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At least 1,135 records · Page 63Linked to original sources
PubMed1979

Occult blood testing using the guaiac method (haemoccult-test) for detection of tumorous lesions induced with 1,2-dimethyl-hydrazine and acetoxymethyl-methyl-nitrosamine in rats.

Colon tumors were induced by 1,2-Dimethylhydrazine (DMH) and Acetoxymethyl-methyl-nitrosamine (AMMN) in male Sprague-Dawley rats. The usefulness of the Haemoccult-test (HT) was investigated for early detection of these chemically induced tumorous injuries. As a prescreening method HT was shown to be unsuitable for early detection of tumours under the conditions of the models used. The accuracy of HT in cases of advanced chemically induced tumors was explored in rats with known colonic tumors, diagnosed by rectoscopy and exploratory laparotomy. In animals with proven colonic tumors HT gave a positive result only in 63% of rats with AMMN-induced tumors and in 50% rats with DMH-induced cancers. Therefore, HT is thought to be an insensitive and thus unsuitable method for the detection of colonic cancer in rats.

Adenocarcinoma↗
PubMed1984

Effects of three sweeteners on rat urinary bladder carcinogenesis initiated by N-butyl-N-(4-hydroxybutyl)-nitrosamine.

The effects of three sweeteners, sodium saccharin, aspartame and stevioside, on urinary bladder carcinogenesis in rats initiated by N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) were evaluated. Male F344 rats were given 0.01% BBN in their drinking water for 4 weeks and then the test sweeteners in their diet for 32 weeks. All surviving rats were sacrificed after 36 weeks, and examined histologically. Treatment with sodium saccharin significantly increased the incidence and extent of preneoplastic lesions, papillary or nodular (PN) hyperplasia, in rats treated with BBN for 4 weeks. Administration of 5% aspartame or 5% stevioside in the diet did not, however, affect the incidence or extent of PN hyperplasia in BBN-treated rats. No preneoplastic or neoplastic lesions of the urinary bladder were observed in rats treated with the test sweeteners only. The results with sodium saccharin were consistent with those in our previous experiments. The data also suggest that aspartame and stevioside do not promote bladder carcinogenesis.

Animals↗
PubMed1984

Induction of oral mucosal tumors in hamsters and rats treated with methyl(acetoxymethyl)nitrosamine.

An oral tumor model has been developed in inbred Syrian golden hamsters by continuous applications every 2 weeks of methyl(acetoxymethyl)nitrosamine [(DMN-OAC) CAS: 56856-83-8; methylnitrosaminomethyl ester acetic acid] at 2 mg/kg body weight alone or by a single application of DMN-OAC followed by continuous twice weekly applications of 12-O-tetradecanoylphorbol 13-acetate (TPA) (1 microgram/animal). Similar studies were done in the W rat buccal mucosa. In the hamsters treated continuously with DMN-OAC, 100% of the tumors were observed in the cheek pouch; none were observed at other sites. In contrast, in the rats treated similarly, only a 67% tumor incidence was observed, of which only 42% were oral tumors. A promoter effect of TPA was observed in hamster cheek pouch tumors induced by DMN-OAC, whereas rat oral mucosa did not respond to TPA treatment.

Animals↗
PubMed1982

[Effect of carboquone (esquinone) on the development of urinary bladder tumors in rats induced by N-butyl-N-(4-hydroxybutyl) nitrosamine].

The effect of carboquone (CQ) by intraperitoneal administration on the development of urinary bladder tumors in Wistar strain male rats induced by N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN) was studied. Urinary bladder tumors were induced in 9 of 11 rats (81.8%) when they were given 0.05% BBN in drinking water for 8 weeks and then given water without BBN for 12 weeks. When CQ 0.25 mg/kg/day was administered intraperitoneally for 7 days after treatment with 0.05% BBN for 8 weeks, incidence of urinary bladder tumors was 19 of 26 rats (73.1%). When CQ 0.25 mg/kg/weekly was given for 12 weeks after treatment with BBN, incidence of urinary bladder tumors was 17 of 27 rats (63.0%). When CQ 0.5mg/kg. B.W./day was given for 7 days after treatment with BBN, tumors developed in the urinary bladder with low incidence as in 8 of 20 rats (40.0%) (P 0.1). When CQ 0.5mg/kg/weekly was given for 12 weeks after treatment of BBN, urinary bladder tumors were induced in 17 of 22 rats (77.3%). Hematotoxity was not observed in any animals treated with CQ. These results showed that CQ inhibited the development of urinary bladder tumors induced by BBN in rats.

Animals↗
PubMed1980

Effects of sodium saccharin and caffeine on the urinary bladder of rats treated with n-butyl-n-(4-hydroxybutyl)nitrosamine.

The effects of sodium saccharin and caffeine on urinary bladder carcinogenesis in Wistar strain rats treated with N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) were studied. Animals were given 0.01% BBN as an initiator for 4 weeks and then sodium saccharin and/or caffeine as promoters for 32 weeks (Experiment I), or were treated simultaneously with 0.001% BBN, sodium saccharin and/or caffeine for 40 weeks (Experiment II). The urinary bladders were then removed and examined by light and electron microscopy. Sequential administration of sodium saccharin after BBN significantly enhanced the induction of hyperplasias compared with administration of BBN alone (Experiment I), and simultaneous administration of sodium saccharin with BBN significantly enhanced the induction of hyperplasia and papillomas compared with BBN alone (Experiment II). Two types of hyperplasias developed in the urinary bladder of rats treated with sodium saccharin alone in both experiments. Caffeine alone had no effect on the rat urinary bladder epithelium, and either sequential or simultaneous administration of caffeine with BBN caused no marked enhancement of carcinogenesis in these experiments.

Animals↗
PubMed1995

[Correlation studies on the alterations of multiple tumor suppressor genes in human esophageal cancer and in human and monkey esophageal epithelial cells treated with N-methyl-N-benzyl nitrosamine].

The correlation between the mutation spectra of tumor suppressor genes Rb, p53, APC and MCC in human esophageal cancer (EC) and in human and monkey esophageal epithelium treated with N-Methyl-N-Benzyl nitrosamine (NMBzA) was studied using PCR amplification and direct sequencing methods. The results showed that in 40.9% (9/22) of the specimen examined, the mutation spectrum of p53 in primary EC was similar to that in the esophageal epithelium of human fetus (in vitro) and monkey (in vivo) treated with NMBzA. The same mutational spectra of tumor suppressor genes Rb, APC, MCC in esophageal epithelium cells of human and monkey treated with NMBzA were also found in some human primary EC. The correlation observed in the mutation spectra of multiple tumor suppressor genes between human primary EC and the esophageal epithelia of human and monkey origin treated with NMBzA wouldsuggest that NMBzA may be the esophageal etiological agent for human esophageal cancer in China.

Animals↗
PubMedDate not supplied

Chemoprevention by indomethacin of N-butyl-N-(4-hydroxybutyl)-nitrosamine-induced urinary bladder tumors.

The effects of indomethacin on the development of N-butyl-N-(4-hydroxybutyl) nitrosamine (OH-BBn)-induced urinary bladder tumors were evaluated in male BDF mice. Preliminary feeding studies revealed that the highest non-toxic dose of indomethacin was 15 mg/kg of AIN-76A diet; thus, dose levels of 15 and 7.5 mg/kg of diet were selected to determine the chemopreventive efficacy of this agent. Diet supplementation with indomethacin was initiated when the mice were 49 days old and continued for the duration of the study. Starting one week after indomethacin treatment, OH-BBN was administered 1x/week for eight weeks. Upon termination of the study (180 days after the initial carcinogen administration), all tumors in the urinary bladder were removed and classified histologically. Mice receiving carcinogen and no indomethacin supplementation had a 24% incidence of urinary bladder tumors; mice receiving 7.5 mg/kg and 15 mg of indomethacin had a 5% and 0% incidence of urinary bladder tumors, respectively. The significant reduction of OH-BBN-induced urinary bladder tumors by indomethacin is consistent with previous suggestions that prostaglandin synthesis inhibitors are effective inhibitors of carcinogenesis.

Animals↗
PubMed1995

Thymosin fraction 5 does not influence urinary tract carcinogenesis by phenacetin and N-butyl-N-(4-hydroxybutyl)nitrosamine in NON/Shi mice.

The effect of thymosin fraction 5 (TF5) on the promotion and progression phases of urinary tract carcinogenesis induced by consecutive administration of phenacetin and N-butyl-N-(4-hydroxybutyl)-nitrosamine (BBN) in NON/Shi mice was investigated. The study was carried out twice with a minor modification to the protocol in the second experiment. Fifty-seven male NON/Shi mice in experiment 1 and 100 mice in experiment 2 were each divided into four groups. Phenacetin was administered for 8 weeks in experiment 1 and 12 weeks in experiment 2, and subsequently BBN was given for 6 weeks in both cases, for total observation periods of 30 and 34 weeks, respectively. Sixty micrograms of TF5 per mouse was inoculated subcutaneously twice a week during (group 2) or after (group 3) BBN exposure, or both periods (group 4). Group 1 served as a control group without TF5 treatment. Histopathological examination revealed no effects on either induction of urinary tract carcinomas or distant metastasis from renal pelvic carcinomas in either experiment.

Animals↗
PubMed1996

A study of antitumor effects of thymosin on rat and mouse urinary bladder carcinoma induced by N-butyl-N-(4-hydroxybutyl)-nitrosamine.

N-Butyl-N-(4-hydroxybutyl)-nitrosamine (BBN), which induces bladder carcinoma in female Wistar rats and female C3H/HeJ mice, was given as 0.025% (w/v) solution to rats and 0.05% to mice in the drinking water. Thymosin fraction 5 (TF5) or thymosin alpha 1 (T alpha 1) dissolved in normal saline, and normal saline (control) respectively were injected into the right thigh IM twice a week in the experimental rats. At the 30th week of BBN oral administration, weights of urinary bladder were different among the three groups. Bladder weights and incidence of bladder carcinoma were significantly lower in the TF5-treated group as compared with control group. Natural killer cell activity of splenic lymphoid cells was significantly elevated in the TF5-treated group as compared with the control group. However, these parameters were not significantly different between the T alpha 1-treated group and control saline-treated group. On the other hand, bladder weights and incidence of bladder carcinoma were not significantly different among TF5-, T alpha 1- and saline-treated groups at 10, 15, 20, and 25 weeks of BBN administration in mice according to the same protocol as rats.

Animals↗
PubMed1998

Chemopreventive effects of nimesulide, a selective cyclooxygenase-2 inhibitor, on the development of rat urinary bladder carcinomas initiated by N-butyl-N-(4-hydroxybutyl)nitrosamine.

The chemopreventive potential of a selective cyclooxygenase-2 inhibitor, nimesulide (NIM), against the development of rat superficial urinary bladder carcinomas after initiation with N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) was examined. Six-week-old Fischer 344 male rats were given 0.05% BBN in their drinking water for 8 weeks, followed by diets supplemented with 0, 100, 200, or 400 ppm NIM for 12 weeks, and they were then sacrificed. NIM decreased, in a dose-dependent manner, the incidence of transitional cell carcinoma (TCC) to 12 of 20 (60.0%), 8 of 16 (50.0%), and 5 of 19 (26.3%) and the multiplicity of TCCs to 0.75 +/- 0.79, 0.56 +/- 0.63, and 0.37 +/- 0.78 per rat at 100, 200, and 400 ppm, respectively, as compared with the BBN alone group values of 18 of 20 (90.0%) and 2.35 +/- 1.23. NIM did not significantly affect the cell differentiation or invasiveness of TCCs. These results indicate clear chemopreventive potential of a selective cyclooxygenase-2 inhibitor against postinitiation development of superficial rat urinary bladder carcinomas.

Animals↗
PubMed1998

[A model of rat's urinary bladder tumor induced by subcutaneous injection of N-butyl-N-(4-hydroxybutyl)-nitrosamine].

A model of urinary bladder tumor was developed in the rat by subcutaneous injection of N-dibutyl-N-(4-hydroxybutyl) nitrosamine. A direct dose-tumor frequency correlation was established. Maximum effect (100%) was recorded with administration of 70 mg of the carcinogenic agent twice a week, for 3 months. Among neoplasms induced were transitional-cell and in situ carcinoma, and multiple papilloma of the bladder. Carcinogenesis was found to involve a significant rise in the activity of urinary beta-gluco-uronidase which may be used as a diagnostic testing procedure.

Animals↗