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PubMed2005

Study of the DNA/ethidium bromide interactions on mica surface by atomic force microscope: influence of the surface friction.

The influence of mica surface on DNA/ethidium bromide interactions is investigated by atomic force microscopy (AFM). We describe the diffusion mechanism of a DNA molecule on a mica surface by using a simple analytical model. It appears that the DNA diffusion on a mica surface is limited by the surface friction due to the counterion correlations between the divalent counterions condensed on both mica and DNA surfaces. We also study the structural changes of linear DNA adsorbed on mica upon ethidium bromide binding by AFM. It turns out that linear DNA molecules adsorbed on a mica surface are unable to relieve the topological constraint upon ethidium bromide binding. In particular, strongly adsorbed molecules tend to be highly entangled, while loosely bound DNA molecules appear more extended with very few crossovers. Adsorbed DNA molecules cannot move freely on the surface because of the surface friction. Therefore, the topological constraint increases due to the ethidium bromide binding. Moreover, we show that ethidium bromide has a lower affinity for strongly bound molecules due to the topological constraint induced by the surface friction.

Adsorption↗
PubMed1988

Comparative cardiac effects of intravenous bolus of ipratropium bromide (itrop) and atropine sulfate in 22 patients.

At the present time, there is no satisfactory pharmacological treatment for arrhythmia or conduction disorders induced by or aggravated by vagal hypertonia. The limited duration of action of the atropine derivatives currently available justifies the development of new compounds with expected longer acting duration. The aim of this study was to compare the effects of a single blind intravenous injection of ipratropium bromide to those of atropine sulfate in 22 patients. These patients were studied with continuous Holter recordings for three days. During the second and the third nights (patient sleeping), boluses of atropine (0.03 mg/kg) and of ipratropium bromide (0.03 mg/kg), respectively, were added to a continuous saline intravenous infusion. Accurate ECG analysis allowed determination of maximal heart rate peak, timing of maximal heart rate, variations in sinus cycle length, atrioventricular conduction, and durations of drug action. A nonsuggestive questionnaire was presented to patients to detect possible occurrence of side effects. The mean maximal heart rate rose significantly (p less than 0.001) for atropine (+46.2%) and for ipratropium bromide (+57.4%). The effects obtained with ipratropium bromide on the heart rate lasted nearly twice as long as those obtained with atropine (respectively, 120 +/- 38.4 min and 70 +/- 30 min- for the pharmacological half-life). Common minor muscarinic side effects (dryness of the mouth) were noted with the two drugs. In conclusion, this comparative intraindividual study confirmed the prolonged vagolytic effects of intravenous ipratropium bromide, which may be valuable in the treatment of patients with vagally mediated automaticity and conduction disturbances.

Adult↗
PubMed1978

Effect of nighttime anisotropine methyl bromide of duodenal ulcer healing and pain: a double-blind controlled trial.

Anisotropine methyl bromide, an anticholinergic, 80 mg given orally at 8 P.M., suppresses gastric acid secretion through the night without significant side effects. Thirty patients with endoscopy-proved symptomatic duodenal ulcer disease completed a randomized, double-blind, placebo-controlled trial of nighttime anisotropine methyl bromide therapy. Eleven (69 per cent) of 16 anisotropine methyl bromide-treated and six (43 per cent) of 14 placebo-treated subjects healed their ulcers within two weeks of starting treatment. The anisotropine methyl bromide-treated subjects averaged 0.63 +/- 0.27 (mean +/- S.E.) episodes of nocturnal pain during the treatment period versus 2.71 +/- 1.08 episodes in the placebo group (P = 0.06). This is the first reported study of this type designed to evaluate the efficacy of an anticholinergic agent in the healing of duodenal ulcers. Although not conclusive, the results suggest nighttime anisotropine methyl bromide therapy may be useful in the treatment of duodenal ulcer disease. Further studies seem warranted.

Adult↗
PubMed1981

Control and virus-transformed baby hamster kidney cells resistant to ethidium bromide. II. Membrane properties.

Aspects of membrane structure and functions were studied in ethidium bromide resistant cells. Submitochondrial particles were solubilized and electrophoresed. The gel patterns, representing mitochondrial membrane proteins, demonstrated qualitative and quantitative alterations in mitochondrial preparations derived from virus-transformed cells and ethidium bromide resistant cells as compared to the control cells. The plasma membrane glycoproteins were labelled by the sodium borohydride method. The glycoproteins were pleased with Triton X-100 and electrophoresed. Fluorograms of the gels demonstrated some marked differences between the ethidium bromide resistant cells and their parental strain. The observed alterations in the membrane glycoproteins did not result in altered glucose transport properties or in the elution patterns of plasma membrane glycopeptides as analyzed by Sephadex G-50 chromatography. Dye uptake and binding studies with intact parental and drug resistant cells and their isolated mitochondria demonstrated no alteration of the membrane permeability or the number of binding sites for ethidium bromide. Similar results were also obtained with a cyanine dye. This latter finding was significant in that it permitted one to exclude dye exclusion as a mechanism for ethidium bromide resistance.

Animals↗
PubMed1978

Reversible tenfod reduction in mitochondria DNA content of human cells treated with ethidium bromide.

Cells of the human line VA2-B in suspension culture have been treated with very low concentrations of ethidium bromide for the purpose of reducing the amount of mitochondrial DNA (mit-DNA) per cell. Cells maintained in the presence of 5 ng/ml ethidium bromide grew at a normal rate for three days; thereafter, their doubling time gradually increased to a stable value of about 60 h. In these cells, the rate of 3H thymidine incorporation into mit-DNA decreased very rapidly to approximately 60% of the normal, and remained thereafter at this level, while the amount of mit-DNA per cell stabilized around a level of 70--80% of the control. In cells long-term treated with 5 ng/ml ethidium bromide, the rate of mitochondrial protein synthesis was about 35% of the normal, and the cytochrome c oxidase activity about 50% of the control. Cells treated with 20 ng/ml of the drug underwent 3--4 cell doublings at control rates, then gradually stopped growing, and eventually died. In these cells, the rate of incorporation of 3H thymidine into mit-DNA was reduced to 50% of the control value after 10 min treatment with ethidium bromide, and became barely detectable after three cell doublings. At this time, the cells had on the average less than 10% of the control amount of mit-DNA, the rate of mitochondrial protein synthesis was reduced to 3% of the normal, and the specific activities of cytochrome c oxidase and rutamycin-sensitive ATPase were less than 20% of the control values. In spite of these marked changes, the cells exhibited only a 20--30% loss in cell viability, as estimated by cloning efficiency, after three days of exposure to the drug. Cells treated with ethidium bromide at 20 ng/ml for three days, and then transferred to drug-free medium, recovered a near-to-normal growth rate and cloning efficiency and a near-to-normal rate of synthesis and amount of mit-DNA in about five days.

Cell Line↗
PubMed1977

Mitochondrial DNA replication in petite mutants of yeast: resistance to inhibition by ethidium bromide, berenil and euflavine.

Mitochondrial DNA (mtDNA) replication in petite mutants of Saccharomyces cerevisiae is generally less sensitive to inhibition by ethidium bromide than in grande (respiratory competent) cells. In every petite that we have examined, which retain a range of different grande mtDNA sequences, this general phenomenon has been demonstrated by measurements of the loss of mtDNA from cultures grown in the presence of the drug. The resistance is also demonstrable by direct analysis of drug inhibition of mtDNA replication in isolated mitochondria. Furthermore, the resistance to ethidium bromide is accompanied, in every case tested, by cross-resistance to berenil and euflavine, although variations in the levels of resistance are observed. In one petite the level of in vivo resistance to the three drugs was very similar (4-fold over the grande parent) whilst another petite was mildly resistant to ethidium bromide and berenil (each 1.6-fold over the parent) and strongly resistant (nearly 8-fold) to inhibition of mtDNA replication by euflavine. The level of resistance to ethidium bromide in several other petite clones tested was found to vary markedly. Using genetic techniques it is possible to identify those petites which display an enhanced resistance to ethidium bromide inhibition of mtDNA replication. It is considered that the general resistance of petites arises because a product of mitochondrial protein synthesis is normally involved in facilitating the inhibitory action of these drugs on mtDNA synthesis in grande cells. The various levels of resistance in petites may be modulated by the particular mtDNA sequences retained in each petite.

Acridines↗
PubMed2000

The cross-link breaker, N-phenacylthiazolium bromide prevents vascular advanced glycation end-product accumulation.

AIMS/HYPOTHESIS: Advanced glycation is postulated to have a pivotal role in mediating diabetic vascular complications. The emergence of thiazolium compounds such as N-phenacylthiazolium bromide which cleave preformed advanced glycation end products (AGEs) has allowed us to explore the effects of these agents on the vascular AGE accumulation and hypertrophy associated with diabetes. METHODS: Control and streptozotocin diabetic rats were selected at random for no treatment or treatment with N-phenacylthiazolium bromide (10 mg/kg intraperitoneally) and followed for 3 weeks. In a separate study, intervention with N-phenacylthiazolium bromide was delayed until after 3 weeks of diabetes and then given for 3 weeks (total of 6 weeks). RESULTS: Diabetes was associated with increased mesenteric vascular advanced glycation end products, as assessed by radioimmunoassay and immunohistochemistry. This increase in vascular AGE accumulation was prevented by N-phenacylthiazolium bromide treatment. Diabetes-associated mesenteric vascular hypertrophy was attenuated by treatment with N-phenacylthiazolium bromide only if given from the time of induction of diabetes. CONCLUSION/INTERPRETATION: Cross-link breakers seem to be effective in preventing or reversing accumulation of advanced glycation end-products in blood vessels and have the potential to play a part in the treatment of diabetic vascular complications.

Animals↗
PubMed1978

Effect of ethidium bromide on the digestion of chromatin DNA with micrococcal nuclease.

Intercalation of ethidium bromide into DNA influences the rate of its digestion with micrococcal nuclease in opposite directions depending on whether it is free DNA or DNA in chromatin. In the case of free DNA the binding of ethidium bromide, starting from a very low concentration, results in the inhibition of the rate of digestion (increasing constantly with the increase of the ethidium bromide/nucleotide ratio). In contrast to free DNA the digestion rate as well as the overall amount of nuclease susceptible DNA is increased upon ethidium bromide binding to chromatin, with maximum enhancement around the saturation of intercalation sites. The saturation of intercalation sites in chromatin leads also to the disappearance of the typical micrococcal nuclease digestion pattern of DNA upon gel electrophoresis. Instead, a random cleavage pattern is observed. These data indicate that partial unwinding of chromatin DNA by ethidium bromide results in unmasking new sites for nuclease action. Interpretation of this finding in terms of the nucleosomal structure of chromatin and the mode of ethidium bromide binding to chromatin DNA indicates that newly unmasked sites are localized within the core particle DNA.

Animals↗
PubMed1979

Charge separation of proteins complexed with sodium dodecyl sulfate by acid gel electrophoresis in the presence of cetyltrimethylammonium bromide.

Globular proteins, casein, and membrane proteins which were reacted with sodium dodecyl sulfate were studied by acid urea gel electrophoresis. The sodium dodecyl sulfate bound tightly to the proteins, producing a more acidic charge which prevented migration into the gel. When cetyltrimethylammonium bromide was added to the sodium dodecyl sulfate-protein complexes, the sodium dodecyl sulfate apparently reacted with cetyltrimethylammonium bromide and dissociated so that the proteins migrated in acid gel in a normal manner as compared to the proteins without any added detergent. The sodium dodecyl sulfate-cetyltrimethylammonium bromide complex could be removed from the proteins by centrifugation. Thus, cetyltrimethylammonium bromide used in conjunction with acid gel electrophoresis allows direct comparison by charge of proteins fractionated in the presence of sodium dodecyl sulfate with the starting mixture of proteins not exposed to detergent. The reaction of cetyltrimethylammonium bromide with sodium dodecyl sulfate in acidic urea also provides a simple convenient method of removal of sodium dodecyl sulfate from proteins.

Cetrimonium Compounds↗
PubMed1984

Pulmonary responses of salbutamol tolerant guinea-pigs to aminophylline and ipratropium bromide.

Groups of guinea-pigs were pretreated with salbutamol (15 micrograms/kg s.c. 3 times/day for 7 days) and compared with controls (saline treated) by measurement of the effects of i.v. dosage with salbutamol (1-10 micrograms/kg), aminophylline (5-20 mg/kg) or ipratropium bromide (1-10 micrograms/kg) on total lung resistance in the anaesthetised state. The bronchodilator effects of these three drugs were measured as attenuation of the bronchoconstrictor response to a standard dose of histamine (3 micrograms/kg i.v.). The salbutamol-pretreated guinea-pigs gave significantly reduced responses to salbutamol (at 2, 5 and 10 micrograms/kg) and to aminophylline (at 10 and 20 mg/kg) whilst the responses to ipratropium bromide were similar to controls. A further group of control guinea-pigs was used to examine the effects of beta-adrenoceptor blockade (propranolol 4 mg/kg) on the responses to the bronchodilators. Propranolol blocked completely the responses to salbutamol (10 micrograms/kg) and to aminophylline (5, 10 and 20 micrograms/kg) without affecting the response to ipratropium bromide. The findings indicate that the pretreatment regime employed causes the development of tolerance to the bronchodilator effects of salbutamol and that this tolerance extends to aminophylline, but not to ipratropium bromide. The effects of propranolol and of tolerance to salbutamol suggest that the bronchodilator response to aminophylline is mediated in large part by activation of airway beta-adrenoceptors. The findings also suggest that ipratropium bromide may provide effective bronchodilation (in the presence of parasympathetic tone) in lungs which have become tolerant to beta-adrenoceptor agonists, though whether this may be extrapolated from the guinea pig to man remains to be demonstrated.

Albuterol↗
PubMed1988

Toxicology and pathology of methyl bromide in F344 rats and B6C3F1 mice following repeated inhalation exposure.

The toxicity of methyl bromide was studied in male and female F344 rats and B6C3F1 mice exposed by inhalation to 160 ppm methyl bromide or air 6 hr/day, 5 days/week for up to 6 weeks. The animals were killed after 3, 10, or 30 exposure days, or when 50% mortality was observed in any group. Only female rats survived the entire 30 exposure days at 160 ppm methyl bromide with less than 50% mortality. There were clear species- and sex-related differences in susceptibility of specific organs to methyl bromide. Primary target organs were the brain, kidney, nasal cavity, heart, adrenal gland, liver, and testis. In rats, neuronal necrosis occurred in the cerebral cortex, hippocampus, and thalamus of the brain whereas in mice neuronal necrosis occurred primarily in the internal granular layer of the cerebellum. Nephrosis occurred in all exposed mice, but not rats, and was likely a major cause of moribundity and death. Necrosis of the olfactory epithelium was more severe and extensive in rats than mice. Myocardial degeneration occurred in male and female rats and to a lesser degree in male mice. There was atrophy of the inner zone of the adrenal cortex in female mice and cytoplasmic vacuolation of the adrenal cortex in rats. Testicular degeneration occurred in rats and mice. The target organ specificity of methyl bromide is similar to that of methyl chloride, suggesting that the two monohalomethanes may have a common mechanism of action.

Administration, Inhalation↗
PubMed1984

Disposition of [14C]methyl bromide in Fischer-344 rats after oral or intraperitoneal administration.

Methyl bromide is used as a disinfectant to fumigate soil. The intent of our study was to determine the disposition of methyl bromide following a single acute administration. Male Fischer-344 rats were given 250 mumol of [14C] methyl bromide/kg body wt by either oral or i.p. administration. Urine, feces and expired air were collected and at the end of 72 h the rats were sacrificed and tissues analyzed to determine 14C excretion and tissue distribution. After i.p. administration of methyl bromide, the dominant route of excretion was exhalation of 14CO2, with 46% of the dose exhaled as 14CO2. In contrast, urinary excretion of 14C was the major route of elimination (43% of the dose) when methyl bromide was given orally. Very little of the 14C appeared in the feces (less than 3% of the dose) regardless of route of administration. In rats with bile duct cannulations, 46% of an oral dose appeared in the bile over a 24-h period. Collection of bile significantly decreased the exhalation of 14CO2 and 14C excreted in urine compared to controls. At 72 h after oral or i.p. administration, 14-17% of the 14C remained in the rats, with liver and kidney being the major organs of retention. Results indicate that route of administration can affect the pathways for excretion. In addition, excretion of 14C in bile, coupled with the low levels of radioactivity found in the feces, indicates that reabsorption of biliary metabolites from the gut plays a significant role in the disposition of [14C] methyl bromide.

Administration, Oral↗
PubMed1990

Action of pinaverium bromide, a calcium-antagonist, on gastrointestinal motility disorders.

1. The evidence reviewed here indicates that pinaverium bromide (Dicetel) relaxes gastrointestinal (GI) structures primarily by inhibiting Ca2+ influx through potential-dependent channels of surface membranes of smooth muscle cells. 2. The in vivo selectivity of pinaverium bromide for the GI tract appears to be due mainly to its pharmacokinetic properties. Because of its low absorption (typical for quaternary ammonium compounds) and marked hepatobiliary excretion, most of the orally-administered dose of pinaverium bromide remains in the GI tract. 3. Orally-administered pinaverium bromide does not elicit adverse cardiovascular side-effects at doses that effectively relieve GI spasm, pain, transit disturbances and other symptoms related to motility disorders. 4. Pinaverium bromide is the only Ca2(+)-antagonist with known therapeutic efficacy in the treatment of irritable bowel syndrome and certain other functional intestinal disorders.

Animals↗
PubMed1990

Oxitropium bromide: an acute dose response study of a new anticholinergic drug in combination with fenoterol in asthma and chronic bronchitis.

The aim of this study was to compare the bronchodilator response of patients with either stable asthma or stable chronic bronchitis to the acute administration of oxitropium bromide and a beta agonist (fenoterol) when given both separately and together in order to determine the responses of these two groups of patients and the optimal doses of these agents when given in combination. The responses of 23 patients with asthma and 25 patients with chronic bronchitis to 400 micrograms of fenoterol, and 200 micrograms of oxitropium given either alone or together with 100, 200 or 400 micrograms of fenoterol was studied. The peak bronchodilator response to oxitropium bromide of the patients with chronic bronchitis was equivalent to the fenoterol response while, in the patients with asthma, the response to oxitropium bromide was approximately 30% of the response to fenoterol. In both groups of subjects the addition of oxitropium bromide to fenoterol significantly increased both the magnitude and the duration of the bronchodilator response without a significant increase in side effects. In both groups of subjects 200 micrograms of oxitropium bromide and 200 micrograms or more of fenoterol gave the optimal response.

Adult↗
PubMed2005

Low cetyltrimethylammonium bromide concentrations induce reversible amorphous aggregation of tobacco mosaic virus and its coat protein at room temperature.

Ordered and amorphous protein aggregation causes numerous diseases. Tobacco mosaic virus coat protein for many decades serves as the classical model of ordered protein aggregation ("polymerization"). It was also found to be highly prone to heat-induced amorphous aggregation and the rate of this aggregation could be easily manipulated by changes in solution ionic strength and temperature. Here, we report that rapid amorphous aggregation of this protein can be induced at 25 degrees C in phosphate buffer by low micromolar (start at about 15 microM) concentrations of cationic surfactant cetyltrimethylammonium bromide. At equilibrium four surfactant molecules bound to the protein subunit. As judged by circular dichroism and fluorescence spectroscopy data, the coat protein molecules retained their native structure upon the cetyltrimethylammonium bromide induced aggregation. No aggregation was observed at the higher surfactant concentrations (above 300 microM). Micromolar concentrations of anionic surfactant sodium dodecylsulfate rapidly reversed the cetyltrimethylammonium bromide induced aggregation of the coat protein due to formation of mixed surfactant-surfactant micelles. Cetyltrimethylammonium bromide (100-300 microM) also induced the reversible intact tobacco mosaic virus virion aggregation. The possible liability to the cetyltrimethylammonium bromide induced amorphous aggregation of other ordered aggregate-producing proteins has been discussed.

Capsid Proteins↗
PubMed2006

A randomized, clinical trial comparing the efficacy of continuous nebulized albuterol (15 mg) versus continuous nebulized albuterol (15 mg) plus ipratropium bromide (2 mg) for the treatment of acute asthma.

Multiple studies have examined adding nebulized ipratropium bromide to intermittent albuterol for the treatment of acute asthma. Although continuous nebulized treatments in themselves offer benefits; few data exist regarding the efficacy of adding ipratropium bromide to a continuous nebulized system. To compare continuous nebulized albuterol alone (A) vs. albuterol and ipratropium bromide (AI) in adult Emergency Department (ED) patients with acute asthma, a prospective, randomized, double-blind, controlled clinical trial was conducted on a convenience sample of patients (IRB approved). The setting was an urban ED. Consenting patients > 18 years of age with peak expiratory flow rates (PEFR) < 70% predicted, between October 15 and December 28, 1999, were randomized to albuterol (7.5 mg/h) + ipratropium bromide (1.0 mg/h), or albuterol alone via continuous nebulization using the Hope Nebulizer (B&B Technologies Inc., Orangevale, CA) for 2 h. Main outcome measures were changed in mean improvement at 60 and 120 min PEFR compared to baseline (time 0). Secondary measures were admission rates. Data were analyzed using appropriate parametric and non-parametric tests (p < 0.05 statistically significant). Sixty-two patients (30 women) completed enrollment: 32 in (AI) and (30) in (A). Four (A) and 2 (AI) patients are without 120 min data: 3 (A) and 1 (AI) were discharged after 60 min, whereas one each (A) and (AI) worsened and were admitted before 120 min. There were no statistically significant differences between treatment groups in age, sex, predicted or initial PEFR. Thirteen (19.4%) patients were admitted. There was no statistically significant difference in improvement of mean PEFR at 60 min or 120 min compared to baseline, between groups, using repeated measures analysis of variance. Mean improvement in PEFR at 60 min compared to baseline (time 0): (A) = 93.2 L/min (95% confidence interval [CI] 64.5-121.8), (AI) = 86.6 L/min (95% CI 58.9-114.3); mean improvement in PEFR at 120 min compared to baseline (time 0) (A) = 116.5 L/min (95% CI 84.5-148.5), (AI) = 126.4 L/min (95% CI 95.4-157.4). There was no statistically significant difference in admission rates between groups: 5/30 (A) and 8/32 (AI) (p = 0.62). There were no significant differences in mean improvement of PEFR at either 60 or 120 min between ED patients with acute asthma receiving continuous albuterol alone vs. those receiving albuterol in combination with ipratropium bromide.

Adult↗
PubMed2006

[Peripheral neuropathy induced by acute methyl bromide skin exposure: a case report].

INTRODUCTION: Methyl bromide is a pesticide used as a fumigating agent in homes, for food storage and soil disinfection. Chronic and acute exposures to methyl bromide are known to cause damage to the central and peripheral nervous system. OBSERVATION: We describe a case of a 31-year-old patient who developed a peripheral neuropathy due to an acute exposure on skin of methyl bromide. This patient was admitted after an accidental dermal exposure to methyl bromide while fumigating dates. The patient suffered dermal burns and vesicles on the upper limbs. Two weeks following exposure, she developed weakness of the lower and upper limbs, ataxia, paresthesiae of both legs and arms, abolition of tendon reflexes in the upper and lower limbs and Babinski sign. An axonal neuropathy was detected at the electrophysiological study. The patient recovered gradually. CONCLUSION: While cases of methyl bromide are rare, this study illustrates the toxic effect on the peripheral nervous system.

Adult↗
PubMed1995

Long-term treatment of perennial allergic rhinitis with ipratropium bromide nasal spray 0.06%.

The purpose of this study was to assess the safety and efficacy of ipratropium bromide nasal spray 0.06% (aqueous solution), 84 micrograms per nostril three times a day, in reducing nasal hypersecretion in the long-term treatment of patients with perennial allergic rhinitis (PAR). This was an open-label 1-year trial. In the first 6 months all patients were treated with two puffs ipratropium bromide nasal spray 0.06%, 84 micrograms per nostril three times per day, unless they were unable to tolerate the dose. In the last 6 months the dose could be reduced to the lowest amount required to control rhinorrhea. Ninety-six patients entered the trial, and 47 completed it. Sixty-three patients completed more than 6 months of treatment. Patient and physician global evaluation suggested that ipratropium bromide nasal spray 0.06% is effective in controlling rhinorrhea associated with PAR and can contribute to control of congestion, postnasal drip, and sneezing. There was also a trend toward reduction of mucosal edema and improvement in quality of life. The most common drug-related adverse events were nasal dryness, epistaxis/nose bleed, and increased rhinitis. Most adverse events were mild and resulted in drug discontinuation in less than 10% of patients. Ipratropium bromide nasal spray was well tolerated and not associated with serious drug-related adverse events or clinically significant anticholinergic side effects. Use of ipratropium bromide nasal spray alone or with other standard medications should be considered in treating patients with PAR.

Adolescent↗