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.

Induction of experimental mammary carcinogenesis in rats with 7,12-dimethylbenz(a)anthracene

Abstract: PURPOSE: To test an experimental model of chemical mammary carcinogenesis induction in rats. METHODS: Twenty young virgin Sprague-Dawley female rats, aged 47 days, received 20 mg of 7,12-dimethylbenz(a)anthracene (DMBA) intragastrically by gavage. Afterwards, at 8 and 13 weeks, their mammary glands were examined. At the end of the experiment, the animals were sacrificed, and the mammary tumors were measured and weighed. Tumor fragments were analyzed using light microscopy. RESULTS: Eight weeks after DMBA injection, 16 rats presented at least 1 breast tumor (80%). After 13 weeks, all of them (100%) developed breast carcinomas that were confirmed by histopathological analysis. CONCLUSION: This experimental animal model of chemical mammary induced carcinogenesis is feasible and can be used in further experiments on the role of tumorigenic biomodulator substances.

Predominant role of prolactin in stimulating the growth of 7, 12-dimethylbenz(a)anthracene-induced rat mammary tumor.

Abstract: Summary The effect of prolactin in supporting the growth of 7,12-dimethylbenz(a)anthracene-induced mammary tumor in adult female Sprague-Dawley rats was investigated when estrogen receptors were blocked by the nonsteroidal antiestrogen, Tamoxifen, ICI 46,474 Following an oophorectomy-induced remission, perphenazine, which stimulates endogenous prolactin release, was able to restore tumor growth whether or not Tamoxifen was added A second course of perphenazine treatment, instituted after the tumors were allowed to shrink, was again effective in stimulating tumor growth After a regression in tumor size induced by oophorectomy and daily administration of Tamoxifen, perphenazine was able to restore original tumor size despite continued treatment with Tamoxifen In intact rats, after regression was obtained by daily administration of Tamoxifen and the prolactin inhibitor, lergotrile mesylate, perphenazine induced tumor growth when the latter was discontinued, even though Tamoxifen was continued for 50 days Estrogen receptors measured at the time of maximum stimulation by perphenazine were undetectable On the other hand, estradiol did not stimulate tumor growth when serum prolactin was depressed to undetectable levels by lergotrile These results indicate that prolactin supports the growth of 7,12-dimethylbenz(a)anthracene-induced rat mammary tumor and that estrogen receptors are not required under these conditions

Products of Binding of 7,12-Dimethylbenz(a)anthracene to DNA in Mouse Skin

Abstract: 7,12-Dimethylbenz( a )anthracene (DMBA):deoxyribonucleoside-adducts, from enzymatic hydrolysis of DNA from mouse skin exposed to [3H]DMBA in vivo , were analyzed by reversephase high-pressure liquid chromatography. Double-labeling studies showed that the adducts were qualitatively identical to those formed in mouse embryo cell cultures. These have been tentatively identified as bay-region anti -dihydrodiol epoxide: deoxyguanosine- and :deoxyadenosine adducts and a bay-region syn -dihydrodiol epoxide:deoxyadenosine-adduct (where the terms syn and anti define dihydrodiol-epoxides wherein the benzylic hydroxyl group and epoxide oxygen are cis or trans to one another, respectively). The relative amounts of individual adducts did not vary substantially with time or with the sex of the mice. However, the syn -dihydrodiol-epoxide:deoxyadenosine-adduct did increase with dose and constituted as much as 40% of the total DNA binding at high doses of DMBA. This is in contrast to the much lower (2 to 3%) levels of binding to deoxyadenosine residues in mouse skin reported for the less potent tumor initiator benzo( a )pyrene. The greater reactivity of DMBA with deoxyadenosine residues in mouse skin may play a role in determining its greater tumor initiating potential.

Dehydroepiandrosterone (DHEA) and 3β-methylandrost-5-en-17-one: inhibitors of 7,12-dimethylbenz[a]anthracene (DMBA)-initiated and 12-O-tetradecanoylphorbol-13-acetate (TPA)-promoted skin papilloma formation in mice

Abstract: Long-term oral administration of the adrenal steroid, dehydroepiandrosterone (DHEA), has previously been shown to inhibit the development of spontaneous breast cancer and chemically induced lung and colon tumors in various mouse strains. In the two-stage skin papilloma system in the mouse, topical application of DHEA inhibits both 7,12-dimethylbenz[a]anthracene initiation and 12-O-tetradecanoylphorbol-13-acetate promotion of these tumors. The synthetic steroid, 3 beta-methylandrost-5-en-17-one, which, unlike DHEA, is not demonstrably estrogenic in the rat, also inhibits papilloma development.

Embryotoxic effects of benzo[a]pyrene, chrysene, and 7,12-dimethylbenz[a]anthracene in petroleum hydrocarbon mixtures in mallard ducks.

Abstract: Studies with different avian species have revealed that surface applications of microiiter amounts of some crude and fuel oils that coat less than 10% of the egg surface result in considerable reduction in hatching with teratogenicity and stunted growth. Other studies have shown that the embryotoxicity is dependent on the aromatic hydrocarbon content, further suggesting that the toxicity is due to causes other than asphyxia. In the present study the effects of three polycyclic aromatic hydrocarbons identified in petroleum were examined on mallard (Anas platyrhynchos) embryo development. Addition of benzo[a]‐pyrene (BaP), chrysene, or 7,12‐dimethylbenz[a]anthracene (DMBA) to a synthetic petroleum hydrocarbon mixture of known composition and relatively low embryotoxicity resulted in embryotoxicity that was enhanced or equal to that of crude oil when 10 μl was applied externally to eggs at 72 h of development. The order of ability to enhance embryotoxicity was DMBA > BaP > chrysene. The temporal pattern of e...