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PubMed2003

Analysis of nitrofuran metabolites in food by high-performance liquid chromatography with tandem mass spectrometry detection.

A reliable and sensitive procedure is presented for the analysis of nitrofuran metabolite residues in foods of animal origin, like poultry and shrimp. The method is based on a one-step extraction/derivatization, followed by solid-phase extraction clean-up with polymeric phase cartridges. The separations were carried out by liquid chromatography coupled with tandem mass spectroscopy detection. Results from the full validation of the procedure and from a survey of food available from the Swiss market, with the analysis of 236 samples of shrimp, poultry, fish and rabbit, are presented and demonstrate that this method is satisfactory in order to control nitrofuran residues in foods of animal origin.

Animals↗
PubMed1991

Inhibition of microsomal lipid peroxidation and cytochrome P-450-catalyzed reactions by nitrofuran compounds.

(5-Nitro-2-furfurylidene)amino compounds bearing triazol-4-yl, benzimidazol-1-yl, pyrazol-1-yl, triazin-4-yl or related groups (a) stimulated superoxide anion radical generated by rat liver microsomes in the presence of NADPH and oxygen; (b) inhibited the NADPH-dependent, iron-catalyzed microsomal lipid peroxidation; (c) prevented the NADPH-dependent destruction of cytochrome P-450; (d) inhibited the NADPH-dependent microsomal aniline 4-hydroxylase activity; (e) failed to inhibit either the cumenyl hydroperoxide-dependent lipid peroxidation or the aniline-4-hydroxylase activity, except for the benzimidazol-1-yl and the substituted triazol-4-yl derivatives, which produced minor inhibitions. Reducing equivalents enhanced the benzimidazol-1-yl derivative inhibition of the cumenyl hydroperoxide-induced lipid peroxidation. The ESR spectrum of the benzimidazol-1-yl derivative, reduced anaerobically by NADPH-supplemented microsomes, showed characteristic spin couplings. Compounds bearing unsaturated nitrogen heterocycles were always more active than those bearing other groups, such as nifurtimox or nitrofurazone. The energy level of the lowest unoccupied molecular orbital was in fair agreement with the capability of nitrofurans for redox-cycling and related actions. It is concluded that nitrofuran inhibition of microsomal lipid peroxidation and cytochrome P-450-catalyzed reactions was mostly due to diversion of reducing equivalents from NADPH to dioxygen. Trapping of free radicals involved in propagating lipid peroxidation might contribute to the overall effect of the benzimidazol-1-yl and substituted triazol-4-yl derivatives.

Aniline Hydroxylase↗
PubMed1975

Correlation between the carcinogenicities of nitrofuran derivatives and their destructive actions on sebaceous glands of mouse skin.

The effects of six nitrofuran derivatives (including a formerly used food preservative) on mouse skin sebaceous glands were investigated. A close correlation was found between the carcinogenicities and destructive activities of nitrofuran derivatives on the sebaceous glands. 5-Nitro-2-furaldehyde semicarbazone and 4-methyl-1-[(5-nitrofurfurylidene)amino]-2-imidazolidinone, which are carcinogenic, caused marked destruction of the glands at a dose of 1-5 mg/mouse. 2-(5-Nitro-2-furfurylidene)-aminoethanol almost completely destroyed the glands at a dose of 5 mg/mouse; its carcinogenicity has not yet been investigated. 1-[(5-Nitrofurfurylidene)amino]-carcinogenic, did not affect the glands, even at a dose of 5 mg/mouse. 2-(2-Furyl)-3-(5-nitro-2-furyl)acrylamide, which is a potent mutagen but not carcinogenic, had no effect on the glands at a dose of 5 mg/mouse. Under similar conditions, the potent carcinogen 7,12-dimethylbenz(alpha)athracene almost completely destroyed the sebaceous glands at a dose of 0.05 mg/mouse, but dimethyl sulfoxide (used as solvent for the test compounds) had no effect.

Animals↗
PubMed1975

Damage to mammalian cell DNA by nitrofurans.

Maximum rates of nitrofuran reduction by intact mammalian cells and homogenates of mouse liver are obtained under anaerobic conditions, although significant reduction does occur with gas mixtures containing 5% oxygen and less. Single-strand breaks in DNA, measured as a decrease in the sedimentation constant on alkaline sucrose gradients, are produced in mammalian L929, KB, AND BHK-21 cells in vitro and Ehrlich ascites cells in vivo by several nitrofuran derivatives under hypoxic conditons.

Aerobiosis↗
PubMedDate not supplied

Liquid chromatographic determination of multiple sulfonamides, nitrofurans, and chloramphenicol residues in pasteurized milk.

A rapid and selective liquid chromatographic method was developed to detect 6 sulfonamides, 3 nitrofurans, and chloramphenicol residues in pasteurized milk. The 10 drugs were extracted with chloroform-acetone and the organic phase was evaporated; the residues were dissolved in an aqueous sodium acetate buffer solution 0.02M (pH = 4.8), and the fat was removed by washing with hexane. The aqueous layer was collected, filtered, and injected. The 6 sulfonamides and chloramphenicol were detected at 275 nm ultraviolet (UV) using a gradient system starting with sodium acetate buffer solution-acetonitrile (95 + 5) and finishing with sodium acetate buffer solution-acetonitrile (80 + 20). Nitrofurans were detected at 375 nm (UV) isocratically with sodium acetate buffer solution-acetonitrile (80 + 20). For 50 ppb fortified milk, the average recoveries were (sulfathiazole) 65.52%; (sulfamerazine) 75.36%; (sulfamethazine) 93.94%; (sulfachlorpyridazine) 75.94%; (sulfamethoxazole) 85.18%; (sulfamonomethoxine) 83.45%; (chloramphenicol) 104.17%; (nitrofurazone) 91.81%; (furazolidone) 100.76%; and (furaltadone) 72.38%. Method detection limits ranged from 4 ppb (nitrofurazone) to 16 ppb (sulfamethazine). Some matrix interferences (3-7 ppb) were observed only with sulfonamides.

Animals↗
PubMedDate not supplied

Stability of sulfonamides, nitrofurans, and chloramphenicol residues in preserved raw milk samples measured by liquid chromatography.

A stability study was made of 10 antimicrobials: 6 sulfonamides, 3 nitrofurans, and chloramphenicol residues in raw milk samples preserved with 0.1 % potassium dichromate (K2Cr2O7) and 0.05% mercuric bichloride (HgCl2) during cold storage for 7 days. Preserved milk samples fortified with 50 ppb of each antimicrobial were analyzed by liquid chromatography (modified AOAC Method 993.32). Drugs were extracted with chloroform-acetone after solvent evaporation residues were dissolved with aqueous sodium acetate buffer solution (0.02M, pH 4.8), and fat was removed with hexane. Sulfonamides and chloramphenicol were detected at 275 nm (UV) by using a gradient system of sodium acetate buffer solution-acetonitrile starting at 95 + 5 (v/v) and finishing at 80 + 20 (v/v). Nitrofurans were detected at 375 nm (UV) isocratically with sodium acetate buffer solution-acetonitrile (80 + 20, v/v). Residues stability was measured through recovery data. Sulfamethoxazole, sulfachloropyridazine, nitrofurazone, furazolidone, and furaltadone residues remained stable in the presence of either preservative for 7 days. Sulfamethazine and chloramphenicol were not affected by K2Cr2O7, but had significant losses (p <0.05) when HgCl2 was used: 26.2 and 13.4%, respectively. Average recoveries of sulfamonomethoxine, sulfamerazine, and sulfathiazole significantly decreased by Day 7, with losses of 17.1, 17.2, and 23.2% for K2Cr2O7, and 23.3, 20.7, and 48.0% for HgCl2, respectively. During 5 days of cold storage all antimicrobials tested, except sulfathiazole, remained stable in milk samples preserved with 0.1 % K2Cr2O7 or 0.05% HgCl2.

Animals↗
PubMed1976

[Comparison of the sensitivity of pathogenic staphylococci isolated in 1974 to certain antibiotics and nitrofuran derivatives].

Sensitivity of 267 strains of pathogenic staphylococci isolated in 1974 was studied with respect to some antibiotics and nitrofuran derivatives by the method of serial dilutions on solid media. Sensitivity to penicillin, oxacillin, olemorphocycline, ristomycin and nitrofuran derivatives (furagin and salafur) was observed in 30.7 +/- 2.8, 61.8 +/-3, 29.2 +/-2.8 and 98.9 +/- 0.8 per cent of the cultures respectively.

Adult↗
PubMed1975

Carcinogenicity of 5-nitrofurans and related compounds with amino-heterocyclic substituents.

Carcinogenicity of eight 5-nitrofurans with heterocyclic substituents at the 2-position of the furan ring was investigated by feeding the chemicals to Sprague-Dawley female rats. N-[5-(5-nitro-2-furyl)-1,3,4-thiadiazol-2-yl]acetamide induced in 30 rats the highest incidence of tumors with the greatest number of tissues involved: forestomach squamous cell tumors (22), kidney pelvis transitional cell carcinomas (15), pulmonary alveolar cell carcinomas (16), hemangioendothelialsarcomas (20) of the intestine, mesentery, liver, lung, and pancreas, and a few tumors of other tissues. 2-Amino-5-(5-nitro-2-furyl)-1,3,4-thiadiazole, 2-amino-5-(5-nitro-2furyl)-1,3,4-oxadiazole, and trans-2-[dimethylamino)methylimino]-5-[2-(5-nitro-2-furyl)vinyl]-1,3,4-oxadiazole produced high incidences of mammary tumors. The other four 5-nitrofurans tested: N-[4-(5-NITRO-2-FURYL)-2-THIAZOLYL]ACETAMIDE;2,3,4-TRIFLUORO-N-[4-(5-NITRO-2-furyl)-2-thiazoly]acetamide;5-(5-nitro-2-furyl)-1,3,4-oxadiazol-2-ol; and N-( [3-(5-nitro-2-furyl)-1,2,4-oxadiazol-5-yl]methyl)acetamide were associated with tumor incidences of 40-60%. Two other chemicals were also tested: 2-Amino-5-nitrothiazole caused a low incidence of breast and kidney pelvis tumors, and 2-amino-4-(p-nitrophenyl)thiazole induced a high incidence of breast and salivary gland adenocarcinomas and lymphomas.

Adenocarcinoma↗
PubMedDate not supplied

[EPR studies and the role of the electron structure of the heterocycle in the metabolic denitrosation of 5-nitrofuran].

The ESR method revealed that the reduction of 5-nitrofuran and nitrobenzene in liver homogenate is accomplished by the appearance of the nitro anion radicals. ESR spectrum of nitroxyl radical for nitrobenzene was recorded. Metabolic denitrosation in liver homogenate and the formation of hemoprotein nitrosyl complexes were present for 5-nitrofuran and were absent for nitro- and nitrosobenzene. Quantum chemical calculations of the electron structure for the molecules of 5-nitrosofuran and nitrosobenzene showed that the electronegative oxygen atom in the aromatic system turns to increase the positive charge of C atom bonded to NO group. The process of denitrosation in the molecules of 5-nitrosofuran and 5-N-furylhydroxylamine was proposed to include the reaction of nucleophilic NO group substitution.

Animals↗
PubMedDate not supplied

Renal handling of 5-nitrofuran nephrotoxins in the rat.

Formic acid 2-[4-(5-nitro-2-furyl)-2-thiazolyl)-hydrazide (FNT) and 3-hydroxymethyl-1-([3-(5-nitro-2-furyl)-allydidene]amino)hydantoin (HMN) were investigated to determine whether differences in the renal handling of these two chemicals might provide evidence to explain their different patterns of toxicity and carcinogenicity. The isolated perfused rat kidney and whole animal were used. In the isolated perfused rat kidney, both FNT and HMN had similar half-lives (t1/2) but the urinary excretion and renal clearance of HMN (2.1 +/- 0.4 greater than those of FNT (0.2 +/- 0.1 nmol/min and 0.06 +/- 0.01 ml/min, respectively). Probenecid increased the t1/2 and decreased the metabolic clearance of HMN but did not have any effect on FNT t1/2 or clearance. These differences in excretion of FNT and HMN could not be explained on the basis of protein binding. The total clearances of FNT and HMN were similar and significantly higher than that of the 5-nitrofuran bladder carcinogen ANFT. In the whole animal, the urinary excretion of HMN was about 10-fold greater than that of FNT. The t1/2 of both FNT and HMN was less than 5 min in the whole animal. Probenecid decreased the urinary excretion of HMN from 9.7 +/- 1.4% to 4.4 +/- 1.0% (p less than 0.05). Compared with HMN, FNT has less urinary excretion but a similar elimination t1/2, suggesting a greater nonrenal clearance. HMN but not FNT has tubular excretion. Thus, alterations in substituents of 5-nitrofurans markedly alter their renal handling and may partially explain their diverse toxic effects.

Animals↗
PubMed1983

[Nitrofuran poisoning in veal calves].

Prolonged administration of furazolidone to calves may give rise to chronic furazolidone poisoning: retardation of growth, thrombocytopenia and leucopenia, occasionally changing into haemorrhagic diathesis. In acute nitrofuran poisoning neurological signs are observed as a consequence of monoamine oxidase inhibition. Five incidents of acute nitrofuran poisoning on veal calf farms are reported in the present paper, each with a mortality rate varying frm 46.7 per cent ot 70 per cent. Ten times the recommended dose of furazolidone or furadoltone was administered in each case.

Acute Disease↗
PubMed1981

Microsomal nitroreductase activity of rabbit kidney and bladder: implications in 5-nitrofuran-induced toxicity.

Reductive metabolism of the aromatic nitro group of 5-nitrofurans is thought to be an important step in the mechanism of their toxicity. Microsomal nitroreductase activity with p-nitrobenzoic acid and N-[4-(5-nitro-2-furyl)-2-thiazolyl[formamide (FANFT) as substrates was assessed in the renal cortex, outer medulla, inner medulla, bladder transitional epithelial and non-epithelial bladder tissue. Cortex and transitional epithelial tissue contained the most p-nitrobenzoic acid reductase activity. However, FANFT reductase activity was similar in all areas tested except nonepithelial bladder tissue, which was 10% of the others. FANFT reduction was inhibited by oxygen, but not by carbon monoxide, allopurinol or aspirin and required NADPH. These results are consistent with NADPH-cytochrome c reductase catalyzed FANFT reduction. In medullary microsomes, the apparent Km and Vmax were 0.125 mM and 0.84 nmol/mg of protein per min, respectively. Transitional epithelial microsomes incorporated approximately 1 and 10% of the total [2-14C]FANFT metabolized into t-RNA and trichloroacetic acid-precipitable material, respectively. Two products of FANFT reduction were demonstrated by high-pressure liquid chromatography. One product was reversibly oxidized to FANFT and the other was tentatively identified by mass spectral analysis as an open chain nitrile. In view of the relatively low oxygen tension in the renal inner medulla and bladder mucosa, these results suggest that medullary and transitional epithelial nitro-reductases may be involved in the pathogenesis of 5-nitrofuran toxicity.

Animals↗
PubMed1980

[Joint action of aminoglycoside antibiotics and nitrofurans with bile on bacteria of the genus Proteus].

The combined effect of monomycin, kanamycin, neomycin and nitrofurans, such as furacillin, furagin, nitrofurantoin and furazolidone with bovine bile was studied on 36 strains of Proteus mirabilis and 14 strains of Proteus vulgaris. It was found that sub-bacteriostatic doses of the bile significantly increased the antiproteus activity of the aminoglycoside antibiotics and nitrofurans. The combinations of the bile with monomycin and kanamycin and the bile with furazolidone and nitrofurantoin proved to be most effective. Clinical trials of the drugs in treatment of inflammatory diseases of the biliferous system of the Proteus etiology are recommended.

Aminoglycosides↗
PubMed1995

[Genotoxic properties of 5-nitrofuran compounds].

5-nitrofurans are a large group of nitro-compounds and worldwide as human and veterinary drugs, food additives or preservatives. However, many adverse effects of these compounds and among mutagenic as well as carcinogenic activities create doubts about safety of their use. Present paper deals with various mechanisms of genotoxic action of 5-nitrofurans. Main metabolic pathways leading to the formation of their active metabolites are discussed.

Bacteria↗
PubMed1998

The 5-nitrofuran-2-ylmethylidene group as a potential bioreductively activated prodrug system for diol-containing drugs.

Acid-catalysed condensation of 5-nitrofuran-2-carboxaldehyde with 1-phenylethane-1,2-diol and with 2,2-dimethyl-1-phenylproane-1,3-diol in boiling benzene gave the expected cyclic nitrofuranyl acetals. Biomimetic reduction of these acetals with sodium borohydride in the presence of palladium triggered release of the parent diols. Thus these nitrofuran acetals may have potential for applications as prodrugs for selective release of diol-containing drugs in hypoxic solid tumours.

Acetals↗
PubMed1983

Transferable nitrofuran resistance conferred by R-plasmids in clinical isolates of Escherichia coli.

A high proportion of nitrofuran-resistant strains has been found in a collection of antibiotic-resistant Gram-negative bacteria isolated from patients with urinary tract infections. Some of the Escherichia coli carried R-plasmids that conferred resistance to nitrofurantoin and nitrofurazone. The mechanism of resistance is not clear; only in lactose non-fermenting recipients was there a decrease in the nitrofuran-reducing ability of whole-cell suspensions. One of the plasmids conferred enhanced resistance to UV light on DNA repair defective mutants but not on repair efficient strains. In some resistant strains, the total resistance was apparently the result of a combination of chromosomal and plasmid-borne genes. The presence of the plasmid may allow the development of higher resistance levels by mutation of chromosomal genes.

Drug Resistance, Microbial↗
PubMed1974

New antimicrobial nitrofuran, trans-5-amino-3-[2-(5-nitro-2-furyl)vinyl]-delta2-1,2,4-oxadiazole: antibacterial, antifungal, and antiprotozoal activities in vitro.

trans-5-amino-3-[2-(5-nitro-2-furyl)vinyl]-Delta(2) -1,2,4-oxadiazole, a new antimicrobial nitrofuran, has shown microbial activity in vitro against a wide range of bacteria and fungi, and against several protozoa. The antimicrobial activity of the nitrofuran is not significantly diminished in vitro in the presence of 50% human serum. The compound is not cross-resistant with a number of common antibiotics or synthetic antimicrobial agents; some cross-resistance with furazolidone is encountered. The development of resistance to the compound in vitro, when it occurs, is mixed, but is unrelated to increase in pathogenicity of the test organism.

5-Amino-3-((5-nitro-2-furyl)vinyl)-1,2,4-oxadiazol↗
PubMed1962

Proteus vulgaris urinary tract infections in rats; treatment with nitrofuran derivatives.

Ascending urinary tract infections with stone formation have been produced experimentally in rats, using a modification of the method of Vermuelen & Goetz (1954a, b). A zinc disc infected with a culture of Proteus vulgaris was inserted into the bladder by suprapubic cystotomy under ether anaesthesia. The pH of the urine rises from 6.9 to 8 or 9 and calculi develop in the bladder within a few days of infection. The bladder and ureters become swollen, distended and inflamed, and renal abscesses develop. Death from renal failure generally occurs within 10 days of infection. Oral treatment with nitrofurantoin was commenced three days after infection and continued for one month. This arrested the initial rise in urine alkalinity and stone formation, and few, if any, macroscopic lesions were found at post-mortem examination. Of nine nitrofuran derivatives examined for activity against this infection several showed slight activity, but only one, N-(5-Nitrofurfurylidene)-gamma-butyric acid, was as active as nitrofurantoin when given at four times the dose, but it was also one-third as toxic. It is concluded that this technique is suitable for the examination of potential urinary antiseptics.

Animals↗