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Biomedical subjects

A Rivenson

Publications and source records attributed to A Rivenson.

102 records · Page 6Linked to original sources
PubMed1981

Comparative carcinogenicity and metabolism of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone and N'-nitrosonornicotine in Syrian golden hamsters.

The tobacco-specific nitrosamines 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and N'-nitrosonornicotine (NNN) were tested for carcinogenic activity in Syrian golden hamsters. In Assay A, 30 hamsters were each given 19 s.c. injections of 0.048 mmol of NNK or NNN. In Assay B, 20 hamsters each received 75 s.c. injections of 0.012 mmol of NNK or NNN. Among the NNK-treated hamsters in Assay A, three developed carcinomas of the nasal cavity, and 19 had adenomas and/or adenocarcinomas of the lung. In the NNN group, one hamster developed a lung adenoma, and five had tracheal papillomas. In Assay B, 11 of the NNK-treated hamsters developed carcinomas of the nasal cavity, 16 had lung adenomas and/or adenocarcinomas, and seven had tracheal papillomas; in the NNN group, we recorded only one hamster with a lung adenoma and one with a tracheal papilloma. These findings in the Syrian golden hamster confirm that NNK is a more powerful carcinogen than NNN, as was shown previously in assays with rats and mice. In metabolism studies, 96 to 98% of the radioactivity of the injected [1-14C]NNK was recovered in the urine, 4% was recovered in the feces, and less than 0.5% was recovered as exhaled 14CO2. The corresponding distribution for [2'-14C]NNN was 62 to 78% in urine, 10% in feces, and less than 0.5% in respiratory 14CO2. The levels of binding of [1-14C]NNK and [2'-14C]NNN to the trichloroacetic acid-insoluble fractions were highest in liver, lung, kidney, and adrenals. The urinary metabolites of NNK and NNN resulted from alpha-hydroxylation, from N-oxidation of NNN to N'-nitrosonornicotine-1-N-oxide, and from reduction of NNK to 4-(methylnitrosamino)-1-(3-pyridyl)butan-1-ol.

Animals↗
PubMed1981

Carcinogenicity in Syrian golden hamsters of N-nitrosamines formed during nitrosation of spermidine.

Several N-nitrosamines are formed during the nitrosation of the polyamines, spermidine and spermine. Since these polyamines may represent a source for the endogenous or exogenous formation of N-nitrosamines, their major nitrosation products were assayed for carcinogenicity in male Syrian golden hamsters. Administration of N-nitroso-3-butenyl(2-propenyl)amine SC once a week for life at a dose of 300 mg/kg induced neoplasms mostly in the upper respiratory tract (nasal cavity, larynx, trachea). Lung microlithiasis (alveolar and bronchial) also developed in all these animals. In contrast, N-nitroso-3-butenyl(3-hydroxypropyl)amine and N-nitroso-4-hydroxybutyl(2-propenyl)amine induced neoplasms, primarily in the digestive tract, including the nonglandular stomach, cecum, colon, and adrenal gland.

Animals↗
PubMed1980

Nephrocalcinosis in 2 young rats: a case report.

Nephrocalcinosis was diagnosed as an incidental histopathological finding in 2 Sprague-Dawley rats of 150 g bodyweight. The calcified material was located along the entire corticomedullary junction. Dietary and other causes of nephrocalcinosis are discussed.

Animal Nutritional Physiological Phenomena↗
PubMed1980

Tumor-initiating activity of dihydrodiols formed metabolically from 5-methylchrysene.

The major dihydrodiols formed from 5-methylchrysene by rat liver 9000 X g supernatant were tested for tumor-initiating activity on mouse skin. The compounds tested were 1,2-dihydro-1,2-dihydroxy-5-methylchrysene, 7,8-dihydro-7,8-dihydroxy-5-methylchrysene, 9,10-dihydro-9,10-dihydroxy-5-methylchrysene, and 5-methylchrysene. Each compound was applied in a total initiating dose of 30 microgram and was followed by promotion with tetradecanoylphorbol acetate. 1,2-Dihydro-1,2-dihydroxy-5-methylchrysene was the most powerful tumor initiator, inducing tumors in 95% of the animals and 7.3 tumors per animal. 5-Methylchrysene and 7,8-dihydro-7,8-dihydroxy-5-methylchrysene induced tumors in 75 and 50% of the animals and gave 3.0 and 1.1 tumors per animal, respectively. 9,10-Dihydro-9,10-dihydroxy-5-methylchrysene was not tumorigenic. The results indicate that 1,2-dihydro-1,2-dihydroxy-5-methylchrysene is a major proximate carcinogen of 5-methylchrysene. Both 1,2-dihydro-1,2-dihydroxy-5-methylchrysene and 7,8-dihydro-7,8-dihydroxy-5-methylchrysene can theoretically form bay-region dihydrodiol epoxides, but the former was more tumorigenic than the latter. The high activity of 1,2-dihydro-1,2-dihydroxy-5-methylchrysene is typical of hydrocarbon derivatives with a methyl group in the bay region adjacent to an unsubstituted angular ring.

Animals↗
PubMed1979

Tumor initiating activity of 5,11-dimethylchrysene and the structural requirements favoring carcinogenicity of methylated polynuclear aromatic hydrocarbons.

The tumor initiating activities of 5,11-dimethylchrysene and 5-methylchrysene on mouse skin were compared. After initiating doses of 30 microgram or 10 microgram, with promotion by 3 times weekly applications of tetradecanoylphorbol acetate, both compounds were highly tumorigenic, inducing tumors in 70--85% of the treated animals. Since 5,12-dimethylchrysene had previously been shown to be only a weak tumor initiator, these results support the generalization that the structural requirements favoring carcinogenicity among the methylated chrysenes and other polynuclear aromatic hydrocarbons (PAH) are a bay region methyl group and a free peri position, both adjacent to an unsubstituted angular ring.

Animals↗
PubMedDate not supplied

Comparative carcinogenicity of o-toluidine hydrochloride and o-nitrosotoluene in F-344 rats.

o-Toluidine hydrochloride and one of its metabolites, o-nitrosotoluene, were administered in the diet (0.028 mol/kg diet) to 2 groups of 30 male F-344 rats for 72 weeks. o-Nitrosotoluene induced significantly more tumors of the bladder (16/30 rats) and liver (20/30) than did o-toluidine hydrochloride (bladder, 4/30; liver, 3/30. Both compounds induced comparable numbers of peritoneal tumors and fibroma of the skin and spleen. o-Toluidine hydrochloride induced more mammary tumors (13/30) than did o-nitrosotoluene (3/30). The results indicate tha N-oxidation is important in the induction of bladder and liver tumors by these single ring compounds but that other mechanisms could be involved in the induction of peritoneal, skin, spleen and mammary tumors.

Animals↗
PubMedDate not supplied

The influence of different varieties of olive oil on N-methylnitrosourea(NMU)-induced mammary tumorigenesis.

Several epidemiological and animal model studies suggest that consumption of olive oil, which is rich in the monounsaturated fatty acid, oleic acid (OA, C18:, n-9) may reduce the risk of breast cancer. There are however, a wide variety of olive oils in the marketplace with levels of OA ranging from a low of 50% to a high of 80% OA. The purpose of this rodent model study was to determine whether the level of OA in olive oil is a key determinant of its protective effects. We compared the inhibitory effects among three different types of olive oil containing 54, 70 and 80% OA and 20, 15 and 5% linoleic acid (LA), respectively, corn oil and a store bought olive oil, using the NMU-induced rat mammary tumor model. While little difference was found in total mammary tumor yields, a differential effect was found in the histological type of tumors formed. Olive oil containing 80% OA and 5% LA exhibited the lowest level of adenocarcinomas and the highest level of the more benign adenocarcinoma arising from within a fibroadenoma. While the reasons for this effect remain to be clarified, these results suggest that future studies on the health benefits of olive oil should take into account the type as well as the amount of olive oil.

Animals↗
PubMedDate not supplied

Chemoprevention of azoxymethane-induced colon cancer by ascorbylpalmitate, carbenoxolone, dimethylfumarate and p-methoxyphenol in male F344 rats.

The chemopreventive effect of 40 and 80% maximum tolerated dose (MTD) levels of ascorbylpalmitate (AP), carbenoxolone (CBX), dimethylfumarate (DMF) and p-methoxyphenol (p-MP) administrated in the diet before and during initiation and postinitiation phases of azoxymethane (AOM)-induced colon carcinogenesis was studied in male F344 rats. The MTD levels of AP, CBX, DMF and p-MP were determined in male F344 rats and found to be 5000 1500, 1000 and 1000 ppm, respectively, in modified AIN-76A diet. Based on these MTD values, 40 and 80% MTD levels of each agent was tested for their efficacy in color carcinogenesis. At 5 weeks of age, groups of animals were fed the control (modified AIN-76A diet or diets containing 40 and 80% MTD levels of each AP, CBX, DMF and p-MP. At 7 weeks of age, all animals, except those in the vehicle (normal saline)-treated groups, were given two weekly s.c. injections of AOM at a dose rate of 15 mg/kg body weight/week. All groups were continued on their respective dietary regimen until the termination of the experiment 52 weeks after the carcinogen treatment. Colonic tumors were evaluated histopathologically. The results indicate that dietary administration of 40% MTD of AP significantly inhibited multiplicities (tumor/animal) of noninvasive and total (invasive plus noninvasive) adenocarcinoma of the colon (P < 0.05) and 80% MTD of AP significantly inhibited the incidence (% animals with tumors) and the multiplicities of invasive and total adenocarcinomas of the colon (P < 0.01). Dietary CBX at 40 and 80% MTD levels suppressed the incidence and multiplicities of invasive and total adenocarcinomas (P < 0.05 to 0.001) whereas 40 and 80% MTD of DMF and p-MP had significantly inhibited invasive adenocarcinoma incidence and multiplicity (P < 0.05 to 0.001). However, DMF and p-MP had no significant effect on noninvasive and total adenocarcinoma incidence and multiplicity (P > 0.05). These results suggest that AP and CBX possess potential chemopreventive properties against colon cancer.

Animals↗