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.

Inhibition by Cysteamine-HCl of Oncogenesis Induced by 7,12-Dimethylbenz(a)anthracene without Affecting Toxicity

Abstract: The effects of cysteamine-HCl, a radical scavenger, on 7,12-dimethylbenz(a)anthracene-induced toxicity and oncogenesis were studied in vitro and in vivo . While the addition of cysteamine-HCl to mouse fibroblasts (M2 line) prior to and after the addition of 7,12-dimethylbenz(a)anthracene did not affect the carcinogen-induced toxicity (reduced plating efficiency), the number of transformed foci was markedly reduced. In vivo , the i.p. administration of cysteamine-HCl to Sprague-Dawley rats, prior to and following the injection of 7,12-dimethylbenz(a)anthracene i.v., did not affect the carcinogen-induced adrenal necrosis and lesions of the small intestinal epithelium. Similar treatment did, however, markedly reduce the number of mammary tumors formed. These results suggest that the toxic and oncogenic changes induced by 7,12-dimethylbenz(a)anthracene are due to two different metabolites, and support the concept that the latter effect may be mediated by a radical.

Effects of 7,12‐dimethylbenz[A]anthracene on immune function and mixed‐function oxygenase activity in the european starling

Abstract: Immune function and hepatic MFO activity were examined in adult and nestling starlings administered a synthetic PAH, 7,12-dimethylbenz[a]anthracene (DMBA). Methods used to examine the starling immune system included immunopa-thology, macrophage phagocytosis, lymphocyte blastogenesis to concanavalin A, and hemagglutination of sheep erythrocytes (SRBC). Concomitant investigations of MFO activity were conducted in starlings exposed to DMBA. Ethoxyresorufin O-dealkylase (EROD) and pentoxyresorufin O-depentylase (PROD) were used as indicators of hepatic MFO activity. Changes in MFO activity were compared to chemically altered immune responses following DMBA exposure. Subcutaneous exposure of adult starlings to 125 mg/kg DMBA resulted in suppression of lymphocyte blastogenesis and antibody production to SRBC. EROD and PROD activity were increased 2.8- and 3.4-fold, respectively. Lymphocyte blastogenesis was impaired in adult starlings orally exposed to 125 mg/kg DMBA. The immune system of nestling starlings exposed orally to 100 mg/kg DMBA was altered, as evidenced by decreased phagocytic ability of macrophages and inhibition of lymphocyte blastogenesis. Oral exposure to DMBA did not induce MFO activity in starlings of either age class. Effects of DMBA on immune function and MFO activity in starlings varied with the age of birds and route and length of chemical exposure.

Characterization of adenocarcinomas of the dorsolateral prostate induced in Wistar rats by N-methyl-N-nitrosourea, 7,12-Dimethylbenz(a)anthracene, and 3,2'-Dimethyl-4-aminobiphenyl, following sequential treatment with cyproterone acetate and testosterone propionate

Abstract: Carcinomas of the rat prostate induced by a single injection of N-methyl-N-nitrosourea, 7,12-dimethylbenz(a)anthracene, and 3,2'-dimethyl-4-aminobiphenyl, after sequential treatment with cyproterone acetate and testosterone propionate, were evaluated as potential animal model for prostatic cancer. All ten carcinomas examined were located in the dorsolateral prostate region and did not involve the distal parts of the seminal vesicle and coagulating glands. The incidence of urinary obstruction leading to the animals' death was 6 of 10 rats, and metastases in the lung, abdominal lymph nodes, and/or liver also occurred in 6 of 10 rats. The tumors were invasive adenocarcinomas, showing frequent perineural invasion and a variable degree of differentiation. There were ultrastructural similarities with human prostatic carcinoas, such as intracellular lumina. Plama acid phosphatase was increased. Enzyme histochemical analysis revealed similarities with the Dunning R3327H and -HI prostatic carcinomas but was not helpful in determining the site or origin of the tumors. The gross and microscopic appearance of the tumors and the observation of preneoplastic lesions exclusively located in the dorsolateral prostate suggest this lobe as site origin of the carcinomas. Preneoplastic lesions (n = 9) included atypical hyperplasias (n = 5) and lesions with all histological characteristics of carcinoma except for local invasion and metastases, which were classified as carcinoma in situ (n = 4). Although androgen sensitivity could not be assessed, the observed characteristics of the tumors [their long latency time (46-80 weeks), the presence of preneoplastic lesions, and the short duration of the treatment, leaving the animals intact] all indicate that the present approach is a valid animal model for the study of prostatic carcinogenesis. Chemicals/CAS: cyproterone acetate, 427-51-0; testosterone propionate, 57-85-2; 2',3-dimethyl-4-aminobiphenyl, 13394-86-0; 9,10-Dimethyl-1,2-benzanthracene, 57-97-6; Acid Phosphatase, EC 3.1.3.2; Aminobiphenyl Compounds; Methylnitrosourea, 684-93-5

Inhibition by actinomycin D of DNA and RNA synthesis and of skin carcinogenesis initiated by 7,12-dimethylbenz[a]anthracene or beta-propiolactone.

Abstract: Summary Application of 84 µg of actinomycin D inhibits skin tumor formation initiated by either 7,12-dimethylbenz[ a ]anthracene (DMBA) or β-propiolactone (BPL). Treatment with this dose of actinomycin D inhibits the binding of DMBA to skin DNA by 40%, but does not affect BPL binding to DNA. Inhibition of binding of initiators to DNA cannot explain more than a small part of the inhibition of tumor formation by actinomycin D. A dose of 10 µg of actinomycin D inhibits tumor formation by 40–50% when given the same day as the initiator (DMBA or BPL) or 1 or 7 days later. Application of this dose of actinomycin D inhibited RNA synthesis only slightly for about 12 hours (6–18 hours after treatment), but inhibited DNA synthesis by 75–90% for at least 2 days (from 24–72 hours after treatment). The inhibition of tumor formation by actinomycin D may be related to its inhibition of the incorporation of thymidine- 3 H into skin DNA. It is not known whether this block of DNA synthesis is reversible or irreversible in potential tumor cells.