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PubMed1985

Neomycin is more efficient than streptomycin in suppressing frameshift mutations.

The effects of streptomycin and neomycin on the phenotypic suppression of frameshift mutations in the lacZ gene of Escherichia coli and on the efficiency of suppression of amber mutations in T4 phage by the informational supE tRNA nonsense suppressor were compared. Neomycin stimulated much more efficiently than streptomycin the phenotypic suppression of frameshift mutations. Because neomycin favors mismatches of the central codon base whereas streptomycin favors mismatches of the first codon base, this result suggests that mismatching of the central codon base pair and shifting of the reading frame are two correlated phenomena. In contrast, both streptomycin and neomycin stimulated about equally the efficiency of the tRNA nonsense suppressor, an effect probably related to their interference with the proofreading control in tRNA selection.

Escherichia coli↗

PubMed1988

The effects of neomycin on membrane properties and discharge activity of an isolated sensory neuron.

The effects of neomycin sulfate were examined upon the discharge activity and electrical membrane properties of an isolated invertebrate sensory neuron, the crayfish stretch receptor neuron. Neomycin depressed cell discharge activity in a concentration-dependent manner over the concentration range of 0.01-1.0 mM. Significant concentration-related increases were observed in the resting membrane potential and the width of the orthodromic action potential. There was a significant concentration-dependent decrease in the fast rising phase of the antidromic action potential. Significant changes also were observed in other electrical properties such as membrane resistance, but these were found not to be concentration related. The most significant change was membrane hyperpolarization, which could account for the depression of cell discharge activity. The observed changes are consistent with a neomycin-induced change in the membrane potassium conductance. It is proposed that the neural effect of neomycin is a selective interaction with the neuronal membrane phospholipids.

Action Potentials↗

PubMed1968

Effect of neomycin on exchangeable pools of cholesterol in the steady state.

Five patients received cholesterol-7alpha-(3)H intravenously during control periods. Specific activity of total serum cholesterol was determined serially during the 1st wk and weekly thereafter. 28-59 wk after the injection of the tracer, when no further radioactivity could be detected in serum cholesterol, 2 g of oral neomycin was given daily to four patients for the remainder of the experiment. Average total serum cholesterol concentrations were reduced by 20, 21, 26, and 29%, respectively, in these subjects. The fifth patient, given placebo, had no change in serum cholesterol. After a period of 12-26 wk of medication the intravenous injection of cholesterol-7alpha-(3)H was repeated, and while neomycin or placebo administration was continued, serum cholesterol specific activity was again determined serially during the 1st wk and weekly thereafter for 23-42 wk. The data were subjected to a two-compartment analysis. During the administration of neomycin, half-times of the cholesterol radio-activity decay curves were decreased in two patients and remained unchanged in two subjects. The size of the "intermediate" pool of cholesterol decreased in each patient during the administration of neomycin by 33, 36, 40, and 44%, respectively. The absolute decrease was much larger in each case than the concomitant reduction of serum cholesterol. There was no significant change in the data during the administration of placebo in one patient. The size of the "intermediate" pool can be calculated by compartmental analysis from the cholesterol decay curves. For the "slow" pool size and the other kinetic parameters only ranges of values can be deduced from the present experiment.

Aged↗

PubMed1971

Action of neomycin on the intraluminal phase of lipid absorption.

Administration of a single 1 g dose of neomycin sulfate to five healthy subjects simultaneously with a test meal caused a marked increase in the proportion of fatty acid and bile acid in the ultracentrifuged deposit of aspirated intestinal contents. Labeled cholesterol was precipitated in a similar manner in two hypercholesterolemic patients. Neomycin had no effect on the pancreatic lipase concentration or on the pH of intestinal contents. These results confirm that the ability of neomycin to precipitate micellar lipids is due to interaction between the polybasic neomycin molecule and ionized fatty acids and bile acids. This mechanism provides an explanation for both the steatorrhea and hypocholesterolemia induced by this compound.

Administration, Oral↗

PubMedDate not supplied

Neomycin ototoxicity.

A case of oral neomycin ototoxicity is presented, followed by a summary of known cases in the English literature. While it is known that neomycin is concentrated in the inner ear fluids, at the present time the biochemical basis of its ototoxic effect has not been definitively elucidated. High frequency audiometry can aid in the early detection of the onset of neomycin-induced deafness. Dialysis has a limited but useful role in preventing neomycin ototoxicity.

Deafness↗

PubMed1992

Bioactive polymers: in vitro and in vivo study of controlled release neomycin.

Neomycin is coupled on xanthan-a polysaccharide of microbial biosynthesis produced by Xanthomonas campestris-through ionic complexation. The kinetics of neomycin release, in vitro, at pH = 8.2 is studied. A controlled release of neomycin, following a zero order kinetics is observed, regardless of the eluent flow. Neomycin complexed on xanthan, administered in a unique daily dose to patients suffering from dysentery in the 100 cases taken in study, has shown a high clinical efficiency as compared with the treatments with ampicillin or furazolidone, administered for 5-10 days or longer.

Adult↗

PubMed1986

Aminoglycoside binding sites in Escherichia coli as revealed by neomycin-gold labeling.

A cytochemical technique for demonstration of neomycin binding sites by electron microscopy was developed and applied to Escherichia coli. Neomycin was conjugated chemically with bovine serum albumin (BSA). Colloidal gold was coated with the conjugated neomycin-BSA. The neomycin-BSA-gold was applied to thin sections of Epon-embedded E. coli and examined. Gold particles were observed on the outer membrane and the cytoplasmic membrane of E. coli. It was probably the ribosomes that were being labeled in the cytoplasm. Different cytochemical controls, including a number of inhibition tests and the use of BSA-gold, proved the specificity of this cytochemical technique and provided the biochemical significance of the observations.

Binding Sites↗

PubMed2003

Glioma cell-associated sustained activation of the transcription factor, nuclear factor-kappa B, was inhibited by neomycin.

Experimental evidence suggests that the transcription factor nuclear factor-Kappa B (NF-kappa B) plays an important role in tumor cell invasion, apoptosis suppression and growth. Malignant glioma is one of the most intractable tumors because of its invasiveness to surrounding brain tissue. Our study investigated the role of neomycin on NF-kappa B activity in glioma cell cultures. We performed immunocytochemical analysis of cells with the antibody NF-kappa Bp65 which results show that neomycin decreases significantly the activation of NF-kappa B when added to glioma cultures for 30 min. This finding supports an important role for neomycin in glioma invasion, apoptosis and growth. Collectively, these data suggest a rationale for clinical trials with neomycin in the treatment of gliomas.

Animals↗

PubMed2003

Antiproliferative action of neomycin is associated with inhibition of cyclin D1 activation in glioma cells.

The progression of mammalian cells through G1 phase of the cell cycle is governed by the D-type cyclins (D1, D2, D3). These proteins are induced at the beginning of the G1 phase and associate with serine/threonine cyclin-dependent kinases to form holoenzymes. Overexpression of cyclin D1 in human cancers as well as in several cancer cell lines has been reported. Here, we employed mitotic selection to synchronize the C6 glioma cell cycle at the start of the G1 phase and assessed the effects of neomycin on cyclin D1 protein detection by immunocytochemical analysis. Cyclin D1 activation as well as cell proliferation were already significantly reduced after 3 h of incubation of the cells with neomycin. These findings suggested that the antiproliferative effects of neomycin in gliomas could be mediated by inhibition of the expression of cyclin D1 gene and support further consideration of therapeutic use of neomycin in a Phase I clinical study for patients with recurrent glioblastoma.

Animals↗

PubMed1993

Neuropharmacological characterization of voltage-sensitive calcium channels: possible existence of neomycin-sensitive, omega-conotoxin GVIA- and dihydropyridines-resistant calcium channels in the rat brain.

We attempted to characterize the functional roles of subtypes of voltage-sensitive calcium channels in the brain. The maximal number of [125I]omega-conotoxin GVIA (omega-CTX) binding sites in rat brain associated with N-type calcium channels (N-channels) was approximately 10 times more than that of [3H]-PN200-110 associated with L-type calcium channels (L-channels). [125I]omega-CTX binding was inhibited by aminoglycoside antibiotics, neomycin and dynorphin A(1-13), but not by various classes of L-channel antagonists. A 6-hydroxydopamine-induced lesion of the striatum resulted in a marked reduction of both [125I]-omega-CTX and [3H]PN200-110 binding. Kainic acid-induced lesion of the striatum reduced [3H]PN200-110 binding by 57%, but did not reduce [125I]omega-CTX binding. Omega-CTX produced a small (18%) but significant reduction of potassium-stimulated Ca2+ influx into rat brain synaptosomes, although it produced a concentration-dependent inhibition in chick brain synaptosomes. Neomycin inhibited Ca2+ influx in both preparations in a concentration-dependent manner. Both omega-CTX and neomycin inhibited potassium-stimulated [3H]dopamine (DA) release from rat striatal slices. The L-channel antagonists had no effect on either Ca2+ influx or [3H]DA release. These results suggest that DA release in the striatum is regulated by Ca2+ influx through N-channels located in presynaptic nerve terminals, and that the most of the Ca2+ influx in rat brain appears to be governed by neomycin-sensitive, omega-CTX- and DHP-resistant calcium channels.

Animals↗

PubMedDate not supplied

Radioactive labeling of phospholipids and proteins by cochlear perfusion in the guinea pig and the effect of neomycin.

Phospholipids and proteins of guinea pig stria vascularis, spiral ligament and organ of Corti were radioactively labeled by perilymphatic perfusion with artificial perilymph containing [32P] orthophosphate or radioactive amino acids. Phospholipids were separated by thin-layer chromatography, proteins by disc gel electrophoresis and quantitated by liquid scintillation counting. The addition of 10-4M to 10-2M neomycin to the perfusion fluid resulted in a dose-dependent increase of tissue permeability to the radioactive precursors, and a specific decrease in the 32P-incorporation into phosphatidylinositol diphosphate in stria vascularis and organ of Corti. No effect of neomycin on protein labeling was observed using a double label approach with [3H]methionine and [35S]-methionine. In vitro, low concentrations of neomycin led to the formation of a complex and polyphosphoinositides. Much higher concentrations of the drug were needed for a comparable reaction with the acid mucopolysaccharide, chondroitin sulfate A. The implications of these findings for the mechanism of neomycin ototoxicity are discussed.

Animals↗

PubMedDate not supplied

Combined effects of noise and neomycin. Cochlear changes in the guinea pig.

Cochlear damage resulting from the combination of neomycin with acoustic overstimulation was investigated in guinea pigs. Four groups of animals received subcutaneous injections and exposure to broad band noise daily for 7 days, as follows: I. Neomycin (200 mg/kg) followed by 10 hours of noise at 115 dB SPL; II. Saline followed by 115 dB noise: III. Neomycin followed by low intensity noise (45 dB as an acoustic control); or IV. Saline followed by 45 dB noise. After a 30 day stabilization period, each ear was examined electrophysiologically and histologically. Measures of cochlear integrity included AC cochlear potentials from 100 Hz through 20 kHz as well as outer hair cell (OHC) counts. A marked interaction leading to augmentation of damage was found when neomycin was combined with 115 dB noise (Group I). Losses in cochlear sensitivity, averaged across all frequencies, amounted to 62 dB in Group I, whereas the averaged losses for Groups II and III were only 16 dB and 17 dB respectively. Loss of OHC's was close to 100% in Group I, while OHC losses were only 17% in Group II and 26% in Group III.

Acoustic Stimulation↗

PubMedDate not supplied

A biochemical mechanism of the ototoxic interaction between neomycin and ethacrynic acid.

The effects of neomycin on tissue levels of ethacrynic acid was studied in vivo and in vitro. In vitro, the addition of neomycin to incubations of synaptosomes and inner ear tissues of guinea pigs raised the concentration of bound ethacrynate approximately two-fold. In vivo, radioactive ethacrynate was determined in the inner ear of mice by radioautography after intravenous injection of the drug (50 mg/kg body weight). Treatment of animals with neomycin (100 mg/kg body weight, intramuscularly) 60 min prior to ethacrynate led to a three-to five-fold higher accumulation of ethacrynate in cochlear structures. It is suggested that neomycin breaks down hemolabyrinthine or tissue permeability barriers and allows increased penetration of the other drug into the inner ear.

Animals↗

PubMed1996

The alteration of ultrastructure and immunoreactivity of human embryonic organ of Corti tissue culture after exposure to aminoglycoside (neomycin) ototoxicity.

Using electron microscopy and GABA immunohistochemistry we evaluated the effects on human embyronic organ of Corti tissue culture of exposure to the ototoxic aminoglycoside antibiotic neomycin at a dose of 1 mM for 48 to 96 hrs. Neomycin induces the formation of multilamellar myeloid structures. These lesions, found only in the basal coil but both in inner and outer hair cells, were characteristic of the membrane-associated neomycin-induced damage. A large amount of lipofucsin and numerous lipoid vacuoles as well as vesicle-filled mound-like protrusions were also observed after exposure to neomycin. It seems there is no obvious effect on GABAergic innervation.

Aminoglycosides↗

PubMed2004

In vitro effect of a buffered chelating agent and neomycin or oxytetracycline on bacteria associated with diseases of fish.

The antimicrobial agents used to treat bacterial fish diseases are archaic, and their uses may result in the emergence of drug-resistant bacterial strains. This study evaluated the in vitro antimicrobial activity of combinations of Tricide and neomycin or oxytetracycline on common disease-causing bacteria of fish and its possible use as an alternative treatment of these diseases. Tricide solutions containing of 8 mM United States Pharmacopeia (USP) disodium ethylenediaminetetraacetate dehydrate (chelator) and 20 mM USP 2-amino-2-hydroxymethyl-1,3-propanediol (buffer) potentate the antimicrobial action of neomycin and oxytetracycline when reacted in vitro with Aeromonas hydrophila, Streptococcus iniae, Pseudomonas aeruginosa, and Staphylococcus aureus. Serial passage of the test organisms in Tricide or Tricide and neomycin or oxytetracycline did not result in the development of resistant forms. Combinations of Tricide and neomycin or oxytetracycline reduced the amount of antibiotics necessary for fish therapy, render drug-resistant bacteria sensitive to antimicrobial therapy, may be used to decontaminate recently shipped fish, and should reduce the formation of antibiotic-resistant forms.

Animals↗

PubMed1977

Ribostamycin, as an intermediate in the biosynthesis of neomycin.

A mutant of a neomycin-producting Streptomyces fradiae was found which synthesizes ribostamycin instead of neomycin. After a reverse mutation new colonies were obtained producting neomycin again. Ribostamycin might thus be considered as an intermediate in the biosynthesis of neomycin.

Anti-Bacterial Agents↗

PubMed1999

Tissue-specific levels and cellular distribution of epidermal growth factor receptors within control and neomycin-damaged neonatal rat Organ of Corti.

Epidermal growth factor receptor (EGFR) levels were assayed by an enzyme-linked immunosorbent assay (ELISA) in microdissected organ of Corti (OC) from neonatal rats directly after isolation and after 3 days in culture with and without neomycin treatment. In addition, the cellular distribution of the EGFR in the OC was determined by immunohistochemistry. The in vitro level of EGFR determined by ELISA assays doubled after neomycin damage to OC, suggesting that EGFR is subject to up-regulation following this treatment. Immunohistochemistry of both in vivo and in vitro controls indicates that EGFR is predominantly localized in the stereociliary bundles of the hair cells; supporting cells and the apical junctions between the remaining Kolliker organ cells were also immunolabeled. In neomycin-treated cultures, sensory cells were degenerated, so no labeling could be seen. However, supporting and Kolliker organ cells continued to show labeling. In addition, nerve fibers in the region of the future osseous spiral lamina and projecting out toward the damaged sensory epithelium were immunostained. The up-regulation of the EGFR and its redistribution within the OC following neomycin damage support the earlier observation that growth factors that act through EGFR, such as EGF and transforming growth factor-alpha can induce neonatal mammalian auditory hair cell replacement under culture conditions, after aminoglycoside treatment.

Animals↗

PubMed2001

Modulation of irinotecan-induced diarrhea by cotreatment with neomycin in cancer patients.

This study was designed to evaluate irinotecan (CPT-11) disposition and pharmacodynamics in the presence and absence of the broad-spectrum antibiotic neomycin. Seven evaluable cancer patients experiencing diarrhea graded > or =2 after receiving CPT-11 alone (350 mg/m(2) i.v. once every 3 weeks) received the same dose combined with oral neomycin at 1000 mg three times per day (days -2 to 5) in the second course. Neomycin had no effect on the systemic exposure of CPT-11 and its major metabolites (P > or = 0.22). However, it changed fecal beta-glucuronidase activity from 7.03 +/- 1.76 microg/h/mg (phenolphthalein assay) to undetectable levels and decreased fecal concentrations of the pharmacologically active metabolite SN-38. Although neomycin had no significant effect on hematological toxicity (P > 0.05), diarrhea ameliorated in six of seven patients (P = 0.033). Our findings indicate that bacterial beta-glucuronidase plays a crucial role in CPT-11-induced diarrhea without affecting enterocycling and systemic SN-38 levels.

Adolescent↗