title: Chemoprevention of 2-amino-1-methyl-6-phenylimidazo [4,5-b]pyridine-induced mammary carcinogenesis in rats.
abstract: Modifying effects of dietary exposure of diallyl disulfide (DAD), aspirin, DL-alpha-difluoromethylomithine (DFMO), beta-naphthoflavone (beta-NF), alpha-naphthoflavone (alpha-NF), indole-3-carbinol (I3C) and protocatechuic acid (PCA) on 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP)-induced mammary carcinogenesis were examined in two experiments with female rats. For both experiments, PhIP in corn oil at a concentration of 85 mg/kg was given to animals via an intragastric tube for eight doses for an initial 4 weeks, and test chemicals were given in the diet (Experiment 1: DAD, 200 ppm; aspirin, 400 ppm; DFMO, 400 ppm; beta-NF, 1000 ppm; Experiment 2: alpha-NF, 1000 ppm; I3C, 1000 ppm; PCA, 2000 ppm) for an initial 4 weeks. The experiments were terminated after 25 weeks. In Experiment 1, exposure of beta-NF decreased the incidence and multiplicity of total mammary tumors (fibroadenoma, intraductal carcinoma and invasive ductal carcinoma) (P < 0.001 and P < 0.0001), and lowered the incidence of ductal carcinoma (P < 0.0001). DAD lowered the incidence of ductal carcinoma and decreased the multiplicity of the total tumors (P < 0.01 and P < 0.005). Furthermore, aspirin decreased the total tumors (P < 0.05). In Experiment 2, alpha-NF decreased the multiplicity of ductal carcinoma (P < 0.05). These results suggest that alpha-NF, beta-NF, DAD or aspirin could be chemopreventing agents for mammary neoplasia.
authors.affiliation: Department of Pathology, Gifu University School of Medicine, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Mori
authors.forename: S
authors.initials: S
authors.lastname: Sugie
authors.forename: W
authors.initials: W
authors.lastname: Rahman
authors.forename: N
authors.initials: N
authors.lastname: Suzui
mesh_terms: D000498:Allyl Compounds / Q000494:pharmacology / Q000627:therapeutic use; D000818:Animals; D016588:Anticarcinogenic Agents / Q000494:pharmacology* / Q000627:therapeutic use; D001241:Aspirin / Q000494:pharmacology / Q000627:therapeutic use; D001571:Benzoflavones / Q000494:pharmacology / Q000627:therapeutic use; D002273:Carcinogens / Q000008:administration & dosage / Q000633:toxicity*; D004220:Disulfides / Q000494:pharmacology / Q000627:therapeutic use; D004336:Drug Antagonism; D000518:Eflornithine / Q000494:pharmacology / Q000627:therapeutic use; D005260:Female; D062385:Hydroxybenzoates / Q000494:pharmacology / Q000627:therapeutic use; D007093:Imidazoles / Q000008:administration & dosage / Q000633:toxicity*; D007211:Indoles / Q000494:pharmacology / Q000627:therapeutic use; D008325:Mammary Neoplasms, Experimental / Q000139:chemically induced* / Q000517:prevention & control*; D051381:Rats; D017207:Rats, Sprague-Dawley; D019324:beta-Naphthoflavone / Q000494:pharmacology / Q000627:therapeutic use
chemical_list: D000498:Allyl Compounds; D016588:Anticarcinogenic Agents; D001571:Benzoflavones; D002273:Carcinogens; D004220:Disulfides; D062385:Hydroxybenzoates; D007093:Imidazoles; D007211:Indoles; C009091:protocatechuic acid; C028009:diallyl disulfide; C011512:alpha-naphthoflavone; D019324:beta-Naphthoflavone; C049584:2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine; C016517:indole-3-carbinol; D001241:Aspirin; D000518:Eflornithine