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PubMed1984

Mutagenicity of urine of various species fed N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide or 2-amino-4-(5-nitro-2-furyl)thiazole.

Rats, mice and hamsters, which are susceptible to the bladder carcinogenesis by N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT), and guinea pigs, which are not, were fed a diet containing 0.188% FANFT or 0.188% 2-amino-4-(5-nitro-2-furyl)thiazole (ANFT) for 1 week and their urine was then examined for mutagenicity for S. typhimurium TA100. The mutagenicities of the urine of these species fed FANFT were approximately equal. Similarly, that of the urine of these species fed ANFT were also approximately equal. However, the urine from FANFT-fed animals was approximately 10 times as mutagenic as that from ANFT-fed animals. ANFT was detected only in the urine of rats, mice or hamsters fed FANFT. A positive correlation between the susceptibility toward bladder carcinogenesis by FANFT and urinary ANFT excretion was demonstrated, although the correlation between this susceptibility and urine mutagenicity was lacking.

Animals↗
PubMed1995

Effect of indomethacin on N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide-induced urinary tract carcinogenesis.

The effects of indomethacin on the urinary bladder and renal pelvis in rats treated with N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT) were studied. Two hundred female Sprague-Dawley rats were divided into four groups. Group 1 received control diet without added chemicals. Group 2 was treated with indomethacin (1 mg/kg per day) in the drinking water throughout the experiment. Groups 3 and 4 received 0.2% FANFT in the diet for seven weeks followed by control diet. In addition to FANFT, Group 4 received indomethacin, 1 mg/kg per day, for the entire experiment. The rats were sacrificed after 92 weeks. There were no urothelial tumors in the control group, one renal pelvic tumor in the indomethacin group, 4 tumors in the FANFT group and 10 urothelial tumors in the FANFT + indomethacin group. The difference between Groups 3 and 4 was statistically significant (P < 0.05). Moderate and severe hyperplasia of the renal pelvic and papillary epithelium was found in 15 of 48 rats in Group 2 (indomethacin only) as compared with 6 of 49 control rats (P < 0.05). Moderate and severe hyperplasia was equally frequent in Groups 3 and 4 (14 and 17 animals in each group, respectively). Twenty-four rats in Group 2 had mammary tumors as compared to 12 animals in Group 1 (P < 0.01). Five of the tumors in Group 2 were adenocarcinomas. There was no difference between the number of mammary tumors in Groups 3 and 4 (36 and 32 animals in each group, respectively). The results suggest that indomethacin enhances FANFT-induced urinary tract carcinogenesis. Indomethacin also seems to exert some tumorigenic activity in the mammary gland.

Animals↗
PubMed1984

Biotransformation of the bladder carcinogen N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide in mice.

The biotransformation of N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT), a potent urinary bladder carcinogen, was studied in mice. About 82% of radioactivity was excreted as 14CO2 within 36 hr after intragastric administration of N-[4-(5-nitro-2-furyl)-2-thiazolyl]-[14C]formamide, suggesting its deformylation to 2-amino-4-(5-nitro-2-furyl)thiazole ( ANFT ). The latter was formed in vitro as a product following incubation of FANFT with mouse liver homogenates. Chromatographic analysis of mouse urine obtained 24 hr after the i.p. administration of N-[4-(5-nitro-2-furyl)-[2-14C]thiazolyl]formamide revealed excretion of ANFT and unmetabolized FANFT, suggesting the prevalence of the deformylation reaction in vivo. In addition, at least two more metabolites were present in urine. One of these metabolites exhibited chromatographic properties similar to those exhibited by a compound derived from the in vitro nitroreduction of ANFT . This metabolite was isolated from urine of FANFT-fed animals and from in vitro enzymatic reduction of ANFT with mouse liver homogenates. The isolated products had chromatographic and spectral properties and a mass spectral fragmentation pattern similar to that of a compound obtained by catalytic reduction of ANFT with palladium and activated carbon. Spectroscopic analyses established the structural identity of the chemical reduction product as 1-[4-(2-aminothiazolyl)]-3-cyano-1-propanone ( ATCP ). Since the chromatographic properties of the enzymatically derived product and the urinary metabolite were identical to those of a compound obtained by chemical reduction, they must be structurally the same and thus correspond to ATCP . About 5% of the urinary metabolites of FANFT is ATCP , and thus ATCP is quantitatively a minor excretory product. ATCP was far less active than was ANFT of FANFT in the Ames mutagenicity assay with Salmonella typhimurium TA.

Animals↗
PubMed1980

Metabolism of N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide by prostaglandin endoperoxide synthetase.

Cooxidative metabolism of the urinary bladder carcinogen N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT) was examined using solubilized and particulate microsomal preparations from the rabbit renal inner medulla and the ram seminal vesicle. Metabolism was measured by the rate of decrease in absorbance at 400 nm. In these soluble and particulate preparations, FANFT metabolism was observed only in the presence of specific fatty acids. These fatty acids are substrates for prostaglandin endoperoxide synthetase. Structurally dissimilar inhibitors of prostaglandin endoperoxide synthetase such as indomethacin, aspirin, 5,8,11,14-eicosatetraynoic acid, ethoxyquin, and meclofenamic acid specifically inhibited FANFT metabolism. Other inhibitor and substrate specificity studies suggest that FANFT was not metabolized by nitroreductase, xanthine oxidase, lipoxygenase, lipid peroxidation, or mixed-function oxidases. In addition, the lack of detectable 2-amino-4-(5-nitro-2-furyl)thiazole formation suggests that arylformamidase was not participating in FANFT metabolism measured in these experiments. The data indicate that prostaglandin endoperoxide synthetase can mediate FANFT metabolism by a cooxidative process.

Animals↗
PubMed1980

Development of an in vitro and in vivo epithelial tumor model for the study of invasion.

Three continuous cell lines were isolated from N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT)-induced carcinoma of the Fischer rat urinary bladder by standard explant techniques. RBTCC-2 carcinoma cells were derived from a noninvasive FANFT tumor of Stage 0, RBTCC-5 carcinoma cells were from an invasive FANFT tumor of Stage B2, and RBTCC-8 carcinoma cells were from a s.c. metastasis of a FANFT tumor of Stage D2. Invasive and metastatic carcinoma cells were differentiated from their noninvasive counterparts by cellular and nuclear pleomorphism, cell size, nuclear:cytoplasmic ratio, number of nucleoli, and abnormalities of occludens junctions. Using low (less than 10) and high (greater than 80) passages of these cell strains, tumorigenicity experiments in syngeneic rats showed that the normal in vivo progression of FANFT tumors was interrupted by the isolation of carcinoma cells to cell culture. Histological appearance and biological behavior of tumor isografts closely resembled those of the original FANFT tumors. This was best demonstrated when tumor cells were inoculated adjacent to rat femurs. The destruction of bone, monitored radiographically and histologically, served as a measure of the invasive potential of the tumor cells. Destruction and deep invasion were observed only with isografts of invasive and metastatic carcinoma cells, presumably due to collagenolytic activity. Despite rapid degradation of bone by these isografts, the natural resistance of cartilage to tumor invasion could not be overcome. These carcinoma cell lines, together with their normal epithelial counterparts and the major supporting cells of connective tissue characterized previously by our laboratory, provide a unique system to study tumor invasion.

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PubMed1977

A long-term study of reversible and progressive urinary bladder cancer lesions in rats fed N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide.

Hyperplasia and, ultimately, neoplasia of bladder epithelium were produced by feeding 0.2% N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT) to weaning male Fischer rats. Hyperplasia induced by FANFT feeding for 2, 4, or 6 weeks, followed by feeding control diet until the end of the 84-week experiment, was reversible, and at the end of the experiment bladder epithelium in these animals was normal by light and scanning electron microscopy. Hyperplasia produced by 8 or more weeks of FANFT feeding was irreversible and by 84 weeks had resulted in bladder tumors in all animals fed FANFT for 12 or more weeks and in 4 of 5 and 6 of 7 animals fed FANFT for 8 and 10 weeks, respectively. The epithelial changes after 6 and 8 weeks of FANFT were similar by light microscopy but different by scanning electron microscopy. Pleomorphic microvilli seen with scanning electron microscopy are the hallmark of irreversible, and possibly progressive, epithelial proliferative change.

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PubMed1984

Tumor production in germ-free rats fed 5-nitrofurans.

Weanling female germ-free Sprague-Dawley rats were divided into 3 groups: the control group rats were fed an autoclaved 5010C diet for 2 years; the nitrofurantoin (NF) group rats were fed this diet supplemented with 0.188% NF for 2 years; and the N-[4-(5-nitro-2-furyl)-2-thiazolyl]-formamide (FANFT) group rats were fed this diet supplemented with 0.188% FANFT for 20 weeks followed by 20 additional weeks of the control diet. The FANFT-group rats were killed following the early appearance of bladder tumors. Six of 11 control rats had tumors: 2 with mammary fibroadenomas, 1 with adrenal adenoma, 1 with leukemic spleen, and 2 with mesenchymal sarcoma of the colon. Ten of 12 NF-group rats had tumors: 9 with mammary fibroadenomas, 1 with adrenal adenoma, and 1 each with leukemic spleen and cervical squamous cell carcinoma. Eight of 12 FANFT-group rats had tumors: 7 with bladder and 1 with renal pelvis transitional cell carcinoma. The incidences of mammary fibroadenoma in the NF group and of lower urinary tract tumors in the FANFT group were significantly greater (P less than 0.01) than those of these tumors in the control group.

Animals↗
PubMed1992

Ras involvement in cells transformed with 2-amino-4-(5-nitro-2-furyl)thiazole (ANFT) in vitro and with N-[4-(5-nitro-2-furyl)-2-thiazoyl]formamide in vivo.

N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT) administration to rats followed by sodium saccharin results in transitional cell carcinomas of the bladder, of which 24% harbor an activated H-ras gene. Since 2-amino-4-(5-nitro-2-furyl)thiazole (ANFT) is the mutagenic and carcinogenic metabolite of FANFT in vivo, we wished to examine ras activation in in vitro ANFT-transformed rat bladder epithelial cells as well as four cell lines established in culture from in vivo FANFT-induced rat bladder tumors. Screening by Western blotting revealed no enhanced levels of p21ras in ANFT-transformed cells nor in cells established in culture from FANFT-induced rat bladder carcinomas. Further investigations using immunohistochemical staining with a different pan-reactive p21 monoclonal antibody (Cetus Corporation) specific for this method, however, showed two groups of cells from FANFT-induced rat bladder tumors had enhanced immunoreactivity. Apart from this, p21ras expression of most of the cells groups varied little from the controls. We examined the reported hot spots (exons 1 and 2) of each of the ras genes (H-, K- and N-ras) by direct sequencing of amplified DNA. No mutations were present. We conclude, therefore, that ANFT transformation of primary rat bladder epithelial cells in vitro may not in this case be mediated by ras activation, although this is difficult to determine since others have observed that optimal culture conditions can select for certain populations of cells without ras activation.

Animals↗
PubMed1986

Effect of dose on the induction of urothelial proliferation by N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide and its relationship to bladder carcinogenesis in the rat.

The effect on urothelial proliferation of a urinary bladder carcinogen, N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT), fed to male F344 rats at doses of 0.2, 0.1, 0.05, 0.01, 0.005 and 0.001% of diet for 4 or 10 weeks was evaluated by autoradiography, using [3H-methyl]thymidine, and by histopathology. At week 4, hyperplasia was induced in 10/11 and 6/11 rats given 0.2% and 0.1% FANFT, respectively. The dose-related increase of labeling index in the bladder epithelium was significant for the groups given 0.01% or higher doses of FANFT. At week 10, histopathologic lesions were observed in groups given 0.05% or higher doses of FANFT. This was accompanied by a significant increase in labeling index for these groups. The results are consistent with the long-term carcinogenicity studies conducted with the same dose levels of FANFT. The interrelationships between numbers of cells (hyperplasia), cell proliferation (labeling index) and cancer induction are discussed utilizing a computerized model of bladder carcinogenesis.

Animals↗
PubMed1983

Multistage carcinogenesis in the urinary bladder.

The induction of cancer of the urinary bladder is a multi-stage process involving multiple exogenous and endogenous factors. Based on the classical initiation-promotion model, we have used N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT) as initiator and sodium saccharin (SAC) or tryptophan as promoters. These latter chemicals have the properties expected of promoters: induction of hyperplasia, reversibility and nonmutagenicity. Also, tumors were induced whether the promoter was administered immediately after FANFT or beginning 6 weeks after FANFT was discontinued, but no tumors resulted if either promoter was given without initiation with FANFT. Factor(s) present in normal urine also are involved in the promotion process, in addition to the role of urine as a carrier of carcinogens. However, administration of SAC to animals with a rapidly proliferating bladder mucosa, induced by ulceration, pellet insertion, or in utero, resulted in bladder tumor induction, even without prior initiation with FANFT. To better understand the complex interaction of the multiple variables in bladder carcinogenesis, a stochastic computer model has been formulated based on long-term carcinogenicity and tissue kinetic studies in vivo. This model indicates the importance of cell proliferation and the development of hyperplasia in carcinogenesis.

Animals↗
PubMed1991

Lack of bladder tumor promoting activity in rats fed sodium saccharin in AIN-76A diet.

Sodium saccharin (NaSac) fed as 5% of Prolab diet promotes bladder tumor carcinogenesis in male F344 rats initiated with N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT) fed as 0.2% of the diet for 4 weeks. NaSac also increases urothelial proliferation if fed for short periods in Prolab diet, but no increased proliferation is seen if it is fed for up to 10 weeks in AIN-76A semisynthetic diet, even at levels as high as 7.5% of the diet. To determine whether NaSac as part of an AIN-76A diet has promoting activity, groups of approximately 30 male, 5-week-old F344 rats were fed AIN-76A diet containing (a) 0.2% FANFT for 4 weeks followed by 5% NaSac for 100 weeks; (b) 0.2% FANFT followed by control diet; or (c) control diet followed by 5% NaSac. Bladder tumor incidences were 10, 23, and 0%, respectively. When fed in Prolab diet, 0.2% FANFT for 4 weeks followed by NaSac or control diet for 100 weeks resulted in bladder tumor incidences of 40 and 17%, respectively. Groups of rats fed 0.1 or 0.2% FANFT for 1 or 2 weeks followed by 5% NaSac or control diet for 100 weeks had bladder tumor incidences of 0 to 7%. These data demonstrate that NaSac does not promote bladder cancer in male rats if fed in AIN-76A diet. Other studies suggest that this is due to the low urinary pH in rats fed AIN-76A diet.

Animals↗
PubMed1986

Effect of sodium phenobarbital and sodium saccharin in AIN-76A diet on carcinogenesis initiated with N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide and N,N-dibutylnitrosamine in male F344 rats.

Promoting activities of sodium phenobarbital (PB) and sodium saccharin (SS), incorporated in a semisynthetic diet (AIN-76A), on 2-stage carcinogenesis initiated with N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT) or N,N-dibutylnitrosamine (DBN) in male F344 rats were investigated. For the first 4 weeks of the experiment, weanling male Fischer rats were fed Wayne diet containing 0.2% FANFT or drinking water containing 0.005% DBN. The control rats were given the basal diet and normal drinking water. Beginning at the fifth week, the rats were given the AIN-76A diet or this diet containing 0.05 or 0.15% PB or 5% SS. The experiment was terminated at the end of 100 weeks. PB significantly increased the incidence of transitional cell carcinoma of the bladder of the rats that had been treated with FANFT (P = 0.027). PB also increased the incidence of bladder carcinoma of the rats that had been treated with DBN, but the increase was not significant (P = 0.081). SS in the AIN-76A diet increased the incidence of bladder carcinoma in the rats which had been treated with FANFT or DBN, but the increase was not significant (P = 0.059 and 0.327, respectively). Both high and low doses of PB, but not SS, significantly increased the incidence of hepatocellular carcinoma in the rats that had been treated with DBN. None of the control rats that had been fed the basal diet or the basal diet containing low or high PB or 5% SS developed either bladder or liver carcinoma. These results demonstrate that PB promotes urinary bladder carcinogenesis of rats initiated with FANFT but not with DBN. In contrast to incorporation in commercial rat chows, SS incorporated in the AIN-76A diet is very weak in promoting bladder carcinogenesis. On the other hand, PB, but not SS, promotes hepatocarcinogenesis initiated with DBN. Neither PB nor SS promoted DBN-induced carcinogenesis of esophagus or forestomach.

Animals↗
PubMed1984

Enhancement by phenothiazine and 2,5-di-O-acetyl-D-glucosaccharo-(1,4)(6,3)-dilactone of bladder carcinogenicity of N-[4-(5-nitro-2-furyl)-2-thiazolyl]-formamide in rats.

Rats concomitantly fed N-[4-(5-nitro-2-furyl)-2-thiazolyl] formamide (FANFT) and phenothiazine, or concomitantly fed FANFT and Glucaron then fed Glucaron alone had significantly greater incidences of transitional cell carcinomas of the bladder than rats fed FANFT alone. Caffeine and cysteamine did not affect FANFT bladder carcinogenesis. Phenothiazine induced nitroreductase activity of hepatic microsomes.

Animals↗
PubMed1996

Analysis of differentiation-associated proteins in rat bladder carcinogenesis.

Uroplakins are the major integral membrane proteins synthesized in terminally differentiated, superficial urothelial cells. Alteration of cell differentiation during rat urinary bladder carcinogenesis was analyzed immunohistochemically for the expression of uroplakins. Expression of uroplakins was compared in N-[4-(5-nitro-2-furyl)-2-thiazolyl]-formamide (FANFT)-, uracil-, sodium saccharin- or sodium ascorbate-induced urothelial simple hyperplasia, papillary-nodular hyperplasia, papilloma and carcinoma. In controls, uroplakins were located only in superficial cells, especially the luminal surface membrane. In FANFT-induced hyperplasia, including simple hyperplasia, intermediate cells also stained and the staining pattern was disorderly and intermittent. In uracil-induced simple hyperplasia, intermediate cells were stained but in an orderly fashion. In sodium saccharin- or sodium ascorbate-induced simple hyperplasia, superficial cells were swollen but alterations were not observed in the staining pattern. In carcinoma induced by FANFT and uracil, uroplakin expression was very disorderly and focal, usually with no expression on surface cells. It appears that disorderly differentiation is an index of bladder malignancy and is an early event in FANFT-induced lesions but a late event in uracil-, sodium saccharin- and sodium ascorbate-induced lesions.

Animals↗
PubMed1983

Co-carcinogenicity of sodium saccharin and N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide for the urinary bladder.

The co-carcinogenic activity of sodium saccharin and N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT) was evaluated in male Fischer rats by co-administering them as 5% and 0.005% of the diet, respectively, for 2 years. The effect of simultaneous administration of two urinary bladder promoting substances, sodium saccharin and L-tryptophan as 5% and 2% of the diet, respectively, was also evaluated. Five of 16 rats administered sodium saccharin plus FANFT developed bladder tumors whereas none of the rats administered FANFT, sodium saccharin, or L-tryptophan alone, sodium saccharin plus L-tryptophan, or the control diet developed bladder tumors. Possible mechanisms for the co-carcinogenic activity of sodium saccharin and FANFT are discussed.

Animals↗
PubMed1985

Immunohistochemical study of keratin in proliferative bladder epithelium induced by freezing, cyclophosphamide or N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide in the rat.

The distribution of intracellular keratin proteins was examined in a variety of urinary bladder lesions of the rat using the immunoperoxidase staining technique. In ethanol-fixed sections, the normal epithelium was strongly positive for keratin staining. Focal regenerative hyperplasia of the bladder epithelium induced by freezing exhibited relatively weak staining. However, diffuse regenerative hyperplasia induced by a single intraperitoneal injection of cyclophosphamide (CP) showed an intensely positive reaction throughout the epithelium. Of the sections fixed with Bouin's solution, the staining reaction was drastically reduced in the normal bladder and the staining was totally negative in the regenerative hyperplasia caused by freezing. Simple hyperplasia induced by a 4-week feeding of N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT) as 0.2% of the diet exhibited strong reactivity, and nodular and papillarly hyperplasia induced by a 10-week feeding of FANFT was also positive for keratin throughout the lesions. In contrast to the preneoplastic lesions, FANFT-induced transitional cell carcinoma showed differential staining within the tumors. These results suggest that different keratin expression is involved in the proliferative bladder lesions induced mechanically by freezing and chemically by CP or by the carcinogen FANFT.

Animals↗
PubMed1988

The influence of antipyrene on N-[4-(5-nitro-2-furyl)-2-thiazolyl]-formamide-induced urinary tract carcinogenesis.

Human over-use of analgesics containing phenacetin, antipyrene (phenazone) and caffeine has been associated with the development of both renal pelvic and bladder tumors. In Sprague-Dawley rats antipyrene has been shown to be a weak complete urinary tract carcinogen. The present study was designed to evaluate the promoting capacity of antipyrene in N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT)-induced urinary tract carcinogenesis. One hundred and eighty male Sprague-Dawley rats were divided into groups of 30 and were treated with the following chemicals in the diet: group 1 received a control diet without chemicals; group 2 was treated with 0.2% FANFT in the diet for five weeks followed by control diet; group 3 received 0.2% FANFT for five weeks followed by 0.535% antipyrene in the diet; group 4 was treated with 0.535% antipyrene; group 5 was treated with 0.102% caffeine; and group 6 was treated with 0.535% antipyrene and 0.102% caffeine in the diet. Ten of 27 rats in group 3 (37%) developed urinary tract tumors (P greater than 0.001, five of which were renal pelvic tumors and five were bladder tumors. The majority of the tumors were well differentiated non-invasive urothelial carcinomas. None of the rats in other groups developed urinary tract tumors. In addition, renal papillary necrosis (RPN) was found in 33% of the rats in group 3, 50% in group 4, and 10% in group 6. The present study clearly shows that antipyrene acts as a promoter of FANFT-induced urinary tract carcinogenesis and that it is nephrotoxic to the renal papilla resulting in renal papillary necrosis.

Animals↗
PubMed1976

Effect of avitaminosis A and hypervitaminosis A on urinary bladder carcinogenicity of N-(4-(5-Nitro-2-furyl)-2-thiazolyl)formamide.

The effect of vitamin A deficiency and hypervitaminosis A on the urothelial carcinogenicity of N-[4-(5-nitro-2-furyl)-2-thiazolyl]formanmide (FANFT) was determined in female weanling Sprague-Dawley rats. Vitamin A deficiency resulted in squamous metaplasia of the urinary bladder and high incidences of cystitis, ureteritis, and pyelonephritis. Administration of FANFT to vitamin A-deficient rats appeared to accelerate the carcinogenic process, with earlier appearance of urinary bladder tumors and the development of ureteral and renal pelvic carcinomas. Most of these tumors were squamous cell, occasionally with transitional cell foci. Hypervitaminosis A prevented the appearance of squamous metaplasia and squamous cell neoplasia in rats fed FANFT, but it did not inhibit the formation of transitional cell hyperplasia or neoplasia in comparison to rats receiving normal levels of vitamin A and FANFT.

Animals↗