimethylbenz[a]anthracene (DMBA)-induced and progestin-accelerated DMBAinduced mammary tumors in Sprague‐Dawley rats. Mammary tumors were induced in female rats with DMBA or DMBA plus progestin treatment. After tumors had reached 5‐25 mm 2 in size, PRIMA-1 was administered twice a day for 3 days via tail vein injection (20 or 50 mg/kg). Tumor size was monitored every day following PRIMA-1 for at least 15 days prior to killing. PRIMA-1 caused regression of w40% of progestin-accelerated DMBA-induced mammary tumors, but did not induce regression of native non-progestin-accelerated DMBA-induced tumors. Importantly, PRIMA-1 also suppressed the emergence of any new progestin-accelerated tumors in this model. Immunological studies with an antibody that selectively reacts with mutant p53 suggested that none of the native DMBA-induced tumors expressed mutant p53. By contrast, six out of eight progestin-accelerated DMBA-induced tumors stained for mutant p53 protein. In PRIMA-1-treated tumor-bearing rats, tumor regression correlated with conversion of mutant to wild-type p53 conformation, reduced expression of vascular endothelial growth factor and estrogen receptor, lack of blood vessel perfusion, increased expression of p21, and massively increased expression of anti-angiogenic protein, secreted protein acidic and rich in cysteine. These pre-clinical results suggest that PRIMA-1, as a single agent or in combination with other anti-cancer compounds, has potential as a novel chemotherapeutic treatment for progestin-accelerated human breast cancer.

Synthesis of trans-3,4-dihydroxy-3,4-dihydro-7,12-dimethylbenz[a]anthracene, a highly carcinogenic metabolite of 7,12-dimethylbenz[a]anthracene

Abstract: Das Benzanthracen (I) wird in die isomeren Hydroxyderivate (II) ubergefuhrt, deren Oxidation nach Swern die isomeren Ketone (IIIa) und (IIIb) liefert, die chromatographisch getrennt werden.

Clerodendron inerme Protects Cellular Integrity During 7,12- Dimethylbenz[A]-Anthracene Induced Hamster Buccal Pouch Carcinogenesis

Abstract: Aim of the present study was to investigate the protective effect of Clerodendron inerme on cellular integrity by measuring the status of glycoconjugates, lipids, osmotic fragility, and membrane bound enzyme activity in 7, 12-dimethylbenz (a) anthracene (DMBA)-induced oral carcinogenesis. Oral squamous cell carcinoma was induced in the buccal pouch of Syrian golden hamsters by painting with 0.5% DMBA in liquid paraffin thrice a week for 14 weeks. The levels of glycoconjugates, lipids, osmotic fragility and membrane bound enzyme activity were analyzed by using specific colorimetric methods. We observed 100% tumor formation in DMBA painted hamsters. Altered glycoconjugates and lipid pattern were observed in DMBA painted hamsters as compared to control hamsters. Erythrocytes from DMBA painted hamsters were more fragile than those from control hamsters. The activity of membrane bound enzyme (Na+ K+ ATPase) decreased in DMBA painted hamsters as compared to control hamsters. Oral administration of aqueous leaf extract of Clerodendron inerme (CiALet) at a dose of 500mg/kg body weight significantly prevented the tumor formation and histopathological abnormalities as well as normalized the above said biochemical variables in DMBA painted hamsters. Our results thus demonstrate the protective effect of Clerodendron inerme on cellular integrity during DMBA induced oral carcinogenesis.

Chemopreventive effect of syringic acid on 7,12-dimethylbenz(a)anthracene induced hamster buccal pouch carcinogenesis.

Abstract: Oral squamous cell carcinoma is most prevalent and refractory cancers worldwide. Recently, chemoprevention could be a promising approach in developing countries. The present study investigates the ...