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PubMed1992

Generation of furazolidone radical anion and its inhibition by glutathione.

Furazolidone is a nitrofuran drug which causes dilated cardiomyopathy in turkeys and serves as an important model of human dilated cardiomyopathy. Although extensively investigated, the chemical mechanism by which furazolidone produces injury remains unknown. In this work we used electron paramagnetic resonance (EPR) spectroscopy to show that furazolidone was reduced to its corresponding nitro anion radical by ascorbate and hypoxanthine. Glutathione prevented the generation of this anion radical. These results document directly, with EPR spectroscopy, the presence of furazolidone anion radical during biochemical reduction and suggest a protective role of glutathione in furazolidone-induced injury. These data enhance our understanding of furazolidone metabolism and may be useful in defining its role in furazolidone-induced dilated cardiomyopathy.

Electron Spin Resonance Spectroscopy↗

PubMed1981

Furazolidone resistance in Salmonella gallinarum: the relationship between in vitro and in vivo determinations of resistance.

Of 22 strains of Salmonella gallinarum isolated from recent outbreaks of infection in poultry in Greece (15). Amman (3), Kenya (2), Lebanon (1) and Yemen (1), 20 were more resistant to furazolidone in vitro than 6 strains that had been isolated in the U.K. in the 1950s; the minimum inhibitory concentration of furazolidone was approximately 0.3 microgram/ml for the sensitive strains and 1.3 or 2.5 microgram/ml for the more resistant strains. Furazolidone given continuously in the food did not control experimental infections in chickens caused by most of the strains that had been classed as more resistant by the in vitro tests. Chloramphenicol, trimethoprim and sulphadiazine or mixtures of the latter two were the best antibiotics for treating these infections, but they were less satisfactory than furazolidone for treating infections caused by the furazolidone-sensitive strains. As a group, the furazolidone-resistant strains and furazolidone-resistant mutants of one of the sensitive strains were less virulent for chickens than the sensitive strains.

Animals↗

PubMed2001

One-week regimens containing ranitidine bismuth citrate, furazolidone and either amoxicillin or tetracycline effectively eradicate Helicobacter pylori: a multicentre, randomized, double-blind study.

BACKGROUND: The metronidazole resistance of Helicobacter pylori strains has increased rapidly. AIM: To evaluate the efficacy and safety of new 1-week regimens containing ranitidine bismuth citrate, furazolidone and either amoxicillin or tetracycline. METHODS: One hundred and twenty patients with H. pylori-positive inactive duodenal ulcer or non-ulcer dyspepsia diagnosed by endoscopy were recruited randomly to receive one of two regimens for 7 days: ranitidine bismuth citrate, 350 mg b.d., furazolidone, 100 mg b.d., and either amoxicillin, 1000 mg b.d. (n=60), or tetracycline, 500 mg b.d. (n=60). H. pylori infection was identified by rapid urease testing and histology. 13C-Urea breath test was performed to evaluate the cure of H. pylori infection at least 4 weeks after completion of triple therapy. RESULTS: The eradication rates of H. pylori by ranitidine bismuth citrate-furazolidone-amoxicillin and ranitidine bismuth citrate-furazolidone-tetracycline regimens were 82% and 85% (P > 0.05), respectively, by intention-to-treat analysis, and 85% and 91% (P > 0.05), respectively, by per protocol analysis. Adverse effects were mild in both ranitidine bismuth citrate-furazolidone-amoxicillin and ranitidine bismuth citrate-furazolidone-tetracycline groups. CONCLUSIONS: One-week regimens containing ranitidine bismuth citrate, furazolidone and amoxicillin or tetracycline are well tolerated and effective for the eradication of H. pylori.

Adolescent↗

PubMed1980

Inhibition of monoamine oxidase by furazolidone in the chicken and the influence of the alimentary flora thereon.

1 The addition of furazolidone to the feed at the therapeutic level (0.04% w/w, 10 days) inhibited monoamine oxidase (MAO) activity by 47 to 72% in chicken duodenal mucosa, heart and brain, but in the liver the enzyme activity was unaffected by the treatment. 2 Furazolidone (200 mg/kg) administered by crop tube inhibited MAO activities in duodenal mucosa, liver, heart and brain. 3 Furazolidone (200 mg/kg) injected intramuscularly did not inhibit MAO activity in the chicken. 4 Pretreatment of the chickens with intramuscular neomycin did not antagonize the inhibition of MAO activity produced by furazolidone (200 mg/kg, crop tube). 5 Pretreatment with neomycin by crop tube to suppress the alimentary flora significantly reduced the effect of furazolidone on MAO activity, suggesting that the drug was transformed by the alimentary flora to an active metabolite which subsequently inhibited MAO activity in other organs. 6 Furazolidone in the feed (0.04% w/w, 10 days) or administered by crop tube (200 mg/kg) had no effect on the activity of aminopyrine demethylase in chicken liver. 7 The activity of aspartate transaminase in plasma was unaffected by the addition of furazolidone to the feed (0.04% w/w, 10 days).

Aminopyrine N-Demethylase↗

PubMed1989

Single-dose treatment of cholera with furazolidone or tetracycline in a double-blind randomized trial.

To evaluate single doses of 400 mg of furazolidone and 1 g of tetracycline given orally to patients with diarrhea due to Vibrio cholerae, we studied 87 adults in a randomized, double-blind, placebo-controlled trial. All patients received intravenous fluids for rehydration and no other drugs. The total volumes of stool (mean +/- standard deviation) during a 6-day period after treatment were significantly smaller in the tetracycline group (10.5 +/- 8.6 liters) than in the furazolidone group (20.9 +/- 15.9 liters) and the placebo group (19.1 +/- 10.5 liters) (P less than 0.01). The duration of diarrhea and volumes of intravenous fluids were also significantly reduced in the tetracycline group (P less than 0.05). However, there were no differences between the furazolidone and the placebo groups with regard to stool volume, intravenous fluid, and duration of diarrhea. Within 48 h of treatment, tetracycline significantly reduced the number of patients with positive stool cultures for V. cholerae (37%) compared with furazolidone treatment (96%) and the placebo (97%) (P less than 0.001). Although the tetracycline group had a significantly higher incidence (61%) of bacteriologic relapse (negative stool cultures on days 2 and 3, followed by positive cultures afterward) compared with that in the furazolidone group (40%) and the placebo group (33%), this was not associated with clinical relapse. There were no differences between the furazolidone and placebo groups with regard to any of the bacteriologic responses examined. These data indicate that a single dose of 1 g of tetracycline is effective in the treatment of cholera, but it is asymptomatic bacteriologic relapse. A single dose of 400 mg of furazolidone is not therapeutically effective in cholera.

Adult↗

PubMed1968

Controlled comparison of tetracycline and furazolidone in cholera.

A controlled comparison of furazolidone and tetracycline in the treatment of cholera indicates that, in either dosage used, furazolidone reduced total stool volume by 50% and duration of diarrhoea by 40%. These results are comparable to those achieved with tetracycline, which was given in presently recommended dosage. Both furazolidone and tetracycline significantly reduced the rate of stool output within 18 to 24 hours of starting antibiotic treatment. Furazolidone was significantly less effective than tetracycline in rapidly and consistently terminating vibrio excretion. One convalescent carrier of cholera vibrios was identified among control patients; none was identified among patients treated with either tetracycline or furazolidone. All Vibrio cholerae strains tested were sensitive to tetracycline and furazolidone, but larger concentrations of the latter were required to achieve inhibition of growth. It is concluded that tetracycline remains the antibiotic of choice in cholera but that furazolidone would be a useful adjunct to cholera therapy when tetracycline is unobtainable or if strains of V. cholerae with clinically significant resistance to tetracycline should be encountered.

Adult↗

PubMed2005

Furazolidone-induced pulmonary hypersensitivity.

OBJECTIVE: To report a case of pulmonary hypersensitivity associated with furazolidone use and review the literature on this topic. CASE SUMMARY: A 43-year-old white female presented with fever and dyspnea. She had recently completed a course of furazolidone 125 mg 4 times daily for 10 days for enteritis. Investigations revealed bibasilar interstitial infiltrates on chest X-ray, hypoxia, and 21% eosinophilia. Her fever, hypoxia, and dyspnea rapidly abated following discontinuation of furazolidone and administration of corticosteroids. DISCUSSION: Furazolidone is a bactericidal agent used to treat infectious enteropathies. It is chemically similar to nitrofurantoin, which is well known to cause pulmonary hypersensitivity reactions. Application of the Naranjo probability scale suggests that a furazolidone adverse reaction in this patient was probable. A MEDLINE search from 1966 to October 2004 revealed 2 previously reported cases suggestive of furazolidone pulmonary hypersensitivity. All published reports closely resemble each other and descriptions of nitrofurantoin-associated pulmonary hypersensitivity reactions. CONCLUSIONS: Furazolidone may induce pulmonary hypersensitivity reactions; clinicians should be aware of this potentially serious adverse effect.

Adult↗

PubMedDate not supplied

[The efficacy of different oral dosage forms of furazolidone for E. coli infections in carrier pigeons].

The clinical efficiacy of furazolidon for treatment of E. coli-induced gastro-intestinal infections in racing pigeons was investigated. 36 adult pigeons were treated with 2 different oral modes of application (capsule/drinking water) with a daily therapeutic dosage of 12.5 mg furazolidon/pigeon. The pigeons used for this study (Columba livia f. domestica) originated from conventional breeders and were housed in 3 different groups (control-, capsule- and powder-group) in different stables. After infection with an E. coli-strain (O150:H8) that proved to be pathogenic for pigeons, the animals developed clinical signs of disease within 2 days. After onset of disease the treatment with furazolidon for 5 days started. This phase was followed by an adspectory phase for 6 days. The negative identification of the E. coli O150:H8 was determined as main parameter for the clinical efficiacy of the treatment with furazolidon. This parameter showed a highly significant (p = 0.0001) difference between both groups treated with furazolidon and the control group. In both groups treated with furazolidon the E. coli strain could not be isolated after the end of the treatment. An improvement of clinical signs was seen 24 hours after treatment via capsule and 48 hours after treatment via drinking water formulation. The time difference might be caused by the high concentration of furazolidon in the capsules due to the single daily application. Considering the inaccurate dosing via drinking water that results from the varying drinking water intake in pigeons, the application by capsule should be prefered. Both furazolidon preparations proved to be effective in treating gastro-intestinal E. coli-infections in racing pigeons in a dosage of 12.5 mg/pigeon for 5 days, however, best results were obtained by application via capsule.

Administration, Oral↗

PubMed1976

Studies on the effects of furazolidon and P-rosaniline on the kinetoplast of Trypanosoma gambiense in mice.

p-Rosaniline-sensitive and -resistant strains of Trypanosoma gambiense were separately passaged in mice treated with furazolidon. After 10 serial passages in mice, the trypanosomes were found to be resistant to furazolidon when tested in mice. The rate of appearance of AK forms after injection of furazolidon into mice infected with a clone obtained from the p-rosaniline resistant strain by repeated treatment with furazolidon (WRF) was lower than that in mice infected with a clone obtained from the p-rosaniline sensitive strain by the same treatment with furazolidon (WSF). Moreover, WSF was resistant to p-rosaniline, although it had not been exposed to it. These results indicate that there is an interaction between the actions of furazolidon and p-rosaniline on the kinetoplast. The existence of this interaction was supported by electron microscopic observations on the kinetoplasts of trypanosomes after the injection with p-rosaniline and furazolidon into mice infected with the p-rosaniline resistant clones, WSF and WRF.

Animals↗

PubMed1981

Furazolidone and quinacrine. Comparative study of therapy for giardiasis in children.

Furazolidone and quinacrine hydrochloride were compared for efficacy, toxicity, and ease of administration in 45 young children with giardiasis. With the initial course of therapy, the cure rate was 89% (17/19) with furazolidone and with quinacrine it was 64% (9/14) in children less than 5 years and 92% (11/12) in older children. Cure rates for all courses of therapy were 92% (24/26) with furazolidone and 53% (9/17) and 92% (12/13) in the younger and older children, respectively, treated with quinacrine. Quinacrine failure was usually due to severe vomiting. When re-treated with furazolidone, patients were cured. The disadvantages of furazolidone are the large volume of doses and the expense. In this study, furazolidone was more effective and better tolerated than quinacrine for the treatment of giardiasis.

Adolescent↗

PubMed1987

Identification of a reactive intermediate of furazolidone formed by swine liver microsomes.

Furazolidone (N-(5-nitro-2-furfurylidene)-3-amino-2-oxazolidone) is metabolized by swine liver microsomes under aerobic and anaerobic conditions (rate: 2.55 and 3.25 nmol/mg protein/min, respectively). Covalent binding to microsomal protein amounted aerobically to 0.29 nmol/mg protein/min. Of all amino acids tested, only addition of cysteine to the incubation mixture decreased microsomal protein binding of furazolidone, indicating that covalent binding may occur at protein thiol groups. Two known metabolites of furazolidone, 3-(4-cyano-2-oxobutylidene-amino)-2-oxazolidone and 2,3 dihydro-3-cyano-methyl-2-hydroxyl-5-nitro-1 alpha,2-di(2-oxo-oxazolidin-3-yl) iminomethyl-furo[2,3-b] furan, were minor metabolites. At least 50% of total metabolites is formed by swine liver microsomes via a reductive process of furazolidone as indicated by the formation of a furazolidone-mercaptoethanol conjugate after the addition of mercaptoethanol to the incubation mixture. The conjugate was identified as 3-(4-cyano-3-beta-hydroxyethylmercapto-2-oxobutylidene amino)-2-oxazolidone, indicating that the open-chain acrylonitrile-derivative is the reactive intermediate of furazolidone which also may be responsible for interaction with protein.

Amino Acids↗

PubMed1992

Effect of furazolidone on tissue sulphydryl groups, ascorbic acid, and lipid peroxide levels in the rat, and the influence of dimethylsulphoxide thereon.

The concentrations of sulphydryl groups (SH), ascorbic acid (AA) and lipid peroxide (LP) were measured in the liver, kidney and brain of rats 24 h after treatment with furazolidone at single oral doses of 75, 150 and 300 mg/kg. The drug produced significant reductions in the concentrations of SH, and significant increases in the concentrations of LP, in the tissues studied. The level of AA was significantly decreased in the livers (but not the kidneys or brains) of rats treated with furazolidone at a dose of 300 mg/kg. The concentrations of AA in the tissues of rats treated with lower doses were unaffected. In another experiment, furazolidone was given orally to rats at a dose of 300 mg/kg, together with a subcutaneous injection of dimethylsulphoxide (DMSO) at a dose of 8 g/kg, and SH measured in the liver 24 h later. DMSO alone had no significant effect on SH concentration. However, when DMSO was given concomitantly with furazolidone, SH concentration was significantly less depressed than when furazolidone was given alone. It is concluded that DMSO protected tissues against toxicity induced by furazolidone.

Analysis of Variance↗

PubMed1992

Production, hatchability and fertility of eggs from breeding Japanese quail (Coturnix coturnix japonica) fed diets containing furazolidone.

1. Breeding Japanese quail were allocated to 8 groups, each group consisting of 20 females and males. The birds were fed one of 4 diets for up to 33 d: a control diet or a diet containing 200 mg/kg, 400 mg/kg or 1000 mg/kg furazolidone. Subsequently, quails were fed a furazolidone-free diet for up to 21 d. Egg production, quality, hatchability and fertility of the groups were measured. 2. Significant reduction in egg production occurred in birds fed 400 mg/kg and 1000 mg/kg furazolidone, the effect being more pronounced at the higher concentration. 3. Hatchability was reduced significantly for all groups of birds fed furazolidone and this effect was both dose and time dependent. The reduction in hatchability was attributable to an increase in infertile eggs rather than an increase in embryonic mortality. 4. Egg quality was affected, with more small eggs being produced by birds fed 1000 mg/kg furazolidone. 5. After removal of the experimental diets egg production of the affected groups returned to control values. Hatchability and fertility of affected groups also returned toward control values, but had generally not attained these values 21 d after the cessation of the experimental diets. 6. It was concluded that standard recommendations for the therapeutic dosage of poultry with furazolidone may not be appropriate for breeding Japanese quail.

Animals↗

PubMed1999

Metabolism of furazolidone: alternative pathways and modes of toxicity in different cell lines.

1. The metabolism and cytotoxicity of the antimicrobial nitrofuran drug furazolidone have been studied in Caco-2, HEp-2 and V79 cell lines. Free radical production, metabolite pattern, formation of bound residues, inhibition of cellular replication and protection by the antioxidant glutathione were compared for the three cell lines. 2. All three cell lines produced the same nitro-anion radical with similar kinetics. Little further metabolic breakdown was observed in V79 cells, whereas Caco-2 and HEp-2 cells showed extensive degradation of furazolidone, but with different end patterns. 3. Under hypoxic conditions, the colony-forming ability was extensively impaired in HEp-2 cells whereas the other two cell lines were less affected, suggesting that irreversible damage to DNA occurred prevalently in HEp-2 cells. In V79 cells the absence of oxygen caused a 25-fold increase in the formation of protein-bound residues. 4. Brief exposure to furazolidone caused a 50% loss of endogenous glutathione in Caco-2 cells, but no loss could be detected in V79 and HEp-2 cells. Consistently, when glutathione was depleted by buthionine-[S,R]-sulphoximine (BSO) and diethylmaleate (DEM) treatment, the viability of V79 and HEp-2 cells was minimally affected by furazolidone, whereas that of Caco-2 cells was substantially reduced. 5. It is concluded that the cytotoxicity of furazolidone in these cell lines can be exerted by a number of different mechanisms, possibly related to different metabolic pathways. The cytotoxicity of nitrofuran drugs, therefore, cannot be ascribed to a single toxic intermediate, but in Caco-2 cells furazolidone is extensively metabolized and detoxified by GSH, in V79 is only partially activated and then bound to proteins, whereas in HEp-2, once activated, may react with DNA.

Anti-Infective Agents, Local↗

PubMed2001

Evaluation of the residues of furazolidone and its metabolite, 3-amino-2-oxazolidinone (AOZ), in eggs.

The use of furazolidone in food-producing animals is banned within the EU. Detection of the protein-bound side-chain metabolite, 3-amino-2-oxazolidinone (AOZ), in animal tissues is the most effective method of enforcing the ban. The study was undertaken to find out if the same applies to eggs. The concentrations of furazolidone and AOZ in eggs reached a plateau of approximately 360-380 microg kg(-1) by the fourth day of treating birds with 400 mg kg(-1) furazolidone. After a 4-day withdrawal from treatment, intact furazolidone could not be detected. AOZ residues could still be detected up to 21 days following withdrawal from treatment. During treatment, most intact furazolidone residues occur in the albumen. For AOZ, there is a more even distribution of residues between albumen and the yolk. The concentration of furazolidone in egg homogenates stored at -20 degrees C decreases by 44% after 55 days. AOZ residues are stable during this period. From these results, it is clear that AOZ is a more suitable marker residue than the parent compound for monitoring concentrations of the drug in eggs.

Animals↗

PubMed1997

The prevalence and possible causes of bound and extractable residues of the furazolidone metabolite 3-amino-2-oxazolidinone in porcine tissues.

Furazolidone is readily metabolized and rarely detectable in animal tissues. An alternative is to measure bound and extractable residues containing the 3-amino-2-oxazolidinone (AOZ) moiety. This compound was used to examine the incidence of furazolidone residues in Northern Ireland pigs. AOZ was found in 32/200 kidney samples. A depletion study showed that none of the samples contained AOZ residues at concentrations greater than that found in pigs fed medicated feed, and subjected to an obligatory 7-day withdrawal period. Furazolidone carry-over from medicated feed to subsequent unmedicated batches of feed was investigated in a local feed mill. Furazolidone could be detected only in the first two batches of ostensibly unmedicated feed. A series of feeds containing levels of furazolidone similar to those found in the feed mill carry-over study were prepared. These were fed to pigs, which were killed without withdrawal. The tissues contained AOZ residues, but at concentrations lower than those found in pigs fed medicated feed and properly withdrawn. The possible cross-contamination of unmedicated pigs following exposure to a cleaned house that had previously housed pigs undergoing furazolidone medication was investigated. Tissue AOZ residues were detected, even after comparatively short periods of exposure. However, the concentrations were again lower than those found in pigs fed medicated feed and properly withdrawn.

Animal Feed↗

PubMed2005

Helicobacter pylori eradication in childhood after failure of initial treatment: advantage of quadruple therapy with nifuratel to furazolidone.

BACKGROUND: Failures of Helicobacter pylori eradication in children are common. AIM: To evaluate the efficacy of amoxicillin, bismuth subcitrate and omeprazole and nifuratel or furazolidone for H. pylori eradication in children who failed initial treatment with a standard triple therapy. METHODS: Seventy-six consecutive H. pylori-positive paediatric out-patients (aged 12-16 years; mean age 13.7 +/- 1.4) with chronic abdominal complaints who had failed one attempt of eradication of H. pylori using metronidazole-containing triple therapy were enrolled. It was an open prospective study. Patients were randomized to receive a 2-week course of bismuth subcitrate (8 mg/kg/day, q.d.s.), amoxicillin (50 mg/kg/day, q.d.s.), with either nifuratel (15 mg/kg/day, q.d.s.) or furazolidone (10 mg/kg/day, q.d.s.), plus omeprazole (0.5 mg/kg, once daily). RESULTS: There were 37 patients in the nifuratel group and 39 in the furazolidone group. Helicobacter pylori was eradicated in 33 of 37 (89%; 95% CI: 74.5-96.9; intention-to-treat) in nifuratel group and in 34 of 39 (87%; 95% CI: 72.5-95.7) in furazolidone group, respectively. Frequency of severe side-effects was greater with furazolidone (21%) than with nifuratel (3%; P = 0.0289). CONCLUSIONS: Nitrofuran-containing therapies consisting of a proton-pump inhibitor, amoxicillin and bismuth citrate plus either nifuratel or furazolidone produced good cure rates even among those who had failed prior therapy. Nifuratel is preferred because of the lower frequency of side-effects.

Adolescent↗

PubMed1975

Furazolidone-pethidine interaction in rabbits.

1 The intravenous injection of pethidine in rabbits pretreated with furazolidone administered orally but not systemically resulted in severe interaction and fatal hyperpyrexia. 2 Treatment with rho-chlorophenylalanine, chloropromazine of cyproheptadine protected the rabbits against the furazolidone-pethidine interaction, while alpha-methyl-rho-tyrosine was ineffective. 3 5-Hydroxytryptophan produced a fatal hyperpyrexia in furazolidone pretreated rabbits. 4 Pretreatment of rabbits with 1,1,1-trichloro-2, 2-bis(rho-chlorophenyl)ethane (DDT) accelerated and enhanced the furazolidone-pethidine interaction, while oxytetracycline pretreatment completely prevented the interaction. 5 It is concluded that furazolidone-pethidine interaction might depend mainly on potentiation of the effects of 5-hydroxytryptamine in the CNS and that the transformation of furazolidone into an active monoamine oxidase inhibitor metabolite might occur mainly in the gut microflora in the gut lumen.

5-Hydroxytryptophan↗