PubMed Health⌕ Search

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 73 records · Page 4Linked to original sources

Phototoxicity from nalidixic acid: oxygen dependent photohemolysis.

Erythrocyte lysis photosensitized by nalidixic acid was investigated. This photohemolysis was found to be oxygen dependent. The effects of various antioxidants and hydroxyl radical scavengers on photohemolysis induced by nalidixic acid suggested a photo-oxidative step. In addition, using the oxygen quencher histidine and the deuterium oxide effect on the singlet oxygen lifetime we obtained evidence indicative of a photodynamic mechanism mediated by oxygen singlet and hydroxyl radicals. On the other hand, pre-irradiated nalidixic acid was not lytic to erythrocytes, yet photoproducts of nalidixic acid demonstrated a greater photohemolytic potential than nalidixic acid itself.

Antioxidants↗

NTP Toxicology and Carcinogenesis Studies of Nalidixic Acid (CAS No. 389-08-2) in F344/N Rats and B6C3F1 Mice (Feed Studies).

Nalidixic acid is an antimicrobial agent to treat bacterial infections of the urinary tract. NTP Toxicology and Carcinogenesis studies were conducted by feeding diets containing nalidixic acid (approximately 99% pure) to groups of F344/N rats and B6C3F1 mice of each sex for 13 weeks or 2 years. Genetic toxicology studies were conducted in Salmonella typhimurium, mouse lymphoma cells, and Chinese hamster ovary (CHO) cells. Thirteen-Week Studies: Nalidixic acid was administered at dietary concentrations ranging from 1,000 to 16,000 ppm. One female rat that received 16,000 ppm nalidixic acid died before the end of the studies; no other compound-related deaths occurred in rats and mice. The final mean body weights of rats that received 8,000 or 16,000 ppm were 23% or 49% lower than those of controls for males and 11% or 31% lower for females. Feed consumption by rats receiving 16,000 ppm was approximately two-thirds that by controls. Liver weight to body weight ratios for male rats that received 2,000 ppm or more and female rats that received 8,000 ppm or more were significantly greater than those for controls. Degeneration of the germinal epithelium in the seminiferous tubules of the testis was observed in 10/10 male rats that received 16,000 ppm; no other compound-related histopathologic effects were observed in rats. The final mean body weights of mice that received 8,000 or 16,000 ppm were 10%-20% lower than those of controls. Feed consumption by dosed mice was similar to that by controls. Liver weight to body weight ratios were significantly greater for male mice receiving 2,000, 8,000, or 16,000 ppm and for female mice receiving 4,000, 8,000, or 16,000 ppm than for the controls. No compound-related histopathologic effects were observed in mice. Based on these results, 2-year studies of nalidixic acid were conducted by feeding diets containing 0, 2,000, or 4,000 ppm nalidixic acid to groups of 50 male and 50 female F344/N rats and 50 male and 50 female B6C3F1 mice. Body Weight and Survival in the Two-Year Studies: Mean body weights of high dose rats were 7%-23% lower than those of controls, and those of low dose male rats were 6%-11% lower than those of controls. The average daily feed consumption by dosed rats ranged from 89% to 96% that by controls. The average amount of nalidixic acid consumed per day was approximately 80 or 175 mg/kg for low dose or high dose rats. Mean body weights of high dose male mice were 1%-8% lower than those of controls throughout the study. Mean body weights of dosed female mice were 5%-17% lower than those of controls. Average daily feed consumption by dosed mice was within 3% of that by controls. The estimated average amount of nalidixic acid consumed per day was approximately 220 or 475 mg/kg for low dose or high dose mice. No significant differences in survival were seen between any groups of rats or mice of either sex after 2 years (male rats: control, 27/50; low dose, 28/50; high dose, 27/50; female rats: 22/50; 31/50; 29/50; male mice: 33/50; 34/50; 31/50; female mice: 40/50; 43/50; 32/50). Nonneoplastic and Neoplastic Effects in the Two-Year Studies: The incidences of preputial gland neoplasms in dosed male rats and of clitoral gland neoplasms in dosed female rats were significantly greater than those in controls (male--preputial gland adenomas, papillomas, or carcinomas, combined: control, 3/49; low dose, 19/49; high dose, 20/47; female--clitoral gland adenomas, papillomas, or carcinomas, combined: 5/46; 15/46; 16/47). A squamous cell carcinoma of the tongue was seen in two high dose male rats. The historical incidence of oral cavity neoplasms in untreated control male F344/N rats is 7/1,596 (0.4%). There were decreased incidences of leukemia (20/50; 9/50; 7/50) and mammary gland neoplasms (10/50; 7/50; 2/50) in dosed female rats and of pituitary gland neoplasms (11/49; 2/50; 2/50) in dosed male rats. Retinal degeneration and cataracts of the eye were observed at increased incidences in dosed rats (degeneration--male: 4/48; 41/48; 47/49; female: 2/47; 40/48; 46/50; cataracts--malee observed at increased incidences in dosed rats (degeneration--male: 4/48; 41/48; 47/49; female: 2/47; 40/48; 46/50; cataracts--male: 11/48; 23/48; 38/49; female: 0/47; 18/48; 14/50). The cause of these cataracts and retinal degeneration is uncertain because cages were not rotated and low and high dose groups of rats may have been exposed to greater light intensity than were the controls. Subcutanous tissue fibrosarcomas and fibromas or fibrosarcomas (combined) were increased in dosed male mice (fibromas or fibrosarcomas, combined: 5/50; 9/50; 14/50). There were no increased incidences of neoplasms in dosed female mice. Genetic Toxicology: Nalidixic acid was not mutagenic in any of several in vitro short-term tests. No gene reversion was observed in S. typhimurium strains TA97, TA98, TA100, or TA1535 after exposure to nalidixic acid in either the presence or absence of exogenous metabolic activation. Results of tests for induction of trifluorothymidine resistance in mouse L5178Y/TK lymphoma cells were negative with or without metabolic activation. In CHO cells, nalidixic acid did not induce sister chromatid exchanges or chromosomal aberrations in either the presence or absence of activation. Conclusions: Under the conditions of these 2-year feed studies, there was clear evidence of carcinogenic activity of nalidixic acid for F344/N rats, as indicated by increased incidences of preputial gland neoplasms in males and clitoral gland neoplasms in females. There was equivocal evidence of carcinogenic activity for male B6C3F1 mice fed diets containing nalidixic acid, as indicated by marginally increased incidences of subcutaneous tissue neoplasms. There was no evidence of carcinogenic activity for female B6C3F1 mice fed diets containing 2,000 or 4,000 ppm nalidixic acid for 2 years. Synonym: 1-ethyl-1,4-dihydro-7-methyl-4-oxo-1,8-naphthyridine-3-carboxylic acid Trade Names: NegGram®.; Dixiben®.; Nalidixan®.; Nalurin®.; Nogram®.; UroNeg®.; Uralgin®.; Urisal®.

Journal Article↗

Controlled comparison of nalidixic acid or lactulose with placebo in shigellosis.

Nalidixic acid and lactulose, respectively, were compared with placebo in a controlled double-blind study in 43 patients with bacteriologically verified shigellosis. All the strains were susceptible to nalidixic acid. Treatment with nalidixic acid resulted in cure in 72%, which was a significantly better result than with placebo (cure in 21%).

Clinical Trials as Topic↗

Chloroplast DNA synthesis during the cell cycle in cultured cells of Nicotiana tabacum: inhibition by nalidixic acid and hydroxyurea.

The effects of nalidixic acid and hydroxyurea on nuclear and chloroplast DNA formation in cultured cells of Nicotiana tabacum were investigated. At low concentrations (5 and 20 micrograms/ml) nalidixic acid, an inhibitor of DNA gyrase, exhibited a greater inhibitory effect on plastid DNA synthesis than on nuclear DNA formation. Since the plastid genome is a circular double-stranded DNA, this is consistent with the proven involvement of a DNA gyrase in the replication of closed circular duplex DNA genomes in procaryotic cells. At a high concentration of nalidixic acid (50 micrograms/ml), DNA synthesis in both the plastid and nuclear compartment was rapidly inhibited. Removal of the drug from the culture medium led to the resumption of DNA synthesis in 8 h. Hydroxyurea, an inhibitor of ribonucleoside diphosphate reductase, also depresses nuclear as well as plastid DNA formation. Removal of hydroxyurea from the blocked cells leads to a burst of nuclear DNA synthesis, suggesting that the cells had been synchronized at the G1/S boundary. The recovery of plastid DNA synthesis occurs within the same time frame as that of nuclear DNA. However, whereas plastid DNA formation is then maintained at a constant rate, nuclear DNA synthesis reaches a peak and subsequently declines. These results indicate that the synthesis of plastid DNA is independent of the cell cycle events governing nuclear DNA formation in cultured plant cells.

Cell Cycle↗

Toxicity and carcinogenicity studies of nalidixic acid in rodents.

Toxicity and carcinogenicity studies of nalidixic acid, an antimicrobial agent used to treat bacterial infections of the urinary tract, were conducted in F344/N rats and B6C3F1 mice of each sex for 13 weeks or 2 years. In the 13-week studies, nalidixic acid was administered at dietary concentrations ranging from 1,000 to 16,000 ppm. Body weights of both rats and mice were reduced in the groups receiving diet containing 8,000 and 16,000 ppm, and feed consumption of rats in the highest treatment groups was approximately two-thirds that of controls. Degeneration of the germinal epithelium in the seminiferous tubules of the testis was observed in male rats that received 16,000 ppm; no other compound-related histopathologic effects were observed in either species. Two-year studies were conducted by feeding diets containing 0, 2,000, or 4,000 ppm nalidixic acid to groups of 50 rats and mice/sex/group. The average daily feed consumption was slightly reduced compared to control groups and resulted in approximate daily doses of 82 or 175 mg nalidixic acid/kg for low dose and high dose rats, and 220 or 475 mg/kg for low dose and high dose mice. Mean body weights of dosed rats and mice were lower than those of controls, except for groups of low dose female rats and male mice. The incidences of preputial gland neoplasms in dosed male rats and of clitoral gland neoplasms in dosed female rats were significantly increased compared to those in controls; responses in low dose groups were similar to those in high dose groups. There were decreased incidences of leukemia and mammary gland neoplasms in dosed female rats and of pituitary gland neoplasms in dosed male rats. Subcutaneous tissue fibrosarcomas were marginally increased in dosed male mice. There were no increased incidences of neoplasms in dosed female mice. Under the conditions of these studies, the dietary administration of nalidixic acid was carcinogenic for rats, causing preputial gland or clitoral gland neoplasms in males and females, respectively. The association of subcutaneous neoplasms with administration of nalidixic acid to male mice was equivocal.

Animals↗

Frequency of appearance of resistant variants to norfloxacin and nalidixic acid.

The clinical use of nalidixic acid has been hampered by the rapid appearance of resistant variants. This study compares the frequency of appearance of resistant variants to nalidixic acid and norfloxacin, a new quinolone-carboxylic acid with superior antimicrobial activity. We found a lower frequency of appearance of resistant variants with norfloxacin, although there was some cross-resistance between the two drugs. A gradation in this frequency was also noted between the species of Gram-negative rods tested, so that larger numbers of resistant variants appeared with the non-fermenters.

Anti-Infective Agents, Urinary↗

Nalidixic acid induced pseudotumour cerebri in children.

Nalidixic acid, the quinolone frequently used in the treatment of acute dysentery, is now emerging as an important cause of pseudotumour cerebri in infants and young children. A study of 20 such cases showed that all the patients had received a higher than recommended dose of nalidixic acid and that 85% of them were given the drug unnecessarily (i.e., for acute watery diarrhoea). A high concentration of the drug in the commercial preparations as well as the lack of awareness about this among doctors, especially the general practitioners, is the possible contributory factor leading to this situation. A simple measure of bringing down the concentration of nalidixic acid in the available preparations and sticking to oral rehydration solution alone in the treatment of acute watery diarrhoea, can bring down the incidence of this condition.

Anti-Infective Agents↗

Metabolic behaviour and tissue distribution of nalidixic acid in chickens.

The metabolic behaviour and tissue distribution of nalidixic acid in normal and E. coli infected chickens were carried out using spectrofluorimetric and microbiological techniques following a single and multiple oral administration of 25 mg/kg b. wt. The obtained results revealed that free nalidixic acid (free NA) is the major fraction of the total drug concentration in serum, liver and kidneys. The free active nalidixic acid was in a higher concentration than hydroxynalidixic acid (free HNA) and both conjugates of NA and HNA following single and multiple oral administration. The obtained results showed that nalidixic acid was highly distributed in all tissues in normal and E. coli infected chickens, with the highest concentrations in kidneys, liver and heart and lowest concentrations in brain, muscles and intestine following oral administration of 25 mg/kg b. wt. twice daily for 5 successive days. Spectrofluorimetic technique was more sensitive for nalidixic acid determination than microbiological method. Nalidixic acid revealed longer withdrawal time in diseased chickens than in normal chickens.

Animals↗

Characterization of a gyrB mutation responsible for low-level nalidixic acid resistance in Neisseria gonorrhoeae.

Nalidixic acid-resistant derivatives of Neisseria gonorrhoeae WR302 were identified and categorized into two classes on the basis of their susceptibilities to this antimicrobial agent. The MIC of nalidixic acid for the derivative strain MUG116 was fourfold greater than that for its isogenic parental strain WR302 (2 versus 0.5 micrograms/ml, respectively). MUG324 was significantly more resistant to nalidixic acid (greater than 64 micrograms/ml). The MICs of other antimicrobial agents known to interact with either the gyrA or gyrB gene products were determined. Although the nalidixic acid MIC for MUG116 increased, no significant increases in the MICs of other agents that interact with the gyrA gene product were seen. The MICs of all agents that interact with the gyrA gene product were significantly increased for MUG324. The gene that imparts low-level nalidixic acid resistance was cloned from strain MUG116. The DNA sequence of this gene was determined, and by comparing the deduced amino acid sequence with sequences of proteins in data bases, this protein was found to be approximately 70% homologous with the gyrB gene product of Escherichia coli.

Amino Acid Sequence↗

The human biotransformation of nalidixic acid.

Authors have developed new chemical methods for studying the human metabolism of nalidixic acid. The methods are suited for the quantitative determination of nalidixic acid, hydroxynalidixic acid, nalidixic acid glucuronide, hydroxynalidixic acid-glucuronide, and of free and total glucuronic acid excretion. The total urinary excretion of NA and its metabolites was found to be 50 to 100% of the ingested dose. The percentual distribution of the individual metabolites was as follows: NA 0,5-5, HNA2,5-6, NAG24-80, and HNAG11-26%. It was unanimously proved by enzymatic decomposition and specific chemical reactions that the excreted conjugates were monoglucuronides. The significance of individual differences, bilirubin metabolism, urinary pH and the pharmacokinetical behaviour of the individual metabolites is discussed from the therapeutic view.

Biotransformation↗

Lactic acidosis, hyperglycaemia and convulsions following nalidixic acid overdosage.

A woman survived ingestion of 32 g nalidixic acid despite developing lactic acidosis, hyperglycaemia, convulsions and abnormal behaviour. The maximum recorded plasma concentration of nalidixic acid was 185 mg/l and the elimination half-life was 3.2 h. Carboxy-nalidixic acid was demonstrated in the plasma. Previously reported cases of nalidixic acid overdosage are reviewed.

Acidosis↗

Resistance of shigella to nalidixic acid & fluorinated quinolones.

It is known that nalidixic acid resistance is a relatively rare phenomenon among shigellae. Between June 1989 and May 1990, six strains of shigellae resistant to nalidixic acid were isolated. These strains also exhibited resistance to three newer fluoroquinolones, viz., ciprofloxacin, pefloxacin and enoxacin. In repeated experiments, nalidixic acid resistance did not transfer to a suitable recipient.

Anti-Infective Agents↗

Comparative efficacy of furazolidone and nalidixic acid in the empirical treatment of acute invasive diarrhea: randomized clinical trial.

Efficacy of furazolidone and nalidixic acid was compared in a randomized trial involving 72 children with acute invasive diarrhea. Thirty six children received furazolidone (7.5 mg/kg/day) and 36 children received nalidixic acid (55 mg/kg/day). Clinical characteristics of the two treatment groups were comparable on admission. Of these, 34 children in furazolidone treated group and 29 children in nalidixic acid treated group completed the full course of treatment and were analyzed finally for clinical efficacy. Clinical cure was observed in 29(85.3%) children treated with furazolidone and 29(100.0%) children treated with nalidixic acid. Nalidixic acid treated group had statistically significantly higher cure rate (p = 0.039) as compared to furazolidone treated group. However, 85% cure rate in furazolidone treated group may be potentially useful for the treatment of acute invasive diarrhea because of decreasing efficacy of nalidixic acid against shigellosis in many countries.

Anti-Infective Agents↗

Growth of coagulase-negative staphylococci on colistin-nalidixic acid agar and susceptibility to polymyxins.

Colistin-nalidixic acid agar, although recently recommended as a replacement for blood agar for primary plating of urine specimens ( Fung et al., J. Clin. Microbiol. 16:632-636, 1982), has also been reported to suppress the growth of some strains of staphylococci that are susceptible to colistin (polymyxin E). The susceptibility of 11 species of staphylococci to polymyxins was determined, and the ability of these species to grow on colistin-nalidixic acid agar was examined. Although the MICs for most of the strains tested were 8 micrograms/ml or less, only a few coagulase-negative staphylococci grew on or were inhibited by colistin-nalidixic acid agar. This descrepancy was explained by the antagonistic effects that medium components, such as physiological concentrations of magnesium and calcium and 5% sheep blood, had on the activity of polymyxin. Colistin-nalidixic acid agar is still recommended for routine urine processing; however, the poor growth of 13% of the Staphylococcus saprophyticus strains tested suggests that blood agar should be included in the primary plating battery of urine specimens obtained from female outpatients.

Agar↗

Fluroquinolone resistance in typhoidal Salmonella and its detection by nalidixic acid disc diffusion.

OBJECTIVE: To determine the presence of fluoroquinolone resistance in Typhoidal salmonellae at Rawalpindi and the role of nalidixic acid in predicting the resistance against fluoroquinolones in Microbiology Laboratory, Department of Pathology, Army Medical College, Rawalpindi. METHODS: One hundred consecutive clinical isolates of Typhoidal salmonellae isolated from blood culture samples were studied. The organisms were identified biochemically and serologically by standard technique. Sensitivity testing was carried out against nalidixic acid and ciprofloxacin by modified Kirby bauer disc diffusion method and minimum inhibitory concentration (MICs) were determined by E-test. RESULTS: Seventeen percent of the isolates were resistant to nalidixic acid. Nalidixic acid disc diffusion and MIC estimation by E-test were 100% comparable. All isolates were sensitive to ciprofloxacin but the isolates which were resistant to nalidixic acid had raised MIC values against ciprofloxacin. CONCLUSION: Typhoidal salmonellae have not shown an overt in vitro resistance against fluoroquinolones in our set up but a significant population has emerged with raised MIC values. Nalidixic acid susceptibility test can be used an indirect evidence of resistance to quinolones.

Anti-Infective Agents↗

Penicillin-binding proteins of filaments of Escherichia coli induced by low concentrations of nalidixic acid, oxolinic acid, novobiocin or nitrofurantoin.

Nalidixic acid, novobiocin, oxolinic acid and nitrofurantoin, each at low concentrations, cause filamentation of Gram-negative bacilli. Filamentation induced by beta-lactam antibiotics has been correlated to the binding of these antibiotics to specific penicillin-binding proteins (PBPs) of the envelope of Gram-negative bacilli. The studies reported herein indicate that the former group of non-beta-lactam antibiotics do not bind to any of the PBPs of Escherichia coli. However, PBP 1a, PBP 4 and PBP 5/6 of the filaments induced by these agents are increased significantly.

Acyltransferases↗

Microcalorimetry studies of energy changes during the growth of Klebsiella aerogenes in simple salts/glucose media: inhibition by nalidixic acid.

The addition of nalidixic acid (NA) to exponentially growing cells of Klebsiella aerogenes in simple salts/glucose media has a marked effect on the thermal and other growth parameters of the cells. Mass and energy balances have been established for normal and inhibited growth. The decrease, with increasing NA concentration, of energy allocated to biomass and the increase in that wasted is discussed in terms of the energy stored in macromolecular species by the cells under conditions of stress. The enthalpy of production of cellular material, and the enthalpy of metabolism of glucose become more negative with increasing inhibition. A dual-dose response of NA was observed; at low concentrations the potency was greater than at high concentrations.

Calorimetry↗

Long-term in vivo carcinogenicity study of nalidixic acid in CDF1 mice.

Nalidixic acid (NA), a drug used for the treatment of urinary-tract infections, was administered in the diet to groups of 51 male and 51 female CDF1 mice at concentrations of 0, 0.08 and 0.16% for 76 wk. All the surviving animals were killed at wk 85 after 9 wk on the basal diet. Survival of the treated male and female mice was similar to that of the corresponding controls. The body weights were slightly lower in high- and low-dose males and in high-dose females than in the controls. All groups showed relatively high incidences of tumours of the small intestine, lung and haematopoietic organs in both sexes, of the liver and Harderian gland in males and of the uterus in females. However, there were no statistically significant differences between NA-treated and control mice of either sex in the incidences of tumours in any organs. It was therefore concluded that, under the conditions of this study, NA showed no carcinogenic potential in either male or female CDF1 mice.

Administration, Oral↗