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Biomedical subjects

A Rivenson

Publications and source records attributed to A Rivenson.

At least 91 records · Page 5Linked to original sources
PubMed1985

The effects of catechol on the urinary bladder of rats treated with N-butyl-N-(4-hydroxybutyl)nitrosamine.

The effect of catechol on the development of urinary bladder tumors in Fischer rats treated with N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) was studied. A solution of 0.05% catechol and 0.001% BBN was administered in the drinking water ad libitum for 78 weeks. The urinary bladders were then removed and examined microscopically. No statistically significant difference was observed between the experimental group receiving 0.001% BBN with 0.05% catechol and animals receiving 0.001% BBN alone with respect to the incidence of hyperplasia, papilloma, or carcinoma of the urinary bladder. Animals receiving 0.05% catechol alone in the drinking water had no macroscopic or microscopic lesions significantly different from those in control animals receiving tap water. Analyses of the urine of animals receiving catechol in their drinking water indicated that greater than 99% of the catechol present was in the form of either glucuronide or sulfate conjugates. In a second bioassay, the potential cocarcinogenicity of catechol, administered together with BBN, was explored by direct instillation into the urinary bladder. The development of calculi and possible infections of the urinary tract within all groups of treated animals suggests that this bioassay technique for cocarcinogenicity is of questionable value. These data show that catechol at the dose and mode of administration employed in this study did not affect the epithelium of the urinary bladder or enhance the carcinogenic activity of BBN.

Animals↗
PubMed1984

Dose-response study of the carcinogenicity of tobacco-specific N-nitrosamines in F344 rats.

Tobacco and tobacco smoke contain relatively high amounts of four tobacco-specific N-nitrosamines. Of these, N-nitrosonornicotine (NNN), 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), and N'-nitrosoanatabine (NAT) were bioassayed at three dose levels by subcutaneous injections into male and female F344 rats in 60 subdoses amounting in total to 9,3, and 1 mmol/kg. Compared with the solvent control group (trioctanoin), both NNN and NNK induced significant numbers of tumors of the nasal cavity (P less than 0.01) at all three dose levels in both male and female rats. Significant numbers of tumors were also induced by NNK in the lung at all three dose levels and in the liver at the highest dose level (P less than 0.05). In addition to nasal tumors NNN also induced esophageal tumors at a significant rate in male rats at the high and medium dose levels and in female rats at the high level (P less than 0.05); NAT was inactive at the three doses tested. Bioassays at lower dose levels as well as biochemical studies are strongly indicated for NNN and NNK since these nitrosamines occur in relatively high amounts in both chewing tobacco and tobacco smoke.

Animals↗
PubMed1984

A study of betel quid carcinogenesis. 3. 3-(Methylnitrosamino)-propionitrile, a powerful carcinogen in F344 rats.

3-(Methylnitrosamino)propionitrile (MNPN) is formed in vitro under mild nitrosation conditions from the major areca alkaloid arecoline. It appears likely that MNPN is generated during betel quid chewing especially when tobacco is added to the quid. Upon subcutaneous injection of 1.1 mmol of MNPN in 60 subdoses, all of the 15 male and of the 15 female F344 rats developed tumors within 24 weeks. Twenty-six of the rats had tumors in two different organs at least. Twenty-seven rats had esophageal tumors, 21 nasal tumors, 11 had tongue tumors and two animals had either pharyngeal carcinomas or papillomas of the forestomach. No tumors were observed in the solvent control group. These data indicate that MNPN is a potent carcinogen.

Animals↗
PubMed1984

Chemically induced rat odontomas: morphogenetic considerations.

Three complex odontomas were found in 30 castrated male rats injected with N-methyl-nitrosourea (MNU) and fed a high-fat diet. Histological studies were performed and the related literature was reviewed. The morphogenesis of the tumors is discussed in the light of the bibliographic data and personal findings.

Animals↗
PubMed1984

A study of betel quid carcinogenesis. II. Formation of N-nitrosamines during betel quid chewing.

In model studies, nitrosation of the major areca alkaloid, arecoline, leads to the formation of N-nitrosoguvacoline, 3-(methylnitrosamino)propionitrile (MNPN), 3-(methylnitrosamino)propionaldehyde and two unknown N-nitrosamines. MNPN is a strong carcinogen in Fischer 344 rats. After subcutaneous injection of 1.1 mmol MNPN in 60 doses, all 15 male and 15 female rats developed tumours within 24 weeks; multiple tumours occurred in 26 of the rats. Eighty-seven percent of the animals had tumours of the oesophagus, 70% had nasal cavity tumours, 37% had tumours of the tongue, 7% tumours of the pharynx and 7% tumors of the forestomach. At the dose used, male and female rats showed no significant difference in tumour incidence or site of tumours. The formation of MNPN during betel quid chewing, although likely, has not yet been proven, while the areca-derived N-nitrosamine, N-nitrosoguvacoline (NG), has been found in the saliva of betel quid chewers at levels of 2.2-348 micrograms/L. N-Nitrosoguvacoline levels were higher in the saliva of chewers who used betel quid together with tobacco. The saliva of these chewers also contained tobacco-specific N-nitrosamines.

Animals↗
PubMed1984

Effects of chronic ethanol consumption on the metabolism and carcinogenicity of N'-nitrosonornicotine in F344 rats.

The effects of chronic ethanol consumption on the carcinogenicity and metabolism of N'-nitrosonornicotine (NNN) in male F344 rats have been investigated. Groups of 26 to 30 rats were maintained on either a control liquid diet (Groups 1, 3, and 5) or an ethanol-containing liquid diet (Groups 2, 4, and 6) for 4 weeks prior to and during treatment with NNN. The carcinogen was injected s.c. (10 mg/kg, Groups 3 and 4) three times weekly or added to the liquid diet (17.5 mg/liter, Groups 5 and 6). The total dose was 1 mmol of NNN per rat. Control rats (Groups 1 and 2) received s.c. injections of 0.9% NaCl solution. The nasal mucosa was the main target tissue of NNN in Groups 3 and 4, but both the nasal mucosa and esophagus were major target tissues in Groups 5 and 6. In rats treated s.c. with NNN (Groups 3 and 4), ethanol consumption had no effect on the distribution and incidence of nasal cavity tumors. In rats treated with NNN added to the control liquid diet or to the ethanol-containing liquid diet, the number of tumors of the nasal cavity was 18 in Group 5 and 26 in Group 6 (p less than 0.05). In contrast, the number of rats with esophageal tumors was 25 in Group 5 and 20 in Group 6 (p less than 0.05). The effects of ethanol on the enzyme system which activates NNN were studied in rats which had been maintained on an ethanol-containing liquid diet for 4 weeks. Explants of nasal mucosae, lingual mucosae, esophagi , and livers were cultured in vitro with NNN. Nasal mucosae of ethanol-consuming rats had a 1.5-fold higher (p less than 0.05) alpha-carbon-hydroxylating activity than did those of control rats. Activating enzymes in the lingual mucosae, esophagi , and livers were not induced by ethanol. The results show that the increased susceptibility of the rat nasal mucosa to the carcinogenic effects of NNN added to an ethanol-containing diet could be due in part to an induction of activating enzymes by ethanol. However, since chronic ethanol consumption had no apparent effect on the incidence of nasal cavity tumors in rats treated by s.c. injection of NNN, factors other than enzyme induction are important in determining the effects of ethanol on NNN carcinogenicity.

Alcohol Drinking↗
PubMed1983

Bioassay for carcinogenicity of 3,2'-dimethyl-4-nitrosobiphenyl, O-nitrosotoluene, nitrosobenzene and the corresponding amines in Syrian golden hamsters.

3,2'-Dimethyl-4-aminobiphenyl and 3,2'-dimethyl-4-nitrosobiphenyl were administered by subcutaneous injection in peanut oil to 2 groups of 15 male and 15 female Syrian golden hamsters. The total dose of each compound was 5.6 mmol/kg. In the group treated with 3,2'-dimethyl-4-aminobiphenyl, 24 animals had bladder tumors. In the group treated with 3,2'-dimethyl-4-nitrosobiphenyl 25 animals had subcutaneous tumors and 2 had bladder tumors. These results indicate that 3,2'-dimethyl-4-nitrosobiphenyl is a potent locally acting carcinogen. Total doses of 99 mmol/kg of aniline, o-toluidine, nitrosobenzene, or o-nitrosotoluene administered by subcutaneous injection failed to induce tumors.

Animals↗
PubMed1983

Effect of sodium ascorbate on transplantable murine tumors.

The possible inhibitory effect of vitamin C (sodium ascorbate) on metastases from two transplantable murine tumors was studied. The first murine tumor, colon carcinoma CA-51, was subcutaneously transplanted into male Balb/c mice. Immediately after tumor implantation, the mice were given either 1.0% sodium ascorbate or tap water. Subcutaneous tumors were surgically removed from one half of the animals in each group when the tumors reached a size of 1.5 cm. Results indicated no differences in survival, in the number of mice with metastases, or in the size of metastases between treated and untreated groups. The second murine tumor, lymphosarcoma 6C3HED, was subcutaneously implanted into C3H male and female mice. Sodium ascorbate (1.0% or 3.0%) was administered as above, but surgery was not performed. Again, no significant differences in the number of mice with metastases were observed between treated and untreated groups, with the exception of brain and regional lymph node metastases (enhanced, in males, by ascorbate).

Animals↗
PubMed1983

Effects of route of administration and dose on the carcinogenicity of N-nitrosodiethanolamine in the Syrian golden hamster.

N-Nitrosodiethanolamine was assayed for carcinogenicity in Syrian golden hamsters by s.c. injection, topical application, and oral cavity swabbing. Three groups of 30 hamsters each received 27 weekly s.c. injections of either 500, 170, or 58 mg of N-nitrosodiethanolamine per kg in 0.9% NaCl solution. In the group treated with 500 mg/kg, 19 of 30 animals developed nasal cavity tumors, 7 of 30 had tracheal tumors, and 2 of 30 had tumors of the larynx. Among the animals treated with 170 mg/kg, 7 of 29 presented with nasal cavity tumors and 4 of 29 presented with tracheal tumors. In the group treated with 58 mg/kg, only two tracheal tumors were observed. Acetone solutions of N-nitrosodiethanolamine were applied to the shaved backs of three groups of 30 hamsters, each three times weekly for 36 weeks, at doses of 25, 8, or 2.5 mg; the total doses were the same as in the groups treated by s.c. injection. At the 25-mg dose level, 5 of 30 animals developed nasal cavity tumors and 4 of 30 animals had tumors of the trachea. No skin tumors were observed. The incidence of respiratory tract tumors in the groups treated with 8 or 2.5 mg was not significant compared to controls. The oral cavities of 40 hamsters were swabbed three times weekly for 45 weeks with 20 mg of N-nitrosodiethanolamine; the total dose was the same as the highest doses given by s.c. or topical administration. Seventeen of 38 hamsters had nasal cavity tumors, 6 of 38 developed tracheal tumors, and 1 of 38 presented with a tumor of the larynx. No tumors were observed in the oral cavity. The results of this study demonstrate that N-nitrosodiethanolamine is organospecific for the Syrian golden hamster nasal cavity and trachea and that it induces tumors in these sites at doses lower than previously reported.

Administration, Oral↗
PubMed1982

Tobacco specific N-nitrosamines: occurrence and bioassays.

A new GC-TEA method for the analysis of tobacco-specific N-nitrosamines (TSNA) has been developed. Four TSNA have thus far been identified; these are N'-nitrosonornicotine (NNN), 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), N'-nitrosoanatabine (NAT) and N'-nitrosoanabasine (NAB). The method is currently being applied to the development of cigarette filter-tips which will selectively remove these carcinogens from cigarette smoke. Since recent epidemiological studies have established a correlation between snuff dipping and oral cancer, we have analysed leading snuff brands for TSNA. Snuff products from Sweden, Denmark, Bavaria and the USA contained 5-106 mg/kg of the TSNA and the saliva of snuff dippers had TSNA levels of 20-890 micrograms/kg. NNN, NNK and NAB induce benign and malignant tumours of the respiratory tract of mice and rats. We have shown that NNN and NNK induce tumours in the upper respiratory tract of hamsters and that NNK is the most active carcinogen of the TSNA, also inducing adenoma and adenocarcinoma in the hamster lung. The reported chemical analyses and bioassay results support the epidemiological findings on the causal association of tobacco use and cancer in man.

Adult↗
PubMed1982

Prostate adenocarcinoma in rats: induction by 3,2'-dimethyl-4-aminobiphenyl.

Five experiments designed for various purposes [mainly for the study of colon carcinogenesis in inbred F344 male rats given sc injections of 3,2'-dimethyl-4-aminobiphenyl (DMAB)] were reviewed as to the production and presence of neoplastic lesions of the prostate gland. The overall incidence of prostate proliferative lesions among 293 animals exposed to DMAB was 32% (95 animals). Early in situ carcinomas were present in 66 animals, larger intra-acinar carcinomas in situ in 28, and invasive carcinoma in 1. None of the control animals in these studies exhibited prostate neoplasms. The conclusion, therefore, is that DMAB can induce adenocarcinomas in the rat prostate gland.

Adenocarcinoma↗
PubMed1982

N-nitrosodiethanolamine: analysis, formation in tobacco products and carcinogenicity in Syrian golden hamsters.

An analytical GC-TEA method has been developed for the quantitative determination of N-nitrosodiethanolamine (NDELA) in tobacco and tobacco smoke. US smoking and chewing tobaccos and experimental cigarette tobaccos contained between 80 and 420 micrograms/kg of NDELA. Two snuff samples contained 3200 and 6800 micrograms/kg of NDELA. NDELA in mainstream smoke of US cigarettes amounted to 10 - 68 ng per cigarette. Evidence was presented which incriminates diethanolamine as a major precursor for NDELA in tobacco and tobacco smoke. Diethanolamine is used as a solubilizing agent for maleic hydrazide, the major sucker-growth inhibitor for US tobacco crops. NDELA was bioassayed in Syrian golden hamsters by skin painting, swabbing of the oral cavity and by subcutaneous injection. Independently of the form of application, NDELA at the higher dose (500 mg/kg) induced carcinomas of the nasal cavity, papillomas of the trachea and tumours of the larynx in some animals. NDELA uptake through the oral cavity in hamsters is presumably greater than through the skin, judging by the higher tumour yield induced by painting of the oral cavity, compared to skin painting. Studies with 14C-labeled NDELA are currently underway to document this observation quantitiatively. The present analytical data for NDELA in tobacco and tobacco smoke, together with the carcinogenicity data reported here and elsewhere, strongly suggest a review of the use of maleic hydrazide-diethanolamine as sucker-growth inhibitor in the cultivation of tobacco and other crops.

Animals↗
PubMed1981

A study of tobacco carcinogenesis XX: mastocytoma induction in mice by cigarette smoke particulates ("cigarette tar").

A significant incidence of cutaneous mastocytomas was observed in female mice of CAF1/J and ARS-HA (ICR) strains upon long-term application of cigarette smoke condensate suspensions ("tar"). The mastocytomas were not detected in control groups treated with acetone, benzo(a)pyrene (BaP), tetradecanoyl phorbol acetate (TPA), nor in mice treated once with an initiator dose of 75 mg 7, 12-dimethylbenz(a)anthracene (DMBA). The skin mastocytomas were constantly accompanied by diffuse dermal mast cell infiltration (DDMI), which was also seen in the tumor-free skin of the "tar"-treated mice. These results indicate that mastocytomas were induced by agents present in the cigarette smoke condensate. DDMI might be a precursor of mastocytomas.

Animals↗