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At least 433 records · Page 24Linked to original sources
PubMed1976

Comparative carcinogenicity of 5-nitrothiophenes and 5-nitrofurans in rats.

We investigated the carcinogenicity of five 5-nitrothiophenes with heterocyclic substituents at the 2-position of the thiophene ring by feeding the chemicals to Sprague-Dawley rats and comparing the type and incidence of lesions with those appearing after exposure to two 5-nitrofurans. Benign and malignant mammary tumors and intestinal tract sarcomas were the most frequent lesions induced by 5-nitrothiophenes. 4-Bis(2-hydroxyethyl)amino-2-(5-nitro-2-thienyl)quinazoline caused a 100% incidence of mammary adenocarcinomas in 28 female rats at risk; it induced 3 benign and 5 malignant mammary tumors and 13 small intestine sarcomas in 20 male rats. A high incidence of similar lesions was observed in male and female rats fed the corresponding 5-nitrofuran analogue, 4-bis(2-hydroxyethyl)amino-2-(5-nitro-2-furyl)quinazoline. In marked contrast, 4 of 28 female rats receiving 4-bis(2-hydroxyethyl)amino-2-(2-thienyl)quinazoline, which lacks the nitro group at the 5-position on the thiophene ring, had solitary benign mammary tumors (P greater than 0.2). Additional 5-nitrothiophenes demonstrating significant oncogenic activity for female rats were 4-morpholino-2-(5-nitro-2-thienyl)quinazoline, 4-(2-hydroxyethylamino)-2-(5-nitro-2-thienyl)quinazoline 4-(2,3-dihydroxypropylamino)-2-(5-nitro-2-thienyl)quinazoline, and 1,2-dihydro-2-(5-nitro-2-thienyl)quinazolin-4(3H)-one. Another nitrofuran, 4,6-dimethyl-2-(5-nitro-2-furyl)-pyrimidine, provided the following types of neoplasms in 30 female rats at risk: squamous cell carcinomas of the forestomach (30), sarcomas of the intestine (21), adenocarcinomas of the kidney (2).

Adenocarcinoma↗
PubMed1978

Effect of intestinal microflora on 2,2'-dimethyl-4-aminobiphenyl-induced carcinogenesis in F344 rats.

The effect of intestinal microflora on colon and breast carcinogenesis induced by 3,2'-dimethyl-4-aminobiphenyl (DMAB) was studied with the use of germfree and conventional F344 rats of both sexes. At 7 weeks of age, all animals except controls were given 20 weekly sc injections of DMAB in corn oil (100 mg/kg body wt/wk). Male animals were autopsied 15 weeks after the last injection, whereas female animals were autopsied 10 weeks after the last injection. Tumors were induced in the colons, duodena, breasts, ear ducts, salivary glands, and skin of conventional rats, and in the colons, breasts, ear ducts, salivary glands, and skin of germfree rats. No consistent difference was found in the incidence of tumors in the ear ducts, salivary glands, and skin between the germfree and conventional rats. None of the germfree rats showed duodenal tumors, whereas 13% of the female and 53% of the male conventional rats developed duodenal tumors. The incidence of intestinal tumors was lower in the germfree rats than in conventional animals. The mammary tumor incidence was lower in germfree female rats than in the conventional female rats than in the conventional females. DMAB induced fewer intestinal and breast tumors in germfree rats than in conventional rats.

Adenocarcinoma↗
PubMed1984

Persistence of DNA single-strand breaks and other tests as indicators of the liver carcinogenicity of 1-nitroso-5,6-dihydrouracil and the noncarcinogenicity of 1-nitroso-5,6-dihydrothymine.

The cyclic nitrosourea 1-nitroso-5,6-dihydrothymine [(NDHT) 1-nitrosodihydrothymine] was not significantly carcinogenic when it was administered for 1 year in drinking water (206 mg/liter) to MRC-Wistar rats. In acute toxicity tests, ip injection of saline solutions of 1-nitroso-5,6-dihydrouracil [(NDHU) CAS: 16813-36-8; 1-nitrosohydrouracil], a strong liver carcinogen in rats, produced only mild liver toxicity but marked focal degeneration of myocardial fibers. NDHU injected ip in water solution produced subcapsular liver damage. NDHU, but not NDHT, induced unscheduled DNA synthesis in hepatocyte primary cultures. NDHU, NDHT, and methylnitrosourea [(MNU) CAS: 684-93-5; N-methyl-N-nitrosourea], a liver carcinogen only under special conditions, were tested for their ability, when injected ip into rats, to produce liver DNA damage measured as strand breaks by alkaline sucrose gradient centrifugation. The three nitrosoureas produced similar maximum DNA damage of 2.2-3.2 strand breaks/10(8) daltons. Eighty percent of the damage due to NDHU persisted for 7 days, and the damage at that time was significantly greater than that produced by NDHT and MNU. The varying persistence of liver DNA damage may explain why NDHU, but not NDHT, is a liver carcinogen.

Animals↗
PubMed1991

Modifying effects of various chemicals on preneoplastic and neoplastic lesion development in a wide-spectrum organ carcinogenesis model using F344 rats.

Modifying potentials of various chemicals on tumor development were investigated in a wide-spectrum organ carcinogenesis model using male F344/DuCrj rats. The animals were treated with N-nitrosodiethylamine (100 mg/kg body weight, ip, single injection at the commencement of the study), N-methyl-N-nitrosourea (20 mg/kg body weight, ip, 4 times during weeks 1 and 2) and N-bis(2-hydroxypropyl)nitrosamine (0.1% in drinking water, during weeks 3 and 4) for multi-organ initiation and then were given one of 14 test chemicals including 6 hepatocarcinogens, 7 non-hepatocarcinogens and 1 non-carcinogen, or basal diet for 16 weeks. All rats were killed at the end of week 20, and the major organs were carefully examined for preneoplastic and neoplastic lesions. Immunohistochemical demonstration of glutathione S-transferase-positive foci was also used for quantitative assessment of liver preneoplastic lesion development. Modifying effects were shown for 11 out of 14 test agents in the liver, forestomach, glandular stomach, lung, urinary bladder or thyroid, 7 of them targeting more than two organs. This was the first demonstration to our knowledge that clofibrate possesses enhancing potential for urinary bladder carcinogenesis and an inhibiting effect on thyroid carcinogenesis. Caprolactam showed no effect in any organ, in agreement with its established inactivity. The results indicated that the system could be reliably applied as a medium-term multiple organ bioassay for assessment of the modification potential of test agents in unknown target sites.

Administration, Oral↗
PubMed1976

Urothelial changes of the renal papillae in Sprague-Dawley rats induced by long term feeding of phenacetin.

Thirty female Sprague-Dawley rats were fed 0.535 per cent phenacetin in the diet for up to 110 weeks. Twenty-six of these rats developed urothelial hyperplasia, partly papillary, of the renal papillae. Twenty-eight rats showed dilatation of the vasa recta frequently associated with thrombus formation and calcification. One phenacetin fed rat had epithelial hyperplasia associated with chronic pyelitis. In 2 of the 30 control rats urothelial hyperplasia was found to be associated with chronic pyelitis. The hyperplastic urothelial changes and vascular changes were often, but not always, present simultaneously. One control rat developed a mammary carcinoma, as compared with 5 rats in the phenacetin group. Four phenacetin fed rats developed carcinoma of the ear duct. The results of the present investigation provide evidence that phenacetin can induce proliferative lesions of the urothelium of the rat renal pelvis with weak carcinogenic activity in the ear duct and mammary glands.

Animals↗
PubMed1988

Tumorigenicity of simian virus 40-hepatocyte cell lines: effect of in vitro and in vivo passage on expression of liver-specific genes and oncogenes.

Five simian virus 40 (SV40)-hepatocyte cell lines were examined for tumorigenicity and the effect of in vitro passage on the expression of four liver-specific genes (albumin, transferrin, alpha 1-antitrypsin, and phosphoenolpyruvate carboxykinase), two oncogenes (c-Ha-ras and c-raf), and two genes associated with hepatocarcinogenesis (alpha-fetoprotein and placental-type glutathione-S-transferase). At low passage (12 to 22), all five cell lines expressed the four liver-specific genes at levels similar to those in the liver and were not tumorigenic or were weakly tumorigenic. At high passage (33 to 61), the cell lines formed carcinomas, and four out of five cell lines produced primary tumors that metastasized. At least two cell lines produced well-differentiated hepatocellular carcinomas that expressed liver-specific RNAs. Levels of expression of liver-specific genes changed with time in culture. Some of the changes in liver-specific gene expression in the tumor tissue (such as for the phosphoenolpyruvate carboxykinase gene) paralleled those that occurred with in vitro passage, while other changes (such as for the albumin gene) did not parallel those that occurred with in vitro passage. Correlations between enhanced expression of c-Ha-ras and tumorigenic potential and between the process of SV40 immortalization and induced expression of c-raf and glutathione-S-transferase-P were observed. Induction of alpha-fetoprotein was detected with in vitro and in vivo passage only in the CWSV14 cell line and was paralleled by diminished albumin expression. In conclusion, we developed a model system with five SV40-hepatocyte cell lines, tumors induced by them, and tumor cell lines to examine changes in gene expression that accompany the progression from a normal cell to a hepatocellular carcinoma. Because the SV40-hepatocyte cell lines and tumor cell lines remain highly differentiated and vary in the magnitude of expression of specific genes, they can be used to study the molecular mechanisms regulating gene expression, in particular those regulating specific genes associated with differentiation.

Animals↗
PubMed1994

Tumor development and apoptosis.

Apoptosis or other types of active cell death may play a major role at various stages of carcinogenesis. Active cell death can be induced, by internal and exogenous signals, in preneoplastic, neoplastic and even malignant cells. It may reverse the effects of initiation and promotion and may lead to tumor regression. Conversely tumor promoters may inhibit active cell death in preneoplastic cells and thereby accelerate cancer development.

Animals↗
PubMedDate not supplied

Tumors and dental and ocular abnormalities after treatment of infant rats with adriamycin.

In rats repeatedly treated subcutaneously as infants with adriamycin in 2 cycles of 4 treatments each, the induction of ocular and dental abnormalities and tumors was studied. Cataracts appeared from 18 to 26 days in 80% of CD rats treated with 1.15 mg/kg/day of adriamycin and from 28 to 104 days in 55% of Wistar-Lewis rats given 0.75 mg/kg/day adriamycin. Abnormal growth of incisors was observed in 30% of the CD rats and in 44% of the Wistar-Lewis rats. At lower doses, no such abnormalities were found. At about 1 year after treatment, 100% of the CD rats treated with 0.75 mg/kg/day adriamycin and about 60% of the Wistar-Lewis rats treated with 0.75 and 0.5 mg/kg/day adriamycin developed tumors, which were histologically classified.

Adenoma↗
PubMedDate not supplied

Chemical modification of tumour blood flow.

The preferential modification of tumour blood flow with chemical agents has been extensively investigated for the purpose of improving the treatment of tumours with ionizing radiation, chemicals and hyperthermia. In this paper I have utilized representative vasoactive drugs to demonstrate the various mechanisms via which tumour haemodynamics can be modified selectively. Chemicals which alter tumour blood flow by changing blood viscosity are also discussed. Of particular interest are the calcium entry blockers, flunarizine and verapamil, which have been shown to increase tumour blood flow, tumour oxygenation, tumour radiation sensitivity and the cytotoxicity of chemotherapeutic agents. These encouraging research results provide compelling evidence that these two drugs may prove to be useful adjuvants for radiation therapy.

Adenocarcinoma↗
PubMed1994

Oxygenation of the rat 9L gliosarcoma and the rat 13672 mammary carcinoma with various doses of a hemoglobin solution.

Tumor oxygen tensions were measured using a computer controlled pO2 microelectrode in two preclinical solid tumor models, the rat 9L gliosarcoma and the rat 13672 mammary carcinoma. Tumor oxygenation profiles were determined under four conditions: 1) normal air breathing, 2) carbogen (95% O2/5% CO2) breathing, 3) after intravenous administration of a solution of ultrapurified polymerized bovine hemoglobin with normal air breathing and 4) after intravenous administration of a solution of ultrapurified polymerized bovine hemoglobin with carbogen breathing. Both tumors had severely hypoxic regions under normal air breathing conditions. Although carbogen breathing increased the oxygenation of the better oxygenated portions of the tumor, it did not impact on the severely hypoxic tumor regions. Administration of the hemoglobin solution was effective in increasing the oxygenation throughout both tumors under normal air breathing conditions. The addition of carbogen breathing to administration of the hemoglobin solution eliminated severe hypoxia in the 9L gliosarcoma and markedly reduced the severely hypoxic regions of the 13672 mammary carcinoma.

Animals↗