Disease relevance of norfloxacin

• Treatment of penicillin-resistant Neisseria gonorrhoeae with oral norfloxacin [1].
• We conclude that a two-dose, single-day regimen of orally administered norfloxacin is effective therapy for uncomplicated urethritis caused by penicillin-resistant strains of N. gonorrhoeae [1].
• We found a significantly lower incidence of infections [1/32 (3.1%) vs. 13/31 (41.9%); P less than 0.005] and spontaneous bacterial peritonitis [0/32 (0%) vs. 7/31 (22.5%); P less than 0.05] in patients receiving norfloxacin [2].
• Norfloxacin prevents bacterial infection in cirrhotics with gastrointestinal hemorrhage [3].
• The prevention of intestinal gram-negative translocation by norfloxacin administration corrects systemic circulatory changes by decreasing NO production in cirrhosis [4].

Psychiatry related information on norfloxacin

• The results of this study suggested that a single dose of oral norfloxacin may be a valuable alternative to the currently recommended treatment regimens for gonococcal eye disease because it combines high efficacy and low toxicity with low cost and excellent patient compliance [5].
• An unusual hallucination with norfloxacin [6].
• The effects of norfloxacin and enoxacin were examined on spontaneous motor activity in the guinea-pig isolated ileum [7].

High impact information on norfloxacin

• Colonization was independently associated with the prophylactic use of both fluconazole (odds ratio, 3.50; P less than 0.001) and norfloxacin (odds ratio, 2.53; P = 0.04) [8].
• Norfloxacin blocked decatenation in wild-type strains, but had no effect in strains with drug-resistance mutations in both gyrase and topo IV [9].
• CPX or NFX plus UV light (NFX*) induce lysosomal membrane permeabilization (LMP), as detected by the release of cathepsins from lysosomes [10].
• Bax-/- Bak-/- double knockout cells fail to undergo MMP and cell death in response to CPX- or NFX-induced LMP [10].
• CPX- or NFX-triggered LMP results in caspase-independent cell death, with hallmarks of apoptosis such as chromatin condensation and phosphatidylserine exposure on the plasma membrane [10].

Chemical compound and disease context of norfloxacin

• This randomized controlled trial was aimed to compare oral norfloxacin vs intravenous ceftriaxone in the prophylaxis of bacterial infection in cirrhotic patients with gastrointestinal bleeding [11].
• Norfloxacin is more potent and broader in spectrum than the earlier developed analogue, nalidixic acid, and is active in vitro against virtually all bacterial pathogens causing urinary tract and gastrointestinal infections, aerobic gram-negative bacilli causing sepsis in neutropenic patients, and Neisseria gonorrhoeae [12].
• CONCLUSION: Bacterial endotoxemia in patients with cirrhosis induces increased synthesis of nitric oxide that can be corrected with norfloxacin [13].
• Responses to NG-monomethyl-L-arginine were greater in patients with cirrhosis but returned to normal after norfloxacin was given [13].
• Herein, using a combination of genomic and functional assays, we demonstrate that specific antibiotics (namely tobramycin, tetracycline, and norfloxacin) at subinhibitory concentrations trigger expression of determinants influencing the virulence of the major opportunistic bacterial pathogen Pseudomonas aeruginosa [14].

Biological context of norfloxacin

• The purpose of the present study was to determine whether changes to the gut flora that occur following norfloxacin-induced selective bowel decontamination alter hepatic regenerative activity [15].
• Norfloxacin was administered to reduce intestinal bacterial translocation [4].
• METHODS: Proinflammatory cytokine levels, Akt and NOS activities, eNOS phosphorylation, and NOS expressions were assessed in aorta from norfloxacin-treated and untreated cirrhotic rats [4].
• Norfloxacin reduces aortic NO synthases and proinflammatory cytokine up-regulation in cirrhotic rats: role of Akt signaling [4].
• The binding of norfloxacin to DNA plasmids is nonintercalative, as shown by the fact that the drug binds preferentially to single-stranded DNA rather than to double-stranded DNA [16].

Anatomical context of norfloxacin

• In a prospective randomized study, selective intestinal decontamination with norfloxacin was performed during hospitalization in 32 cirrhotic patients with low ascitic fluid total protein levels [2].
• Norfloxacin is an oral fluoroquinolone antimicrobial agent recently released for the treatment of uncomplicated and complicated urinary tract infections [12].
• Norfloxacin administration resulted in the suppression of gastrointestinal tract colonization by aerobic bacteria without the development of norfloxacin resistance [17].
• Also the effect of norfloxacin on translocation (as defined by culture positivity of mesenteric lymph nodes) has received little attention [18].
• Previous studies have shown that anaerobic bacteria are susceptible to norfloxacin at the levels attained in the feces [19].

Associations of norfloxacin with other chemical compounds

• Gemfibrozil (GFZ) blocks organic anion transport in J774 cells, thereby facilitating the intracellular accumulation of NFX (Cao, C., H.C. Neu, and S.C. Silverstein. 1991. J. Cell Biol. 115:467a [Abstr.]) [20].
• Thus ursodeoxycholic acid plus norfloxacin may prevent stent clogging [21].
• After oral norfloxacin administration, we saw a significant increase of C3 in serum (p less than 0.05) and ascitic fluid (p = 0.01) [22].
• In the cirrhotic patients with high LBP, norfloxacin normalized (P <.01) LBP (from 16.6 +/- 0.5 to 5.82 +/- 0.8 microg/mL) and sCD14; reduced the level of cytokines, NOx/creatinine, and renin; and increased vascular resistance; but lacked effect in patients with normal LBP [23].
• The primary renal mechanism of elimination for norfloxacin, ciprofloxacin, enoxacin, fleroxacin, temafloxacin, and lomefloxacin is glomerular filtration and tubular secretion [24].

Gene context of norfloxacin

• Instead, norfloxacin causes DNA damage, as evidenced by the induction of the SOS pathway for DNA repair; the increase in susceptibility to the drug by mutations in genes for DNA repair pathways including recA, recB, and uvrD; and the efficient detergent-induced linearization of plasmid DNA in drug-treated cells [25].
• To test this hypothesis, we determined whether macrophage sequestration, lung iNOS expression and activity, and HPS severity were decreased after norfloxacin was given for 5 weeks to prevent Gram-negative bacterial translocation in rats with common bile duct ligation-induced cirrhosis [26].
• The same experiment with a non-Ts background revealed a twofold increase in the norfloxacin MIC at both 30 and 42 degrees C. These data identify the nfxD conditional resistance locus as a mutant allele of parE [27].
• Cells of E. coli transformed with a plasmid carrying the norM gene showed elevated energy-dependent efflux of norfloxacin [28].
• Four parent isolates exhibited a single mutation in gyrA which required < or = 12 mg/L of norfloxacin to be inhibited [29].

Analytical, diagnostic and therapeutic context of norfloxacin

• Group 1 (n = 60) received norfloxacin orally or through a nasogastric tube, 400 mg twice daily for 7 days beginning immediately after emergency gastroscopy; group 2 (n = 59) was the control group [3].
• Adult rats (n = 6 per group) were treated with norfloxacin (10 mg/day) or vehicle for 10 days before 70% partial hepatectomy [15].
• Breath-expired H(2) volume decreased with norfloxacin (37 +/- 8 to 12 +/- 5 mL per 2 hours; P < 0.01) and amoxicillin-clavulanic acid (24 +/- 6 to 8 +/- 4 mL per 2 hours, respectively; P = 0.01), but H(2) breath test result was negative in only 3 and 5 patients [30].
• The binding of plasmid DNA to norfloxacin, a quinolone antibacterial agent, was investigated by fluorescence, electrophoretic DNA unwinding, and affinity chromatography techniques [31].
• Effect of selective bowel decontamination with norfloxacin on spontaneous bacterial peritonitis, translocation, and survival in an animal model of cirrhosis [18].

References