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At least 307 records · Page 17Linked to original sources
PubMed1989

A preliminary report on the derivatization-gas chromatographic determination of nalidixic acid and 3,7-dicarboxynalidixic acid in urine.

A preliminary study on the gas chromatographic analysis of urine spiked with nalidixic acid and 3,7-dicarboxynalidixic acid is described. The method is based on the transfer of an ion-pair of NA or CNA with tetradecyldimethylbenzylammonium chloride (benzalkonium chloride) from alkaline aqueous solution into methyl isobutyl ketone (MIBK), the organic phase, where these salts are derivatized with pentafluorobenzyl bromide. The derivatives formed by this process are chromatographed on an analytical column packed with 1.5% OV-101 and detected with a flame-ionization detector. Several parameters affecting the transfer and/or derivatization of NA or CNA were investigated. These parameters include the phase transfer catalyst employed, the organic solvent used, the concentration of the acid and base added, the amount of derivatizing agent required, and reaction time and temperature.

Chemical Phenomena↗
PubMed1975

Bullous photoreaction to nalidixic acid.

Curtaneous blisters developed after exposure to the sun in two women who were taking nalidixic acid. Blisters continued to appear even after therapy was discontinued and there was no further exposure to the sun. Phototesting showed abnormal sensitivity to both short and long wavelength ultraviolet spectra in one patient. The low incidence of this phenomenon suggests a photoallergic mechanism, but features of both photoallergy and phototoxicity are present.

Adult↗
PubMed1980

Mode of action of a new nalidixic acid derivative, AB206.

A new chemotherapeutic agent, AB206, shows potent antibacterial activity against gram-negative bacteria, including most of the nalidixic acid-resistant strains tested. It strongly inhibits deoxyribonucleic acid (DNA) synthesis in Escherichia coli, but only slightly inhibits ribonucleic acid and protein synthesis. Its activity on DNA synthesis in vivo and in vitro is greater than that of nalidixic acid. AB206 also strongly inhibits in vivo DNA synthesis in nalidixic acid-susceptible and -resistant clinical isolates of Proteus and Serratia. AB206 shows high penetrability into E. coli cells, as demonstrated by antibacterial activity with or without ethylenediaminetetraacetic acid, inhibition of in vivo and in vitro DNA synthesis, and uptake of the drug into cells, as compared to nalidixic acid. It appears that the high antibacterial activity of AB206 may be explained both by its potent inhibitory action against DNA synthesis and also by its high penetrability into bacterial cells.

4-Quinolones↗
PubMed1975

[Resistance to nalidixic acid in tetracycline-resistant mutants of E. coli].

The studies on the effect of nalidixic acid (negram) on the synthesis of DNA and determination of its minimal inhibitory concentrations revealed a regular decrease in the sensitivity levels to negram of the tetracycline resistant mutants selected on media with tetracycline. Heterogene ty of the tetracycline resistant mutants to EDTA showed that one of the causes of insensitivity of the mutants to negram was a change in the surface structures of the microbial cell.

Culture Media↗
PubMed1988

Nalidixic acid and oxolinic acid reversibly suppress 3-methylcholanthrene-induced cell transformation of BALB/3T3 mouse cells.

The effects of nalidixic acid (Nal) and oxolinic acid (Oxl), synthetic antibacterial compounds that inhibit bacterial DNA gyrase, on 3-methylcholanthrene (MC)-induced transformation of BALB/3T3 mouse cells were investigated. Exposure of the cells to Nal or Oxl for 2 weeks at any time during 4 weeks of incubation following MC treatment suppressed MC-induced transformation. Nal and Oxl also suppressed the enhancement of transformation by 12-O-tetradecanoylphorbol-13-acetate (TPA) initiated by MC. The suppression of transformation by Nal was released by exposure of the cells to TPA after removal of Nal. Since the suppressive effects of Nal and Oxl on transformation were time-related, they may be due to epigenetic changes.

Animals↗
PubMed1991

Selective medium containing fosfomycin, nalidixic acid, and culture supernatant of Rhodococcus equi for isolation of Corynebacterium pseudotuberculosis.

FNR medium containing fosfomycin, nalidixic acid, bovine blood and culture supernatant of Rhodococcus equi was prepared by the present authors, and the medium did not inhibit growth of Corynebacterium pseudotuberculosis but completely hampered the growth of Bacillus subtilis, Staphylococcus aureus, and Escherichia coli. The culture supernatant of R. equi facilitated detection of suspected colonies of C. pseudotuberculosis due to synergistic hemolysis. Rate of isolation of the organisms (from the trachea, larynx and nasal cavity of 16 slaughtered sheep with caseous abscess in the lung) was higher with FNR, the selective medium, than with nonselective medium. The selective medium was thus found to be useful for isolation of C. pseudotuberculosis from sheep.

Animals↗
PubMed1987

In vitro release and in vivo absorption of nitrofurantoin and nalidixic acid from ethylcellulose microcapsules.

Ethylcellulose was used as an efficient retarding material to prepare nitrofurantoin or nalidixic acid microcapsules. The dissolution rates of the different preparations have found to increase in alkaline rather than in acidic media. Considerable retardation in the rate and extent of release from 2:1, 1:1 and 1:2 drug-polymer ratios were observed as compared with those of the plain drugs. Absorption study in man proved that formulations containing 2:1 ratios have delayed urinary excretion rates by 2 h, however, the total cumulative amounts excreted from all samples remained almost constant. Man volunteers administered the 2:1 drug-polymer microcapsules did not suffer gastric irritation, usually produced after three consecutive d from taking the plain drugs. Experiments in male albino rats showed that the coated drugs did not produce gastric hemorrhage seen with the same doses of the uncoated ones.

Adult↗
PubMed2000

[Increasing nalidixic-acid-resistance in Salmonella strains isolated from sporadic cases in Tokyo].

A total of 118 nalidixic-acid (NA)-resistant Salmonella strains consisting of 68 domestic strains and 50 imported strains isolated during 1988-1998 in Tokyo were examined regarding their annual incidence, serovars, drug-resistance patterns, and minimum inhibitory concentrations(MIC) to fluoroquinolones (NFLX, OFLX, ENX, and CPFX). NA-resistant strains accounted for 1.3% of all Salmonella (5,302 strains) isolated from domestic cases, and 2.5% of all Salmonella (1,981 strains) isolated from imported cases. The incidence of NA-resistant strains has increased since 1995, and it has been remarkable in imported cases. The results of the serotyping showed that the NA-resistant strains were classified into 25 serovars, excluding untypable strains. Among those, S. Enteritidis (21 strains), S. Blockley (13 strains), S. Litchifield (13 strains), S. Typhimurium (13 strains), S. Hadar (9 strains), and S. Virchow (8 strains) were predominant. Drug-resistance patterns of NA-resistant strains, including other drugs (CP, TC, SM, KM, ABPC, ST, FOM, and NFLX) tested varied among the 26 types. Among those, multidrug-resistant strains accounted for 61.9% (73 strains), and one strain among them was high-resistant to NFLX. MIC distribution of NA-resistant strains to fluoroquinolones showed that the ranges of all drugs were 4-128 times higher than NA-sensitive strains used for controls.

Anti-Infective Agents↗
PubMedDate not supplied

In vitro activity of nalidixic acid and its iron (III) complex on Entamoeba histolytica.

The in vitro activity of the antibacterial agent nalidixic acid (HNal) and its iron (III) complex (FeNal) against Entamoeba histolytica HM1 strain trophozoites in axenic or monoxenic (associated with Clostridium symbiosum) cultures was investigated. Using a dilution test with TYI-S-33 medium, this protozoan was found to be susceptible to both drugs, but FeNal showed amoebicidal activity only at concentrations higher than those used with HNal.

Animals↗
PubMed1985

DNA metabolism during infection of Anacystis nidulans by cyanophage AS-1. VI. Effect of hydroxyurea and nalidixic acid on the development of cyanophage AS-1.

The use of the DNA inhibitors hydroxyurea (HU) and nalidixic acid (NAL) to elucidate patterns of DNA metabolism in AS-1 infected A. nidulans have led to several conclusions. First, HU and NAL at concentrations of 500 and 100 micrograms/ml, respectively, inhibited DNA synthesis in synchronized A. nidulans. Protein and chlorophyll synthesis remained essentially unchanged as did turbidity increases. Second, the complete burst size of the cyanophage AS-1 was severely affected by HU and NAL treatment and burst sizes of 8 and 2.6, respectively, were obtained. Third, inhibitor treatment of infected cultures caused a premature release of phage at 12 h instead of 16 h post infection. Finally, HU treatment of the host cell had no effect on the formation of PIL-DNA, whereas NAL pretreatment blocked its formation.

Chlorophyll↗
PubMed1991

The effect of infinitesimal drug dilutions on the pharmacokinetics of nalidixic acid and atenolol.

1. Ten healthy subjects received two treatments: a single 1 g oral dose of nalidixic acid (NA) followed 1 h later by either an infinitesimal dilution of the drug (NA 7CH) or by succussed water which served as placebo. The study was repeated 18 months later in 10 different subjects. 2. A further 10 healthy subjects received three treatments: a single 100 mg oral dose of atenolol (AT) followed 3 h later by either placebo or a dilution of AT (AT 7CH) or of bisoprolol (BI 7CH). The homoeopathic preparations were administered by the sublingual route. 3. In the first NA experiment NA 7CH significantly shortened the elimination half-life of NA from 8.6 +/- 2.2 (placebo) to 6.4 +/- 1.6 h (NA 7CH). In the second NA experiment none of the pharmacokinetic parameters was modified significantly by the administration of NA 7CH. Neither AT 7CH nor BI 7CH modified the pharmacokinetics of AT.

Administration, Oral↗
PubMed1985

Susceptibility of Campylobacter species to nalidixic acid, enoxacin, and other DNA gyrase inhibitors.

Nalidixic acid-resistant mutants of Campylobacter jejuni and C. coli as well as "C. laridis" strains showed cross-resistance to another DNA gyrase subunit A inhibitor, enoxacin (MIC, 32 micrograms/ml), whereas C. fetus subsp. fetus, C. fetus subsp. venerealis, and "C. hyointestinalis" strains were all susceptible to enoxacin (MIC, less than or equal to 2 micrograms/ml). All Campylobacter species were resistant to novobiocin (MIC, 32 to 512 micrograms/ml), but most strains were susceptible to the other DNA gyrase subunit B inhibitors coumermycin A1 and clorobiocin.

Anti-Bacterial Agents↗
PubMed1995

Mutations sensitizing yeast cells to the start inhibitor nalidixic acid.

The regulatory step Start in the cell cycle of the budding yeast Saccharomyces cerevisiae is inhibited by nalidixic acid (Nal). To study this inhibition, mutations were identified that alter the sensitivity of yeast cells to Nal. Nal-sensitive mutations were sought because the inhibitory effects of Nal on wild-type cells are only transient, and wild-type cells naturally become refractory to Nal. Three complementation groups of Nal-sensitive mutations were found. Mutations in the first complementation group were shown to reside in the ARO7 gene, encoding chorismate mutase; tyrosine and phenylalanine synthesis was inhibited by Nal in these aro7 mutants, whereas wild-type chorismate mutase was unaffected, These aro7 alleles demonstrate 'recruitment', by mutation, of an innately indifferent protein to an inhibitor-sensitive form. The Nal-sensitive aro7 mutant cells were used to show that the resumption of Nal-inhibited nuclear activity and cell proliferation takes place while cytoplasmic Nal persists at concentrations inhibitory for the mutant chorismate mutase. Mutations in the second complementation group, nss2 (Nal-supersensitive), increased intracellular Nal concentrations, and may simply alter the permeability of cells to Nal. The third complementation group was found to be the ERG6 gene, previously suggested to encode the ergosterol biosynthetic enzyme sterol methyltransferase. Mutation or deletion of the ERG6 gene had little effect on the inhibition of Start by Nal, but prevented recovery from this inhibition. Mutation of ERG3, encoding another ergosterol biosynthetic enzyme, also caused Nal sensitivity, suggesting that plasma membrane sterol composition, and plasma membrane function, mediates recovery from Nal-mediated inhibition of Start.

Cell Cycle↗
PubMed1985

Transmission and expression of mutations to nalidixic acid resistance among products of protoplast fusion crosses of Candida albicans.

Earlier studies suggested that heritable resistance to nalidixic acid (Nal) induced in the asexual, pathogenic yeast Candida albicans by growth on Nal results from mitochondrial mutation. To determine conclusively whether mutations to Nal resistance are cytoplasmic or nuclear, several stable Nal-resistant (Nalr) mutants exhibiting distinctive differences in degrees of Nal resistance were obtained from each of two doubly auxotrophic strains (Ade-, Thr- and Arg-, His-), both derived from the same wild-type stock. Inheritance of Nal resistance was then assessed in a series of protoplast fusion crosses between complementing auxotrophs. The initial, intact cellular products of a fusion cross are prototrophic heterokaryons which frequently assort single parental nuclei into monokaryotic blastospores containing biparental cytoplasms. Occasional karyogamy within heterokaryons also yields prototrophic hybrid monokaryons which can undergo recombinations for chromosomal markers through spontaneous or induced mitotic crossing-over. Segregation and expression of Nal resistance among non-hybrid, parental-type monokaryons from Nalr X Nals heterokaryons showed that Nalr mutations are nuclear and that their expressions are not noticeably affected by admixture of cytoplasms of sensitive and resistant parental strains. Analyses of heterokaryons and hybrid monokaryons from Nalr X Nals and Nalr X Nalr crosses demonstrated that Nal resistance is recessive to sensitivity, and that independent Nalr mutations arise at one gene in the Ade-, Thr- strain and at a separate, complementing single gene in the Arg-, His- strain. Prior work demonstrated that induction of Nalr mutations in wild-type C. albicans depends profoundly on the (i) carbon and nitrogen, (ii) growth temperature, (iii) contact with particular metabolic inhibitors and (iv) division stage of cells during exposure to Nal. The present observations indicate that the character of cellular auxotrophies can determine the genetic loci at which Nalr mutations can be recovered.

Alleles↗
PubMed1981

A new citrated formulation of nalidixic acid (Mictral U.K.) for the treatment of acute cystitis.

A 3-day course of a new citrated formulation of nalidixic acid (Mictral) was assessed in fifty-four women presenting with acute uncomplicated cystitis. Over 96% of women with a significant Gram-negative bacteriuria were cured of the infection following a course of treatment. Only two relapses occurred in this group during the follow-up period. Relief of symptoms occurred in nearly 90% of infected patients and generally by the second day of treatment. Although the incidence of side-effects was about 20% they were not considered serious.

Acute Disease↗
PubMed1993

High-performance liquid chromatographic determination of nalidixic acid in rat serum, brain and cerebrospinal fluid.

A high-performance liquid chromatographic method for the determination of nalidixic acid (NA) in rat serum, brain and cerebrospinal fluid (CSF) was developed. NA in rat serum and brain homogenate was extracted and injected onto a reversed-phase column. CSF was directly analysed without extraction procedure. The limits of detection were 0.05 microgram ml-1 for serum, 0.07 microgram g-1 for brain and 0.02 microgram ml-1 for CSF, respectively. Calibration curves were linear over the concentration ranges 0.1-50 micrograms ml-1 for serum, 0.12-9 micrograms g-1 for brain and 0.05-10 micrograms ml-1 for CSF, respectively. The reproducibility of NA assay in rat biological media ranged from 1 to 4% relative standard deviations (RSD). The recoveries of NA added to serum and brain were higher than 96% with an RSD of less than 4%. The present method was found to be applicable to pharmacokinetic study of NA in rat serum, brain and CSF.

Animals↗
PubMed1981

Epidemiologic features of urinary infections due to enterobacteriaceae resistant to nalidixic acid and trimethoprim.

For a period of one year we identified all urinary isolates of Enterobacteriaceae resistant to either nalidixic acid (NA) or trimethoprim (TMP). Host and organism characteristics associated with the occurrence of 68 NA and 61 TMP-resistant isolates were compared with 61 matched antimicrobial-susceptible controls. Minimum inhibitory concentrations to NA and TMP were carried out on all isolates, Escherichia coli isolates were biotyped and TMP-sulfamethoxazole (SMX) synergy studies were performed on TMP-resistant isolates. Study patients were reviewed with regard to age, renal function, presence of structural urinary tract abnormality, history of antimicrobial treatment and persistence of study strains within the urinary tract. Resistance to both drugs was associated with prior treatment with the relevant antimicrobial and with underlying urinary tract abnormality. No association was noted between resistance and patient age or renal function. Once resistant organisms infected an abnormal urinary tract, they were able to persist almost indefinitely. Patients with persistent urinary infections associated with structural urinary tract abnormality account for most NA or TMP-resistant infections in our hospital and constitute an identifiable group in whom the therapeutic usefulness of these drugs is limited.

Adult↗