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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: Findings thus confirm the anti-lipid peroxidative and antioxidant efficacy of vanillic acid in DMBA induced hamster buccal pouch carcinogenesis.
Abstract: INTRODUCTION Vanillic acid, a naturally occurring bioactive substance, possesses diverse pharmacological potential including free radical scavenging and anticancer properties. Excessive generation of Reactive Oxygen Species (ROS) and insufficient antioxidant potential has been involved in numerous pathological disorders, including cancer. AIM To explore the anti-lipid peroxidative and antioxidant efficacy of vanillic acid in Dimethylbenz[a]Anthracene (DMBA) induced oral carcinogenesis. MATERIALS AND METHODS Topical application of DMBA for 14 weeks in the buccal pouch of hamsters resulted in well developed oral squamous cell carcinoma. Vanillic acid at a dosage of 200 mg/kg body weight was orally administrated to the hamsters for 14 weeks. The status of lipid peroxidation and antioxidants were measured in the plasma and buccal mucosa of hamsters using specific colorimetric methods. RESULTS Altered levels of lipid peroxidation by-products {Thiobarbituric Acid Reactive Substances (TBARS)} and disturbances in antioxidants status {Superoxide Dismutase (SOD), Catalase (CAT), Glutathione Peroxidase (GPx), vitamin E, vitamin C and reduced Glutathione (GSH)} were observed in the plasma and buccal mucosa tissues of hamsters treated with DMBA alone. Vanillic acid (200 mg/kg bw p.o) significantly restored the above mentioned plasma and buccal mucosa biochemical variables to near normal range in DMBA treated hamsters. CONCLUSION Present findings thus confirm the anti-lipid peroxidative and antioxidant efficacy of vanillic acid in DMBA induced hamster buccal pouch carcinogenesis.
14 citations
TL;DR: It is proved that Vicenin‐2 prevents DMBA‐induced buccal carcinogenesis in hamsters via improving antioxidants by modulating apoptotic and cytokines signaling pathways.
Abstract: Buccal mucosa carcinoma is a significant cause of death in developing nations. Vicenin-2 is a significant bioactive compound found in Ocimum sanctum Linn or Tulsi that possesses several pharmacologic properties. Our focus is to understand the possible impact of Vicenin-2 on 7,12-dimethylbenz[a]anthracene (DMBA)-induced oral carcinogenesis in hamsters. Buccal carcinoma was induced by treatment with carcinogenic DMBA, three times a week for 14 weeks. We determined 100% tumor incidence, abnormal tumor volume, inclined tumor burden, and deduced body weight in DMBA-induced oral squamous cell carcinoma (OSCC) hamsters. The upregulation of cytokine levels (interleukin [IL]-6, IL-1β, and tumor necrosis factor-alpha [TNF-α]) was observed in DMBA-induced OSCC hamsters. Moreover, dysplastic, hyperplastic, and squamous cell carcinoma was identified in the DMBA-induced OSCC hamsters. The diminished activities of lipid peroxidation and enzymatic/nonenzymatic antioxidants were observed in DMBA-induced hamsters. Furthermore, the high expression of proliferating cell nuclear antigen (PCNA), Cyclin-D1, and Bcl-2, and attenuated Bax expression were observed in DMBA-induced hamsters. Our study results explored that Vicenin-2 (30 mg/kg) treated with DMBA-brushed hamsters averted tumor incidence, improved the antioxidant status, and inhibited lipid peroxidation. Moreover, Vicenin-2 inhibited the immunohistochemical expression of PCNA, Cyclin-D1, and Bcl-2, and significantly restored apoptotic Bax levels. The Vicenin-2 treatment prevents the lesion formation in the oral epithelium of the DMBA-induced hamsters. The Vicenin-2 treatment potentially halts the proinflammatory cytokines (IL-6, IL-1β, and TNF-α) production in OSCC hamsters. Thus, we proved that Vicenin-2 prevents DMBA-induced buccal carcinogenesis in hamsters via improving antioxidants by modulating apoptotic and cytokines signaling pathways.
14 citations
TL;DR: Tumor growth is enhanced and the permissive effects of hormones on mammary carcinogenesis are potentiated in rats fasted during the promotion phase, and fasting before beta-estradiol and haloperidol injection resulted in a more pronounced effect on tumor yield and latency than hormones or fasting alone.
Abstract: The effect of fasting-refeeding during the promotion phase of dimethylbenz[a]anthracene (DMBA)-induced mammary carcinogenesis has been investigated. Female Sprague-Dawley rats were given 130 mg/kg of DMBA and divided into four groups: Group 1 was fed ad libitum; Group 2 was fed ad libitum and, in addition, received daily subcutaneous injections of beta-estradiol and haloperidol for eight days, beginning two weeks after DMBA administration; Group 3 was exposed to three days of fasting one week after carcinogen injection, then fed ad libitum until the end of the experiment; Group 4 was treated as Group 2, except the animals were fasted for three days beginning one week after DMBA administration. Treatment with beta-estradiol and haloperidol enhanced the development of DMBA-induced mammary tumors. Rats fasted after DMBA administration showed increased genesis and growth and reduced latency of mammary tumors. Fasting before beta-estradiol and haloperidol injection resulted in a more pronounced effect on tumor yield and latency than hormones or fasting alone. The data indicate that, in rats fasted during the promotion phase, tumor growth is enhanced and the permissive effects of hormones on mammary carcinogenesis are potentiated.
14 citations
Journal Article•
TL;DR: Although the demethylated antiestrogens have a 20- to 50-fold enhanced affinity for the mammary tumor estrogen receptor in vitro as compared to their parent compound in vivo, both forms are equally potent antitumor and antiuterotrophic agents.
Abstract: This study compares the antitumor activities of the nonsteroidal antiestrogens α-{ p -[2-(1-pyrrolidino)ethoxy]phenyl}-4-methoxy-α′-nitrostilbene (CI628) and cis -{3-[ p -(1,2,3,4-tetrahydro-6-methoxy-2-phenyl-1-naphthyl)phenoxy]-1,2-propanediol} (U23,469) with their demethylated metabolite forms in the dimethylbenz( a )anthracene-induced rat mammary tumor system. Since these demethylated forms are generated during the action of the parent antiestrogens in vivo and are selectively accumulated in the nuclear estrogen receptor fraction in preference to the parent compound, we investigated whether direct administration of the metabolites might prove more effective than administration of the parent antiestrogens in eliciting tumor regression. We have therefore compared the potencies of the parent antiestrogens and their demethylated forms α-{ p -[2-(1-pyrrolidino)ethoxy]phenyl}-4-hydroxy-α′-nitrostilbene (CI628M) and cis -{3-[ p -(1,2,3,4-tetrahydro-6-hydroxy-2-phenyl-1-naphthyl)-phenoxy]-1,2-propanediol} (U23,469M) in stimulating the regression of established dimethylbenz( a )anthracene-induced mammary tumors; and we have monitored the effects of these antiestrogens on estrogen receptors and the enzyme peroxidase as a specific marker for estrogen action in mammary tumors and in uteri of tumor-bearing animals. In mammary tumor cytosol in vitro , the antiestrogens competed with [ 3 H]estradiol for binding to estrogen receptor with affinities of 113% (CI628M), 5% (CI628), 31% (U23,469M), and 0.6% (U23,469), where the affinity of estradiol is considered to be 100%. However, all four antiestrogens were equally effective as antagonists of tumor growth in vivo . Administration of 25 or 100 µg daily of either parent (CI628 and U23,469) or the demethylated (CI628M and U23,469M) antiestrogens was able to elicit the regression of the majority of dimethylbenz( a )anthracene tumors, while low doses (2.5 µg/day) of any of these four compounds had no effect on tumor growth. The 25- and 100-µg doses of antiestrogens markedly reduced tumor cytoplasmic estrogen receptor levels, but they failed to elevate significantly tumor peroxidase activity. Uterine weights were significantly decreased below the diestrus controls following treatment with 25- or 100-µg daily dosages of the antiestrogens; and these treatments resulted in the nuclear localization of approximately 80% of total estrogen receptors. Uterine peroxidase activity, which was high in diestrus control females, was dramatically reduced to 5 to 25% by the intermediate- or high-dose levels of the antiestrogens. These results indicate that, although the demethylated antiestrogens have a 20- to 50-fold enhanced affinity for the mammary tumor estrogen receptor in vitro as compared to their parent compound in vivo , where the parent compounds are rapidly converted to the demethylated metabolites, both forms are equally potent antitumor and antiuterotrophic agents. These high-affinity antiestrogens should be excellent ligands for experiments designed to elucidate the mechanism of antiestrogen action in breast cancer.
14 citations