Disease relevance of furazolidone

• Furazolidone in peptic ulcer [1].
• In-vitro sensitivity of Campylobacter pyloridis to furazolidone [2].
• It is proposed that furazolidone in the turkey produces primary hepatic damage that is reflected in lowered total serum proteins, including trypsin inhibitory capacity, and that the alterations produced by furazolidone are superimposed on round heart disease in the inbred flock [3].
• Increasingly recognized myocardial diseases include cardiomyopathies in cats, dogs, and birds; anthracycline cardiotoxicity; furazolidone cardiotoxicity; ionophore cardiotoxicity; myocardial damage associated with central nervous system injuries; myocardial hypertrophy in[4]
• Furazolidone, although not dramatically effective, has a spectrum of activity that includes Shigella, enterotoxigenic E. coli, Campylobacter, and Giardia lamblia [5].

Psychiatry related information on furazolidone

• Furazolidone-induced mood disorder during the treatment of refractory giardiasis in a patient with AIDS [6].
• Furazolidone administered per os was found to alter the in vivo antioxidative enzymatic defense mechanisms [7].

High impact information on furazolidone

• One-week-old turkey poults were fed furazolidone for 14 days to induce dilated cardiomyopathy [8].
• The recovery of NF expression in good regenerators was independent of axon growth across the lesion, because excision of a segment of spinal cord caudal to the transection site blocked regeneration but did not prevent the return of NF-180 mRNA [9].
• During the first 4 weeks after operation, NF message levels were reduced dramatically in all axotomized reticulospinal neurons, on the basis of semiquantitative in situ hybridization for the single lamprey NF subunit (NF-180) [9].
• The pathways participating in the metabolism of the nitrofuran antimicrobial drug N-[5-nitro-2-furfurylidene]-3-amino-2-oxazolidinone (furazolidone) in intact cells were investigated in the human intestinal cell line Caco-2 [10].
• The first reducing equivalent required for the formation of the nitroanion derivative of furazolidone appeared to be provided essentially by the microsomal cytochrome P450 reductase [10].

Chemical compound and disease context of furazolidone

• The IC50 of the most potent antigiardial agent, 1,3-di(4-amidino-2-methoxyphenoxy)propane compared favorably with the IC50s of the compounds currently used to treat giardiasis, i.e., furazolidone (1.0 +/- 0.03 microM), metronidazole (2.1 +/- 0.80 microM), quinacrine HCl (0.03 +/- 0.02 microM), and tinidazole (0.78 +/- 0.48 microM) [11].
• Efficacy of combined furazolidone and neomycin in the control of contamination in Leptospira cultures [12].
• High cure rate of Helicobacter pylori infection using tripotassium dicitrato bismuthate, furazolidone and clarithromycin triple therapy for 1 week [13].
• Low cure rate of Helicobacter pylori infection with omeprazole and furazolidone dual therapy for one week [14].
• AIM: To test the efficacy of omeprazole, furazolidone and amoxicillin triple therapy for the treatment of Helicobacter pylori infection after failure of standard first-line therapy recommended by the Asia-Pacific Consensus on the management of H. pylori infection [15].

Biological context of furazolidone

• These results indicate that cardiomyopathy induced by furazolidone is associated with decreased myocardial lipid peroxidation [16].
• In contrast, furazolidone-induced cardiomyopathy of similar severity to the spontaneously occurring model was not associated with changes in nucleoprotein composition or degree of phosphorylation [17].
• Antibiotic resistance patterns of aerobic coryneforms and furazolidone-resistant Gram-positive cocci from the skin surface of the human axilla and fourth toe cleft [18].
• An intervention program based on water chlorination, shed drinking system cleaning and disinfection, and withdrawal of furazolidone from feed reduced the proportion of birds colonized with campylobacter from 81 to 7% and was associated with a 1,000- to 10,000-fold reduction in campylobacters recoverable from the carcasses [19].
• All strains that were susceptible to furazolidone and resistant to Taxo A disks (bacitracin, 0.04 U; BBL Microbiology Systems, Cockeysville, Md.) were staphylococci [20].

Anatomical context of furazolidone

• Myocardium from poultry had remarkably decreased myoglobin compared to mammals (34 +/- 4 micrograms/g) with heart failure produced either by furazolidone or salt toxicity causing a further 50% reduction [21].
• 2 Furazolidone (200 mg/kg) administered by crop tube inhibited MAO activities in duodenal mucosa, liver, heart and brain [22].
• Furthermore, neurons of the cranial motor nuclei did not express NF-180 until later developmental stages and the extraocular motor neurons did not label until metamorphosis [23].
• Free carnitine was elevated by 126% in left ventricle and by 54% in skeletal muscle of the furazolidone-treated turkeys (p less than 0.05) [24].
• Swine liver microsomes convert the nitrofuran furazolidone into N-(4-cyano-2-oxo-3-butenylidene)-3-amino-2-oxazolidone, a reactive open-chain acrylonitrile derivative [25].

Associations of furazolidone with other chemical compounds

• In vitro effect of tinidazole and furazolidone on metronidazole-resistant Trichomonas vaginalis [26].
• In separate in vitro experiments furazolidone (2-10 mg.g wet weight-1) did not increase malondialdehyde production in turkey (or rat) left ventricular homogenates [16].
• When multiple treatment regimens fail, salvage therapy regimens such as bismuth or furazolidone quadruple therapy (a bismuth and tetracycline HCl 4 times a day along with a proton pump inhibitor twice a day, and either metronidazole 400 or 500 mg three times daily or furazolidone 100 mg three times daily for 14 days) can be used [27].
• 1 The intravenous injection of pethidine in rabbits pretreated with furazolidone administered orally but not systemically resulted in severe interaction and fatal hyperpyrexia [28].
• Digoxigenin-labeled RNA probes complementary to NF-180 were used to determine the distribution and timing of expression of neurofilament message in the brain and spinal cord of the lamprey [23].

Gene context of furazolidone

• The two new sites are adjacent to a conserved peptide sequence (VEEIIEET-V) found once in higher vertebrate NF-M molecules and twice in lamprey NF-180 [29].
• The mutational specificity of furazolidone in the lacI gene of Escherichia coli [30].
• E. coli strain TC3960 (delta uvrB, pKM101) was treated with 10 microM furazolidone, yielding an induced mutation frequency of 30 times over the spontaneous frequency [30].
• The supernatants from probiotic and furazolidone co-incubation exhibited rather strong suppression on SOS induction produced by furazolidone on E. coli PQ 37 (sfiA: lacZ) [31].
• Mutations in Helicobacter pylori porD and oorD genes may contribute to furazolidone resistance [32].

Analytical, diagnostic and therapeutic context of furazolidone

• Detection of furazolidone in human biological fluids by high performance liquid chromatography [33].
• HPLC is a rapid and sensitive method for the quantitation of furazolidone in biological fluids [33].
• The two isolates with the highest ID50 values for furazolidone in vitro were from patients who had persistent symptoms after treatment with this drug; these patients subsequently responded to treatment with a nitroimidazole with greater in vitro potency [34].
• After 19 new cases were detected early in the summer of 1985, oral administration of furazolidone throughout their entire hospital stay (2.5 mg/kg twice daily) was recommended for all subsequently hospitalized infants [35].
• A control group of Broad Breasted White turkey poults was given regular feed without additive, whereas the experimental group was given the control ration with 700 ppm of furazolidone at 1 week of age for 3 weeks (DCM) [36].

References