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.

Anticarcinogenic and antilipidperoxidative effects of Tephrosia purpurea (Linn.) Pers. in 7, 12-dimethylbenz(a)anthracene (DMBA) induced hamster buccal pouch carcinoma

Abstract: Objectives: To investigate the chemopreventive potential and antilipidperoxidative effects of ethanolic root extract of Tephrosia purpurea (Linn.) Pers. (TpEt) on 7,12-dimethylbenz(a)anthracene (DMBA)- induced hamster buccal pouch carcinoma. Materials and Methods: Oral squamous cell carcinoma was developed in the buccal pouch of Syrian golden hamsters, by painting with 0.5% DMBA in liquid paraffin, thrice a week, for 14 weeks. The tumor incidence, volume and burden were determined. Oral administration of TpEt at a dose of 300 mg/kg, b.w., to DMBA (on alternate days for 14 weeks)- painted animals significantly prevented the incidence, volume and burden of the tumor. Results: TpEt showed potent antilipidperoxidative effect, as well as enhanced the antioxidant status in DMBA- painted animals. Conclusion: TpEt has potent chemopreventive efficacy and significant antilipidperoxidative effect, in DMBA-induced oral carcinogenesis. Further studies are needed to isolate and characterize the bioactive principle.

Inhibition of 7,12-Dimethylbenz(a)anthracene-induced Tumors in Syrian Hamsters by Prior Infection with H-1 Parvovirus

Abstract: Hamsters, given injections s.c. at birth of H-1 parvovirus and 1 month later given a single injection of 7,12-dimethylbenz(a)anthracene, had a 38% tumor incidence compared with a 95% incidence in animals receiving 7,12-dimethylbenz(a)anthracene alone. Thus, H-1 which, it has already been shown, invokes a resistance to the incidence of spontaneous and adenovirus-induced neoplasms in hamsters also produces a suppression of a carcinogen-induced tumor in these animals; this suggests that the H-1-induced barrier to successful oncogenesis by these diverse agents has a common mechanism which, present experiments indicate, is not related to a positive or negative H-1 serology. The pathology of the 7,12-dimethylbenz(a)anthracene-induced tumors was similar for both control and H-1-infected hamsters. Although all but one of the primary neoplasms were anaplastic fibrosarcomas as reported previously by others, 25% of the affected females had, in addition, mammary adenocarcinomas, an extremely rare tumor in hamsters.

Mechanism of metabolic activation of the potent carcinogen 7,12-dimethylbenz[a]anthracene

Abstract: The DNA adducts of 7,12-dimethylbenz[a]anthracene (DMBA) previously identified in vitro and in vivo are stable adducts formed by reaction of the bay-region diol epoxides of DMBA with dG and dA. In this paper we report identification of several new DMBA-DNA adducts formed by one-electron oxidation, including two adducts lost from DNA by depurination, DMBA bound at the 12-methyl to the N-7 of adenine (Ade) or guanine (Gua) [7-methylbenz[a]anthracene (MBA-12-CH2-N7Ade or 7-MBA-12-CH2-N7Gua, respectively]. The in vitro systems used to study DNA adduct formation were DMBA activated by horseradish peroxidase or 3-methyl-cholanthrene-induced rat liver microsomes. The biologically-formed depurination adducts were identified by high-pressure liquid chromatography and by fluorescence line narrowing spectroscopy. Stable DMBA-DNA adducts were analyzed by the 32P-postlabeling method. Quantitation of DMBA-DNA adducts formed by microsomes showed about 99% as depurination adducts: 7-MBA-12-CH2-N7Ade (82%) and 7-MBA-12-CH2-N7Gua (17%). Stable adducts (1.4% of total) included one adduct spot that may contain adduct(s) formed from the diol epoxide (0.2%) and unidentified adducts (1.2%). Activation of DMBA by horseradish peroxidase afforded 56% of stable unidentified adducts and 44% of depurination adducts, with 36% of 7-MBA-12-CH2-N7Ade and 8% of 7-MBA-12-CH2-N7Gua. Adducts containing the bond to the DNA base at the 7-CH3 group of DMBA were not detected.(ABSTRACT TRUNCATED AT 250 WORDS)

Aryl hydrocarbon hydroxylase, epoxide hydrase, and 7,12-dimethylbenz(a)anthracene-produced skin tumorigenesis in the mouse.

Abstract: Mouse skin tumorigenesis initiated by 7,12-dimethylbenz[ a ]anthracene and promoted by repeated applications of phorbol ester is unrelated to genetic diffrences in the extent of aryl hydrocarbon hydroxylase induction by polycyclic hydrocarbons in inbred or hybrid C57BL/6N and DBA/2N mice. Thus, if aryl metabolism of 7,12-dimethylbenz[ a ] anthracene is a necessary step in the initiation of chemical carcinogenesis, the constitutive level of the hydroxylase activity in the skin of these mice is sufficient, Levels of hepatic epoxide hydrase activity are the same among inbred and hybrid C57BL/6N and DBA/2N mice and, in contrast to the hydroxylase, are not inducible by 3-methylcholanthrene. Epoxide hydrase activity could not be detected in the skin of these mice. ACKNOWLEDGMENT We thank Francine Goujon and Noreen Morris for valuable technical assistance.