SEARCH · PubMed Health

Results for “NALIDIXIC ACID”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 217 records · Page 12Linked to original sources

PubMed1978

The effect of nalidixic acid group compounds on reduction of cytochrome c from horse heart and Candida krusei.

Reduction of cytochrome c from both horse heart and Candida krusei by FeSO4 has been demonstrated. This reaction was stimulated by nalidixic acid and structurally related compounds, and the effect was more pronounced for the yeast cytochrome. Divalent metal ions other than Fe2+ lessened or abolished the stimulation by these compounds. Fe2+ and other metal ions altered the spectra of nalidixic acid and related compounds indicating the formation of metal chelate complexes. 1,10-Phenanthroline inhibited reduction of cytochrome c b Fe2+. Other divalent metal ions relieved the inhibition, probably by forming chelates with 1,10-phenanthroline. The results suggest that metal ion chelation may be involved in the molecular mode of action of nalidixic acid and related drugs. The relevance of this artificial electron transfer system to bacterial electron transfer in vivo is discussed.

Animals↗

PubMed1997

Resistance of Vibrio cholerae 01 to nalidixic acid.

Until 1987 all isolates of V. cholerae 01 at a tertiary care hospital in south India were susceptible to drugs commonly used to treat gastroenteritis including cholera. Since July 1987 strains resistant to co-trimoxazole have been encountered and since October 1995 strains resistant to nalidixic acid are being isolated. In this study the latter strains were examined by determining minimum inhibitory concentration levels of nalidixic acid as well as norfloxacin, the fluoroquinolone extensively used to treat diarrhoea. No cross resistance to norfloxacin was found in any of the nalidixic acid resistant V. cholerae 01 strains.

Anti-Infective Agents↗

PubMed1977

Media supplemented with nalidixic acid for the isolation of gram negative anaerobic bacteria.

The minimum inhibitory concentrations (MIC) of nalidixic acid were determined for thirty-four strains of Clostridium sp. by an agar dilution technique. The MIC range of Clostridium perfringens ran from 0.03 microgram/ml to 64 microgram/ml, according to a bimodal distribution. One half of the strains was inhibited by 0.25 microgram/ml. 64 microgram/ml was able to inhibit all the strains tested. The author suggests a systematic utilization of media with and without 40 microgram/ml nalidixic acid. These two media were parallely inoculated with clinical specimens where anaerobic bacteria were suspected, and allowed the isolation of gram negative anaerobes.

Anaerobiosis↗

PubMed1982

[Comparison of the antimicrobial activity of pefloxacin (1589 RB), nalidixic acid and flumequin (author's transl)].

The MIC of the four quinolones were determined for 839 bacterial isolates. The mean in vitro activity of pefloxacin against strains susceptible to nalidixic acid was found to be four times greater than flumequin, eight times greater than pipemidic acid, sixteen times greater than nalidixic acid. On resistant strains pefloxacin, at levels lower than 32 micrograms/ml, remained active against 67 go 100 per cent of the strains as a function of bacterial species. Streptocoques D and Pseudomonas aeruginosa, resistant to other quinolones, were found to be susceptible to pefloxacin.

Anti-Infective Agents, Urinary↗

PubMed1980

Kinetics of induction and decay of error-prone DNA repair activity in Escherichia coli after treatment with nalidixic acid.

Inducible error-prone DNA repair activity was detected by infecting nalidixic acid-pretreated E. coli cells with UV-irradiated phage phi X174. Induction and decay kinetics of reactivation very much resembled that of mutagenesis of the UV-damaged phage. Repair as well as mutagenic activity increased for about 30 min. The maximal error-prone repair capacity, which was induced in the cell during the 30 min nalidixic acid treatment, rapidly died out during subsequent cell growth in absence of nalidixic acid. Induction of this repair mode was not observed in a recA- mutant. In the presence of nalidixic acid plus rifampicin both repair and mutagenic effects were abolished.

Bacteriophage phi X 174↗

PubMed1996

Effect of nalidixic acid on recombination and DNA repair of Escherichia coli K-12 strains.

Bacterial DNA gyrase enzyme plays a role in replication, transcription, recombination and repair. Escherichia coli gyrase enzyme is composed of two types of subunit, the gyr A and gyr B gene products called subunit A and B. Each type of subunit can be inhibited with temperature-sensitive mutations or by treating cells with specific antibiotic. Quinolones class of drugs such as nalidixic acid, oxonilic acid and norfloxacin affect gyr A protein. This effect due to inactivation of gyrase arises from the change in DNA superhelical tension. Mutant bacteria resistant to nalidixic acid show structural alterations in subunit A. Nalidixic acid resistant mutants of E. coli strains showed lower recombination efficiency, linkage, DNA repair, and mutation frequency than their wild types.

Anti-Infective Agents↗

PubMed1987

Penetration of nalidixic acid into Escherichia coli K-12 cells.

Transport of nalidixic acid (NAL) into Escherichia coli cells subjected to osmotic shock, permeabilised with toluene or treated with DNP, CCCP or EDTA, was studied. It was found that osmotic shock and protonophores do not inhibit the transport of [3H]NAL, however, the transport of [3H]DAP and [3H]glucose is reduced. EDTA and toluene enhance penetration of [3H]NAL. This effect is, however, abolished in the presence of Mg++ ions. It is suggested that NAL penetrates into the cell by simple or facilitated diffusion and that the outer membrane of E. coli is the penetration barrier for the drug.

Carbonyl Cyanide m-Chlorophenyl Hydrazone↗

PubMed1978

The effect of nalidixic acid, rifampicin and chloramphenicol on the synthesis of phospholipase C in Bacillus cereus.

The effect of nalidixic acid, rifampicin and chloramphenicol on the synthesis of phospholipase C (EC 3.1.4.3) has been studied in washed Bacillus cereus cells resuspended in nutrient broth. In the absence of inhibitors, the synthesis showed a biphasic pattern. No synthesis of release of enzyme was found in the presence of chloramphenicol. When rifampicin was added, phospholipase C synthesis continued for 10-15 min. Nalidixic acid, at concentrations which inhibited DNA synthesis completely, permitted the synthesis of phospholipase C at the same rate and for a similar length of time as rifampicin.

Bacillus cereus↗

PubMed1976

Nalidixic acid as a selective agent for the isolation of enterobacteria from river water.

Enterobacteria are more resistant to nalidixic acid than the majority of other Gram-negative organisms isolated from river water, so allowing their selection on MacConkey agar containing nalidixic aicd. Selection is further improved by anaerobic incubation which, with nalidixic acid, virtually eliminates oxidase-postivie strains such as Pseudomonas or Aeromonas.

Ampicillin↗

PubMed1992

[Comparative activities in vitro of 4 quinolones (nalidixic acid, pefloxacin, norfloxacin, ofloxacin) on 13 bacterial species].

Nalidixic acid and three fluoroquinolones were tested on 389 strains belonging to 13 bacterial species, all isolated in Algeria. Ofloxacin, norfloxacin and pefloxacin have the same activities on E. coli, Acinetobacter and S. aureus. Norfloxacin has the best activity on Proteus, Enterobacter, Shigella and Klebsiella. Norfloxacin and ofloxacin have the same activities on S. typhi, Salmonella and choleric Vibrio. Norfloxacin has the same activity than pefloxacin on P. aeruginosa. It is necessary to prescribe a quinolone in the right way and to consider the pharmacokinetic properties.

Anti-Infective Agents↗

PubMed1991

Mechanisms of quinolone resistance in a clinical isolate of Escherichia coli highly resistant to fluoroquinolones but susceptible to nalidixic acid.

Two associated resistance mechanisms were found in a nalidixic acid-susceptible (4 micrograms/ml) but fluoroquinolone-resistant (8 to 16 micrograms/ml) strain of Escherichia coli Q2 selected under norfloxacin therapy. As compared with the susceptible E. coli Q1 isolated before treatment, changes in outer membrane proteins and lipopolysaccharides in Q2 were associated with a 1.5- to 3-fold decrease in the uptake of fluoroquinolones but not nalidixic acid. A 50% inhibition of DNA synthesis in toluene-permeabilized cells of the resistant strain E. coli Q2 required up to 500-fold increased quantities of fluoroquinolones, whereas such inhibition was obtained in both E. coli Q1 and Q2 with similar amounts of nalidixic acid. Selection from E. coli Q1 on norfloxacin of one-step resistant mutants resembling E. coli Q2 was unsuccessful. From these results we infer that a decrease in outer membrane permeability, associated with a peculiar alteration of the DNA gyrase, was responsible for the unusual quinolone resistance phenotype of E. coli Q2.

Anti-Infective Agents↗

PubMed1984

groEL and dnaK genes of Escherichia coli are induced by UV irradiation and nalidixic acid in an htpR+-dependent fashion.

Two proteins with molecular weights of 61,000 and 73,000 were found to be induced by UV light in Escherichia coli mutants in which the SOS responses are constitutively expressed. The induction of these proteins by UV light and nalidixic acid was shown to be independent of the recA+ lexA+ regulatory system. Analysis of these proteins by two-dimensional gel electrophoresis and comparison with the "heat-shock" proteins of E. coli revealed that the Mr 61,000 protein comigrated with the groEL gene product, that the Mr 73,000 protein comigrated with the dnaK gene product, and that other heat-shock proteins were also induced. The induction of groEL and dnaK by UV light and nalidixic acid is controlled by the htpR locus. The results suggest that the regulatory response of E. coli to agents such as UV light and nalidixic acid is more complex than previously thought.

Alleles↗

PubMed1966

Mechanism of Action of Nalidixic Acid on Escherichia coli V. Possible Mutagenic Effect.

Cook, Thomas M., (Sterling-Winthrop Research Institute, Rensselaer, N.Y.), William A. Goss, and William H. Deitz. Mechanism of action of nalidixic acid on Escherichia coli. V. Possible mutagenic effect. J. Bacteriol. 91:780-783. 1966.-With a streptomycin-dependent organism, Escherichia coli ATCC 11143, it has been shown that exposure to nalidixic acid, under conditions permitting some bactericidal action, results in an increased number of streptomycin-independent bacteria among the survivors. This effect is evident only with proliferating cultures, and is related to the concentration of nalidixic acid and the duration of exposure.

Journal Article↗

PubMed2000

Single-use phosphorimetric sensor for the determination of nalidixic acid in human urine and milk.

A single-use phosphorimetric sensor to determine the germicide nalidixic acid is proposed. The sensing action is based on the absorption of the analyte into the sensing zone and the subsequent measurement of the phosphorescence intensity emitted by the analyte fixed in the sensor. This plane drop sensor is made up of a 3 x 1.6 cm sheet of the polyester Mylar as solid support, and a circular film 5 mm in diameter and 20 microns in thickness, formed by poly(vinyl chloride) and tributyl phosphate as the plasticizer, adhered to its surface. The sensor is introduced for 2 h into the sample solution, after which it is dried and the phosphorescence intensity is measured directly at lambda ex = 332 nm, lambda em = 412 nm, with a delay time of 0.15 ms and a gate time of 10 ms, under a dry nitrogen stream. The characteristic parameters of the construction of the sensing zone and of the processes of fixing the analyte along with the emission of phosphorescence were studied. The applicable concentration range was from 60 to 1500 ng ml-1, with a detection limit of 20 ng ml-1 and a precision of 2% expressed as relative standard deviation. The method was applied to the determination of nalidixic acid in milk and human urine with recoveries ranging between 96.0 and 103.7%. The calibration process was carried out by applying a mathematical method of finite elements that expresses the analytical signal as a function of the analyte concentration and equilibration time between the sensor and the sample solution.

Anti-Infective Agents↗

PubMed1985

Laboratory evaluation of enoxacin: comparison with norfloxacin and nalidixic acid.

Enoxacin displayed activity similar to that of norfloxacin against enterobacteria, Pseudomonas aeruginosa, staphylococci, streptococci and Bacteroides spp. The activity of enoxacin against many strains was reduced in acid conditions, but the pH effect was not so marked as that seen with norfloxacin. Nalidixic acid was found to be more active in acid conditions, particularly against staphylococci, Streptococcus faecalis and Ps. aeruginosa. In conditions simulating the treatment of bacterial cystitis, a single dose of enoxacin, achieving a peak concentration of 50 mg/l, suppressed growth of nalidixic acid-sensitive and -resistant Gram-negative bacilli for periods of between 18 and 25 X 5 h. Reduced susceptibility of bacteria surviving exposure to enoxacin was observed in one nalidixic acid-resistant strain of Escherichia coli and in nalidixic acid-sensitive strains exposed to low doses (peak concentration = 5 mg/l) of enoxacin. These results are similar to those obtained with norfloxacin and substantially better than those obtained with nalidixic acid.

Anti-Bacterial Agents↗

PubMed1977

The effect of nalidixic acid on the cell cycle of synchronous Rhodopseudomonas palustris cultures.

The influence of the DNA synthesis inhibitor, nalidixic acid, on the properties of synchronous cultures of selected Rhodopseudomonas palustris swarmer cells was examined. There was little alteration in the changes in morphology, extinction, volume distribution and leucine incorporation up to bud development, and photosynthetic membrane lamellae were still synthesized de novo in the bud. However, there was no subsequent division, or flagellum or holdfast synthesis. Instead cells elongated by continued outgrowth of the abortive bud. Since DNA synthesis was also inhibited, this suggested a dependence of cell division, and flagellum and holdfast synthesis, on the completion of chromosome replication. By addition or removal of nalidixic acid at various times in the cell cycle, periods were demonstrated when the organism was insensitive to the antibiotic indicating that there was a pre-synthetic and post-synthetic gap in the pattern of DNA synthesis in R. palustris swarmers.

Cell Division↗

PubMed1988

Influence of nalidixic acid on killing and mutation of V79 cells exposed to different damaging agents.

The effect of treatment with nalidixic acid, an inhibitor of DNA topoisomerase, after exposure of V79 cells to different DNA-damaging agents on the induction of killing and mutation has been studied. The DNA-damaging agents were ultraviolet light, gamma-rays and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). It was seen that treatment with nalidixic acid potentiated the killing by MNNG and suppressed the induction of mutation. However, it had no influence upon killing and mutation by UV light and gamma-rays. The difference in the observed results could be due to the nature of the damage induced and its repair in relation to the function of topoisomerases.

Animals↗

PubMed1981

Thin-layer chromatographic method for the quantitative analysis of nalidixic acid in human plasma.

A sensitive and highly selective thin-layer chromatographic method for determining plasma levels of nalidixic acid is presented. Plasma (50 microliter) was acidified with 50 microliter M orthophosphoric acid and extracted with 100 microliter toluene. A 40-microliter aliquot of the extract was spotted onto the thin-layer plate with the aid of a Desaga Autospotter and, after irrigation, the nalidixic acid on the plate was converted into a fluorescent compound by exposing the plates to hydrogen chloride gas for 10 min and then to strong ultraviolet radiation from a mercury lamp for 10 min. The fluorescence was measured quantitatively using a spectrofluorimeter equipped with a thin-layer chromatogram scanning attachment.

Chromatography, Thin Layer↗