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At least 19 recordsLinked to original sources
PubMed1983

Furazolidone-induced congestive cardiomyopathy in ducklings: regression of cardiac lesions after cessation of furazolidone ingestion.

Newly hatched male White Pekin ducklings (n = 92) were allotted to 2 groups of 46 each and fed 750 mg of furazolidone (FZ)/kg of feed either for 8 weeks (group 1) or for 4 weeks followed by 4 weeks of no FZ intake (group 2). Regression of FZ-induced toxicosis was observed in ducklings of group 2 after cessation of FZ consumption, as evidenced by decreased mortality, progressive decrease in ascites, and increases in body weight gains. Necropsy of 8-week survivors revealed decreased frequency and severity of ascites in ducklings of group 2. The severity of FZ-induced cardiac alterations also was diminished, with a decrease in left ventricular dilatation score and an increase in absolute heart weights in 8-week survivors in group 2. Further evidence of regression of FZ-induced congestive cardiomyopathy after cessation of FZ ingestion was gained from development of intermediate cardiac damage severity scores and frequency and severity of ascites at necropsy in ducklings (previously studied) examined after 4 weeks of FZ feeding, compared with those found in group 1 (FZ 8 weeks) or in group 2 (FZ 4 weeks, no FZ 4 weeks) of the present study. Furazolidone-induced cardiac disease in ducklings offers an attractive model for studies of the pathogenesis of congestive cardiomyopathy and cardiac failure.

Animals↗
PubMed2003

Disposition of 3-(4-cyano-2-oxobutylidene amino)-2-oxazolidone, a cyano-metabolite of furazolidone, in furazolidone-treated grouper.

The cyano-metabolite of furazolidone (FZ), 3-(4-cyano-2-oxobutylidene amino)-2-oxazolidone, was isolated from the mixture of FZ incubated with the post-9000 g hepatic supernatant of grouper. Its structure was confirmed by mass spectrometric and nuclear magnetic resonance spectroscopic studies. Thereafter, the disposition of the cyano-metabolite in the orange-spotted grouper (Epinephelus coioides) after oral and bath treatment with FZ was investigated. Qualitative and quantitative analyses of cyano-metabolite in the fish were performed by high-performance liquid chromatography. Mean recoveries of the metabolite in serum, muscle, liver and kidney were 99.8 +/- 4.1, 98.6 +/- 3.5, 53.1 +/- 7.4 and 64.0 11.4%, respectively. Cyano-metabolite was mainly distributed in the serum and muscle rather than in the liver and kidney. After oral treatment of FZ, the peak cyano-metabolite concentrations, 167.2 ng x ml(-1) in serum and 283.2 ng x g(-1) in muscle, were reached at 5.1 and 6.7 h, respectively. The elimination half-life of cyano-metabolite was 4 h. During 24-h bath treatment of FZ, the maximum concentrations of cyano-metabolite, 258 ng x ml(-1) in serum and 204 ng x g(-1) in muscle, were found at 0.25 and 6 h, respectively. The half-life of cyano-metabolite was 0.5 h after transferring the fish to fresh seawater.

Animals↗
PubMed1989

[Use of urinary furazolidone determination in calves in laboratory diagnosis].

We examined 41 samples of calf urine in order to determine the urinary furazolidone excretion. 26 calves were administered furazolidone in the form of Terapeutan T in a therapeutic dose of 5 kg per os individually, which represents approx. 3 mg of furazolidone per kg body weight per day over 5 days. 11 calves were administered with twice the therapeutic dose, i.e. 6 mg furazolidone per kg live body weight over the same 5 days. A triple strength dose was administered to two calves on the 2nd and 3rd days and after administration we observed the furazolidone excretion in urine. The dynamics of furazolidone excretion in urine of one calf we determined even after the fivefold dose in comparison with the therapeutic dose, administered in the course of 2 days after application of the double dose, which was administered over 4 days. During administration of 3 mg and 6 mg furazolidone respectively per kg of live weight per kg furazolidone was excreted in urine minimally and only rarely (7.6%). During administration of higher doses furazolidone was found in the urine of all individuals. The highest urinary concentration of furazolidone in calves was determined after administration of the fivefold dose in comparison with the therapeutic dose, i.e. 15 mg furazolidone per kg live weight in the 4th hour after urine collection (23.0 mg furazolidone per liter urine). When this dose was administered over 2 days, it did not effect any clinical symptoms of disease. It has proved to be well founded to determine the furazolidone level in calf urine in laboratory diagnostics. The examination contributes to the estimation of the furazolidone dose, administered to calves. Urinary furazolidone concentrations greater than 1.0 mg.l-1 provide warning signals of overdosage with this chemotherapeutic. For urine furazolidone determination we utilized the photometric method, described by Herret and Buzard (1960).

Animals↗
PubMed2004

Effects of furazolidone pretreatment of Salmonella enteritidis PT4 at sub- and suprainhibitory concentrations on phagocytosis and intracellular survival in chicken macrophages.

The antimicrobial effect of the nitrofuran derivative furazolidone at sub- and suprainhibitory concentrations on Salmonella enteritidis PT4 and the influence with regard to interaction with avian macrophages was investigated in this study. Phagocytosis of furazolidone-sensitive (FzS) S. enteritidis with chicken macrophages in the presence of furazolidone at concentrations of 1/8, 1/4, 1/2 and 8x MIC resulted in an increase in the rate of phagocytic killing of approximately 3-, 6-, 6.5- and 9-fold, respectively, with 1/2 and 8x MIC concentrations producing statistically significant (P<0.05) increases in phagocytosis. Treatment of the FzS Salmonella with furazolidone at concentrations of 4x and 10x MIC, for 15 min prior to phagocytosis, also significantly (P<0.005) increased phagocytic uptake when compared with untreated bacteria. The rate of phagocytosis monitored over 90 min was highest between 30 and 60 min with the furazolidone pretreated salmonella, compared with the delayed rate of the control between 60 and 90 min. Exposure of FzS and FzR strains with suprainhibitory concentrations of furazolidone at 4x, 8x and 10x MIC for 30 min prior to phagocytosis demonstrated an increase in bacterial killing. Exposure of strains to sub-inhibitory concentrations of furazolidone led to an increase in chemiluminescence during phagocytosis with macrophages, suggesting an increase in oxidative metabolism in the macrophages as a result of an increase in activation and phagocytosis. Pretreatment of the strains with suprainhibitory concentrations of furazolidone for 30 min prior to phagocytosis demonstrated a similar increase in oxidative metabolism in the macrophages. Measurement of the amount of 14C-furazolidone associated with chicken macrophages was determined over 20 h incubation. The level of radioactivity of 14C-furazolidone alone was used to estimate the amount of cell-associated nitrofuran when incubated with the macrophages by means of regression analysis. Incubation with concentrations of 16, 32 and 64 microg/ml for 20 h resulted in the cell association of >or=1 microg/ml of furazolidone, which is the concentration required for the agent to exhibit bactericidal activity on furazolidone-sensitive Salmonella strains. Furazolidone was able to reduce intracellular salmonella viability at all concentrations, but total killing was achieved only with concentrations of >or=8 microg/ml, which supports the results for furazolidone association with the macrophages. This substantiates that the bioactivity of the nitrofuran was not inhibited or diminished in the intracellular environment of the macrophage and that exposure of salmonella to nitrofurans enhances phagocytosis.

Animals↗
PubMed1989

Furazolidone-enhanced production of free radicals by avian cardiac and hepatic microsomal membranes.

Furazolidone produces a dilative cardiomyopathy and hepatitis in turkeys exposed to this drug in their diets. The ability of furazolidone to enhance free radical reactions when incubated with turkey cardiac or hepatic membranes was determined to evaluate if free radical reactions might contribute to the pathology. Furazolidone (0.135 mM) incubated with NADPH and hepatic microsomes increased oxygen consumption 350% over control incubations. Superoxide dismutase and catalase attenuated the furazolidone-mediated stimulation of oxygen consumption, indicating that the drug promoted the formation of superoxide and hydrogen peroxide. Lipid peroxidation was also stimulated by furazolidone incubated with microsomes, NADPH, and ferric chloride. At concentrations as low as 0.017 mM, lipid peroxidation was more than doubled by furazolidone. Incubation of cardiac sarcosomes with NADPH and furazolidone (0.135 mM) increased oxygen consumption 72% the rate of cytochrome c reduction 72%, and epinephrine oxidation 238% over control. Epinephrine oxidation was enhanced by concentrations of furazolidone as low as 0.017 mM (69% increase over control). This effect of furazolidone was blocked by superoxide dismutase or incubation in an argon atmosphere. These data establish the potential for furazolidone to enhance free radical reactions in cardiac, as well as hepatic tissue. Free radical reactions are therefore potential determinants of furazolidone-mediated hepatic and cardiac toxicities.

Animals↗
PubMed1982

Anorexia and antagonism of thiamin utilization in poultry treated with furazolidone.

Furazolidone (0.4% w/w in the feed, 10 days) reduced the feed intake and growth in 9 week old chickens, and increased the amount of 5-hydroxytryptamine (5-HT) in the brain. The drug also increased the stimulation of transketolase activity by thiamine pyrophosphate (TPP) in lysed blood cells (TPP effect), and the concentrations of pyruvate and lactate in the blood. Experiments with pair-fed birds showed that the reduction in feed intake in furazolidone-treated chickens could account for the reduced growth. The drug also produced anorexia in ducklings and turkey poults. In chickens, the anorectic action of furazolidone was unaffected by methergoline (1 mg/kg, twice daily, I.M), and in ducklings furazolidone did not consistently produce anorexia, although it always inhibited monoamine oxidase (MAO) activity in the brain. These observations suggest that the anorectic action of the drug was not tryptaminergic in nature. The increase in the TPP effect found in preparations from furazolidone-treated chickens was absent in preparations from pair-fed birds on unmedicated feed. Thus the TPP effect could be used as an indicator of the effect of the drug on the thiamine status of chickens. However, the increase in the concentrations of pyruvate and lactate in blood was found both in furazolidone-treated birds and pair-fed birds on unmedicated feed, showing that they were attributable to the reduction in feed intake. The TPP effect in furazolidone-treated chickens, 14-49 +/- 2.33% (n = 10), was sufficient to suggest a mild deficiency of thiamin pyrophosphate. Thiamin, given at a dosage above the requirement of the vitamin for chickens, did not reduce the anorexia or the TPP effect of furazolidone-treated birds, although it stimulated the feed intake and growth of birds on unmedicated feed. It is proposed that furazolidone antagonized the utilization of thiamin, perhaps by inhibiting its phosphorylation. Following the withdrawal of furazolidone, the TPP effect returned to the control value and the rate of growth of the birds increased and matched that the controls. Thus the effect of the drug was reversible. Addition of furazolidone to the feed at a concentration of 0.01% w/w for 28 days did not produce anorexia in chickens or affect the amount of 5-HT in the brain. Thus at this level, it is unlikely that the drug would produce adverse effects in poultry.

Animals↗
PubMed1994

Furazolidone increases thapsigargin-sensitive Ca(2+)-ATPase in chick cardiac myocytes.

Furazolidone is a nitrofuran antibiotic that causes dilated cardiomyopathy in turkeys and chicks and serves as an important model of human dilated cardiomyopathy. The mechanism by which furazolidone produces cardiac injury remains unknown. We investigated the hypothesis that furazolidone alters Ca2+ homeostasis in cardiac muscle cells. Myocytes harvested from 7-day-old chick embryos were treated with furazolidone (0.02, 0.1, and 1 mM) for 24-52 h and then coloaded with seminaphthorhodafluor-1 (SNARF 1) and fura 2 to measure simultaneously intracellular pH (pHi) and intracellular Ca2+ concentration ([Ca2+]i), respectively. Furazolidone did not affect steady-state [Ca2+]i levels in cardiac myocytes. Na+ removal was associated with a rapid increase in [Ca2+]i due to the Na+/Ca2+ exchanger, which was similar in control and furazolidone-treated cells. The rate of [Ca2+]i recovery after Na+ removal was significantly increased in the furazolidone-treated cells compared with controls. In most cells, recovery from Ca2+ load is accomplished by the activity of Ca(2+)-adenosinetriphosphatases (ATPases). Thapsigargin, inhibitor of sarcoplasmic reticulum Ca(2+)-ATPase, prevented the furazolidone-induced changes. These results demonstrate that furazolidone increases the activity of thapsigargin-sensitive Ca(2+)-ATPase without affecting Na+/Ca2+ exchange. These data enhance our understanding of the mechanism of furazolidone-induced injury in cardiac myocytes and may be useful in determining mechanisms of injury in dilated cardiomyopathy.

Animals↗
PubMed2004

Low-dose furazolidone in triple and quadruple regimens for Helicobacter pylori eradication.

BACKGROUND: Furazolidone-based regimens for the eradication of Helicobacter pylori are low cost and effective. Unfortunately, the usual dose of furazolidone is not tolerable in many patients. Lower doses of furazolidone are expected to cause fewer adverse effects. AIM: To investigate the efficacy of low-dose furazolidone in the eradication of H. pylori. METHODS: One hundred and fifty patients with duodenal ulcer and H. pylori infection were randomly assigned to one of three treatment groups: omeprazole 20 mg b.d., amoxicillin 1000 mg b.d. and furazolidone 100 mg b.d. for 14 days (OAF); omeprazole 20 mg b.d., amoxicillin 1000 mg b.d., furazolidone 100 mg b.d. and bismuth subcitrate 240 mg b.d. for 14 days (OABF1); or omeprazole 20 mg b.d., amoxicillin 1000 mg b.d., furazolidone 200 mg b.d. and bismuth subcitrate 240 mg b.d. for 14 days (OABF2). RESULTS: Of the 150 patients, 145 completed treatment. The intention-to-treat and per protocol eradication rates were 54% (27/50), 72% (36/50) and 92% (46/50) for the OAF, OABF1 and OABF2 groups, respectively. The OAF and OABF1 groups showed significantly lower eradication rates than the OABF2 group (P<0.001 and P<0.01, respectively). CONCLUSIONS: Triple and quadruple furazolidone-based H. pylori eradication regimens do not yield acceptable success rates when a low dose of furazolidone (100 mg b.d.) is used.

Adult↗
PubMed1991

Efficacy of a single dose of furazolidone for treatment of cholera in children.

To test the efficacy and safety of furazolidone given as a single dose for childhood cholera, a randomized double-blind placebo-controlled trial was carried out among 118 culture-positive dehydrated children with diarrhea. Patients were randomly assigned to one of four groups to receive medication orally in liquid suspension: furazolidone at 7 mg/kg/day once, furazolidone at 7 mg/kg/day divided into four doses for 3 days, placebo once, or placebo for 3 days. After 12 patients with furazolidone-resistant infections were excluded from the analysis of efficacy, it was determined that both groups treated with furazolidone showed significantly higher rates of bacteriologic success (stool cultures negative for Vibrio cholerae on days 2 to 4 after start of therapy) and clinical success (cessation of diarrhea within 72 h after start of therapy) than corresponding placebo groups (P less than 0.001). There were no significant differences between responses to the 3-day and single-dose regimens of furazolidone, but there was a trend toward better clinical responses in patients who received furazolidone for 3 days. No patient treated with furazolidone dropped out because of side effects. These results indicate that furazolidone, given as either a single dose or divided doses for 3 days, is effective treatment for childhood cholera.

Adolescent↗
PubMed1984

Efficacy of furazolidone in grower diets on subsequent performance of swine--a cooperative study.

Nine experiments were conducted at three stations to evaluate the efficacy of furazolidone as a growth promoter in diets for young swine and to determine if an early growth response is maintained after the additive is withdrawn from the diet. A total of 528 pigs (24 replications, 132 pigs/treatment) initially averaging 12 kg body weight were fed a nonmedicated basal diet or a diet with 110 ppm furazolidone for 5 wk, 165 ppm furazolidone for 3 wk or 220 ppm furazolidone for 2 wk. After withdrawal of furazolidone, the basal diet was fed to the end of the test, at which time the pigs averaged 93 kg. During the initial 2-wk period, pigs fed furazolidone gained 15.4% faster (P less than .001) and required 8% less (P less than .001) feed per unit of gain than control pigs fed the nonmedicated diet. At 5 wk, pigs previously fed furazolidone gained 8.4% faster (P less than .001) and 4.5% more efficiently (P less than .001) than controls. By 10 wk, pigs previously fed furazolidone maintained a slight advantage in growth rate over controls (2.6%, P less than .10), but feed/gain responses were similar for the two groups. By the end of the experiment, the early growth response from furazolidone was completely lost. Although there were differences in growth responses among stations, the treatment response patterns were similar for each station, with no evidence of a treatment X station interaction.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed2005

[In vitro activity of furazolidone and nitrofurantoin in Helicobacter pylori clinical isolates and study of mutation rate].

Clarithromycin, amoxicillin, tetracycline and metronidazole are the most frequently used antimicrobials for Helicobacter pylori infection treatment. While tetracycline and amoxicillin resistance are rare, clarithromycin and metronidazole resistance vary in different populations and are considered factors for treatment failure. The aim of this study was to determine the in vitro activity of furazolidone and nitrofurantoin in 164 H. pylori clinical isolates by agar dilution and to determine the spontaneous mutation rate. Metronidazole and clarithromycin resistance were 23.77% (CI95%: 18.96-29.14) and 16.78% (CI95%: 12.64-21.62), respectively; moreover, 1.4% (CI95%: 0.38-3.54) were intermediate to clarithromycin. All the isolates were susceptible to amoxicillin and tetracycline. Furazolidone and nitrofurantoin resistance rates were 1.82% (CI95%: 0.37-5.25) and 0.6% (CI95%: 0-3.35), respectively. The three furazolidone-resistant strains were nitrofurantoine-susceptible (MIC 4 mg/l for furazolidone and 2 mg/l for nitrofurantoin) and the nitrofurantoin-resistant strains were furazolidone-susceptible (MIC 4 mg/l for nitrofurantoin and 1 mg/l for furazolidone). These four strains were metronidazole-resistant (MIC 16 mg/l). Furazolidone or nitrofurantoin spontaneous mutants were not detected in the eight H. pylori strains tested. However, mutants with resistance to metronidazole were found with all the strains with a mutation rate of 7.4 x 10(-10) to 9.4 x 10(-10). Furazolidone and nitrofurantoin showed an excellent in vitro activity against the H. pylori clinical isolates included herein, supporting the usefulness of furazolidone as second-line antimicrobial after treatment failure or as first-line therapy in populations with low economical resources.

Anti-Infective Agents↗
PubMed1982

Tolerance of young turkey poults to various combinations of dietary furazolidone and salt.

Three feeding trials were conducted to study the tolerance of young turkey poults to furazolidone and to various combinations of salt and furazolidone in the diet. Poults of mixed sexes tolerated up to 0.03% dietary furazolidone from hatch to six weeks of age without harmful effects as judged from the data on mortality rate, feed intake, body weight and plasma composition. High mortality with cardiac dilation and ascites occurred in poults fed the same basal diet containing 0.05 or 0.07% furazolidone. Mortality was positively related to levels of dietary furazolidone, and occurred mainly between two and four weeks of age. The cumulative feed intake and body weight of these poults were significantly lower than those of the control poults at six weeks of age. There was indication of decreased renal function in poults on high furazolidone intake and the mechanism of furazolidone-induced cardiac dilation is discussed. Mortality rate, incidence of cardiac dilation with ascites and heart, liver and body weights and feed efficiency were similar in poults fed diets containing 0.022% furazolidone and varying levels of salts (0.5, 1.0 or 1.5%) compared with the control fed the same basal diet containing 0.5% salt from hatch to eight weeks of age. It is concluded that a starter diet containing 0.022% furazolidone and up to 1.5% salt does not affect the performance of poults from hatch to eight weeks of age.

Age Factors↗
PubMed1989

A comparison of furazolidone and ampicillin in the treatment of invasive diarrhea.

A single-blind, parallel, randomized study comparing the efficacy of furazolidone and ampicillin in the treatment of children with acute invasive diarrhea was conducted among outpatients at the Hospital General de Ciudad Nezahualcoyotl in Mexico between August 1986 and October 1987. Seventy-eight patients were admitted to the study; 39 were randomized to receive furazolidone (5 mg/kg/day for 5 days), and 39 were randomized to receive ampicillin (100 mg/kg/day for 5 days). The enteropathogens Shigella sp, Salmonella sp, and Escherichia coli were isolated in 87.2% of the initial stool cultures. A preliminary assessment of the patients' clinical status was made on day 3. At that time 97.4% of furazolidone patients had improved, compared with 65.7% of patients in the ampicillin group (p = 0.002). At the end of the treatment period (day 6), 100% of evaluable patients treated with furazolidone had a negative stool culture, compared with 71% of evaluable patients treated with ampicillin (p = 0.002). Both absence of watery stools by day 5 and a negative day 6 stool culture determined treatment success. Overall, there was a greater percentage of treatment successes in the furazolidone group than in the ampicillin group (92.3% versus 51.3%, p = 0.001). Tolerance to both drugs was very good. One patient treated with ampicillin developed urticaria, which required discontinuation of treatment; the reaction resolved spontaneously after treatment discontinuation. No adverse reactions were reported in the furazolidone group. The results of this study showed that furazolidone was more effective than ampicillin in the treatment of acute invasive diarrhea. It is suggested that furazolidone should be the treatment of choice for this disease.

Ampicillin↗
PubMed1993

Randomized clinical trial of furazolidone for typhoid fever in children.

The efficacy of furazolidone and chloramphenicol was compared in a randomized trial involving 133 children with bacteriologically confirmed typhoid fever. Sixty-five children were randomized to receive furazolidone, 7.5 mg/kg/day, and 68 children to receive chloramphenicol, 75 mg/kg/day. Both drugs were administered orally. The clinical characteristics of the two treatment groups were comparable on admission. All the strains of Salmonella typhi isolated from the furazolidone group were susceptible to furazolidone. However, of the 68 strains of S. typhi isolated from the chloramphenicol group, 10 were susceptible and 58 were resistant to chloramphenicol. Clinical and bacteriologic cure was observed in 56 (86.2%) children treated with furazolidone and in 35 (51.5%) children given chloramphenicol who were infected with S. typhi strains, irrespective of susceptibility pattern (P = 0.00003). Cure was achieved in 86.2% of furazolidone recipients and 90.0% of chloramphenicol recipients who were infected with strains of S. typhi susceptible to both drugs (P = 0.6). The difference in cure rate was statistically significant (P = 0.000003) when the two treatment groups infected with furazolidone-susceptible but chloramphenicol-resistant strains of S. typhi were compared. There was no relapse or carriers in either of the groups. Furazolidone appears to be a satisfactory alternative to chloramphenicol in the treatment of typhoid fever caused by chloramphenicol-resistant strains of S. typhi.

Carrier State↗
PubMed1994

Furazolidone disposition after intravascular and oral dosing in the channel catfish.

1. The pharmacokinetics, tissue distribution and excretion of the nitrofuran drug furazolidone have been examined in the channel catfish. [14C]Furazolidone was administered by intravascular or oral routes in a single dosage of 1 mg/kg body weight. 2. A two-compartment pharmacokinetic model best described parent furazolidone concentrations in the plasma after intravascular dosing. Elimination of parent compound was extremely rapid, with a terminal half-life of 0.27h and total body clearance of 1901 ml/h/kg. 3. After oral dosing, furazolidone concentrations in the plasma were highest at 1 h and were below the limit of determination (< 20 ng/ml) at 5 h. The oral bioavailability of parent furazolidone administered in solution was 58%, compared with 28% in a feed mixture. 4. Concentrations of furazolidone and its metabolites were highest in the excretory tissues and lowest in the muscle after oral dosing. Parent furazolidone comprised 10% of the total 14C in the muscle at 8 h and was not detectable (< 1 ng/g) at 24 h; total 14C concentrations declined from 274 to 59 ng furazolidone equiv./g between 8 and 168 h. Non-extractable (bound) residues comprised 18% of total 14C in muscle at 8 h and 33% at 168h. 5. Renal excretion was the primary route of elimination of 14C residues and accounted for nearly 55% of the oral dose.

Administration, Oral↗
PubMed1996

The mutational specificity of furazolidone in the lacI gene of Escherichia coli.

The mutational specificity of the 5-nitrofuran derivative furazolidone was determined in the lacI gene of Escherichia coli. 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. Mutations from 88 furazolidone-induced mutants were analyzed by DNA sequencing: 74 were base substitutions, 7 were frameshift mutations, 3 were tandem base substitutions, 3 were complex mutations and 1 deletion was detected. The specificity of mutation was compared to that of furylfuramide (AF2). Differences were observed in both the site specificity and the mutagenic specificity of the two 5-nitrofuran derivatives. (1) Furazolidone-induced point mutations were observed at both G:C and A:T base pairs; 93% of AF2-induced point mutations were targeted to G:C sites. (2) At G:C sites approximately equal numbers of G:C-->T:A transversions and G:C-->A:T transversions and G:C-->A:T transitions were induced by furazolidone; AF2-induced G:C-->T:A transversions outnumbered G:C-->A:T transitions 76:49. (3) There was no observable preference for particular sequences of furazolidone-induced mutations; the prominent hotspots for AF2-induced G:C-->T:A transversions, G:C-->A:T transitions and -(G:C) frameshifts were at 5'-TGC-3' sequences in the lacI gene. (4) Furazolidone-induced frameshifts occurred at homopolymeric sequences suggesting that the mutations arose through a strand slippage mechanism; AF2-induced frameshifts occurred at a nonreiterated G:C base pair and could be templated, through formation of a palindrome, by a sequence 110 base pairs upstream from the site of mutation. The significant differences that we observe between the two spectra do not support the notion that structurally different 5-nitrofuran derivatives might react in a similar manner with DNA to produce premutational lesions with similar characteristics.

Bacterial Proteins↗
PubMedDate not supplied

Induction of lambda prophage by furazolidone.

A dose-dependent prophage induction by furazolidone exhibited a gradual rise to a maximum, corresponding to an exposure dose of 1.2 microgram/ml X h and a gradual fall thereafter. A 2-3-fold higher level of induction was achieved when the lysogens were treated with furazolidone in the presence of a metabolizing mixture. A maximum of about 70% efficiency of induction was achieved. Kinetics of prophage induction by any concentration of furazolidone exhibited a common pattern, viz., an initial rise for 15-20 min, then a plateau extending up to about 60 min and a faster rise thereafter. Higher concentrations of the drug (10 micrograms/ml) exhibited a toxic effect. Chloramphenicol at a concentration of 20 micrograms/ml inhibited the furazolidone-induced prophage induction, the plaque-forming units gradually decreasing from several minutes after the chloramphenicol treatment. The burst size of the lysogens was not significantly affected by treatment with 2 micrograms/ml of furazolidone up to a period of about 10 min, but thereafter, decreased faster with the duration of furazolidone treatment. The "latent period' of induction decreased linearly with the duration of furazolidone treatment.

Bacteriophage lambda↗