PubMed HealthSearch

SEARCH · PubMed Health

Results for “Bromides”

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 19 recordsLinked to original sources

Ethidium bromide complexes with self-complementary deoxytetranucleotides. Demonstration and discussion of sequence preferences in the intercalative binding of ethidium bromide.

The binding of ethidium bromide to the self-complementary deoxytetranucleotides containing guanine and cytosine bases has been studied by circular dichroism, visible absorption, and fluorescence spectroscopies. The circular dichroism spectrum of each of the four deoxytetranucleotides was measured and compared to the spectrum calculated by a nearest-neighbor approximation method which utilized the circular dichroism spectra of the deoxydinucleotides as a basis set. Reasonable agreement was obtained between the calculated and experimental spectra for three of the four deoxytetranucleotides; however, pdC-dC-dG-dG exhibited poor agreement between the actual and nearest-neighbor calculated spectra, which suggests that pdC-dC-dG-dG may exist in an unusual conformation. A nearest-neighbor method was also used to calculate the extinction coefficients for each of the deoxytetranucleotides: these values differ substantially from values recently published by Patel and Canuel [(1977), Proc. Natl. Acad. Sci. U.S.A. 74, 2624--2628] in which the method used for the determination of the extinction coefficients was not stated. The magnitude of the extinction coefficients is important in determining the stoichiometry of complex formation as well as the relative sequence preferences for ethidium binding. The visible absorption titrations, the fluorescence titrations, and the circular dichroism titrations with ethidium bromide clearly show that two ethidiums will intercalate into a (pdC-dG-dC-dG).(pdC-dG-dC-dG) double helix presumably at the two (dC-dG).(DC-dG) sequences. Results from the pdG-dC-dG-dC titrations with ethidium bromide are not as definitive. Raising the temperature from approximately 2 to 26 degrees C diminishes the strength of complex formation for the EthBr plus pdC-dG-dC-dG system and makes it more difficult to unequivocally determine the stoichiometry of the complex formation. These data thus confirm and extend our earlier observation that ethidium bromide preferentially binds to pyrimidine-purine sequences as opposed to purine-pyrimidine sequences. Experiments monitoring the binding of ethidium bromide to pdC-dC-dG-dG and pdG-dG-dC-dC indicate that ethidium will bind strongly to the (dG-dG).(dC-dC) sequence. We conclude that the relative ordering of the sequence preferences for the binding of ethidium to the three sequences available in the tetranucleotides studied is (dC-dG).(dC-dG) congruent to (dG-dG).(dC-dC) greater than (dG-dC).(dG-dC).

Base Sequence

Some aspects in the pharmacology of diclonium bromide (2-(3,4-dicholoroanilino)quinolizinium bromide). Part II: Gastric acid-antisecretory and antiulcerogenic actions.

Diconium bromide, 2-(3,4-dichloroanilino)-quinolizinium bromide, a potent antispasmodic in the lower bowel of the dog, was found in the present study to exert gastric acid-antisecretory and antiulcerogenic activities in the rat stomach. These effects were demonstrated by means of short- and long-term pyloric ligation, acetylsalicylic acid (ASA)-induced ulcerogenesis, and cold-and-restraint stress studies. A reduction of gastric acid concentration by the drug was probably responsible for the decrease in the degree of ulceration and hemorrhagic lesion formation. The drug's inhibition of stress hemorrhagic lesions may be related to an effect both on gastric HCl secretion and on the vasculature in the glabdular mucosa. The delay of gastric emptying by diclonium bromide results from its known antispasmodic or smooth-muscle depressant action. The toxicity of diclonium bromide, perorally, was low in rats and overt signs of drug effect were not evident until toxic doses were administered. It is concluded that diclonium bromide may represent a useful non-anticholinergic drug effective in treating both peptic ulcers and spasticity of the colon (irritable-colon syndrome) in man.

Animals

Relative potency of the atropine-like effects of a new parasympatholytic drug, scopolamine-N-(cyclopropyl methyl) bromide and those of hyoscine-N-butyl bromide.

A double-blind crossover trial with a 4-point bioassay was carried out in 8 convalescent in-patients to study the relative potency of scopolamine-N-(cyclopropyl methyl) bromide (DA 3177), a new parasympatholytic drug, administered at doses of 2.5 mg and 5 mg i.v., and hyoscine-N-butyl bromide, administered at doses of 10 mg and 20 mg i.v., in producing atropine-like effects. The results showed that the effects on heart rate and near point of accommodation were slightly less with DA 3177, while its effects on salivary secretion were a little greater than those of hyoscine-N-butyl bromide. It is suggested that study of the pharmacodynamic effects of parasympatholytic drugs is a relatively simple way of predicting which doses should be effective spasmolytically.

Accommodation, Ocular

Some aspects in the pharmacology of diclonium bromide (2-(3,2-dichloroanilino)quinolizinium bromide). Part I: Antispasmodic action.

Diclonium bromide (EU-2972; 2-(3,4-dichloroanilino)quinolizinium bromide) was demonstrated to possess an effective, prolonged inhibitory action on contractions in response to stimuli or propulsive movements in the lower bowel of the dog. The compound's antagonism to contractile activity was greater in the distal colon than in the duodenum or upper bowel. Diclonium bromide was a nonselective antispasmodic but, unlike papaverine, caused profound antagonism against smooth muscle contractile responses to intrinsic motor neural excitation. The drug had weak specific anticholinergic action, but its lack of antagonistic effect on other cholinergic responses in this study indicates that the anticholinergic action contributes very little, if at all, to its overall antispasmodic effect. The compound has potential application in the treatment of spastic-colon disease.

Acetylcholine

[Comparison of the effects of ethidium bromide and of the ethidium bromide-deoxyribonucleic acid complex in Ehrlich tumor cells].

When injected into the peritoneal cavity, ethidium bromide can strongly inhibit the multiplication of mouse Ehrlich ascites tumour cells. This antitumour effect is increased when ethidium bromide is linked to DNA and also injected into the peritoneal cavity. The cellular alterations are identical after a treatment with E.B. either free or bound to DNA. However, when the cells are treated with E.B.-DNA they contain E.B. for a longer period than after a treatment with E.B.

Animals

Comparison of the effects of ethidium bromide and of ethidium bromide-deoxyribonucleic acid complex in fibroblasts cultivated in vitro.

Chick embryo fibroblasts cultivated in vitro were treated with ethidium bromide (E.B.) or with DNA-E.B. complex (DNA-E.B.). E.B. (5 mug/ml) provokes morphological alterations and cell death, inhibits DNA synthesis and mitotic activity. DNA-E.B. (E.B. 5 mug/ml) is less toxic to the fibroblasts as far as cell structure, DNA synthesis and mitotic activity are concerned. DNA alone has no apparent effect on the fibroblasts. As shown by fluorescence microscopy, the lower toxicity of DNA-E.B. seems to be related to its mode of penetration into the cells.

Animals

[Ipratropium Bromide, an Anticholinergic Bronchodilator/Behavior of airways resistance in patients with reversible respiratory obstruction following inhalation of various doses of ipratropium bromide].

A dose- and time-response study using different doses of an inhaled derivative of atropine, (8r)-3alpha-hydroxy-8-isopropyl-1 aH, 5aH-tropaniumbromide-(+/-)-tropate (Sch 1000, ipratropium bromide, Atrovent) was performed in 12 patients with reversible chronic obstructuve airways disease. The drug was shown to be an effective bronchodilator with the typical action of reducing airways resistance with 2 puffs (0.02 mg per puff). Increasing the dose to 4 and 8 puffs did not produce any relevant difference in time response. The onset of action was rapid and reached a maximum between 30 and 60 min after inhalation. The duration of bronchodilation was maintained during the observation period of 3 h. 30 min after inhalation the results corresponded to those following the inhalation of 2 puffs of orciprenaline (0.75 mg per puff). Isolated side-effects were independent of the dosage.

Adult

[Ipratropium bromide in controlled clinical trials. Short communication (II): Time-response measurements of pulmonary function after ipratropium bromide and isoprenaline].

(8R)-3alpha-Hydroxy-8-isopropyl-1alphaH, 5alphaH, 5alphaH-tropaniumbromide (+/-)-tropate (ipratropiumbromide, Sch 1000, Atrovent) was compared with isoprenaline in a cross-over study with randomized selection in 12 stable asthmatics, using total airways resistance (Rt) measured by whole-body plethysmography, peak expiratory flow (PEF) and pulse rate as parameters. 2 puffs ipratropiumbromide (0.02 mg per puff) or isoprenaline (0.1 mg per puff) were administered by metered dose inhaler and measurements taken at 5, 20, 35, 50, 90 min, 2, 3, 4, and 6 h later. Drugs were given on alternate days. Rt decreased significantly (p less than 0.001) for 4 h to 53% of the initial value after ipratropiumbromide and to 70% of the initial value after isoprenaline, but only for about 2 h after the latter. The maximum 20-min effect on Rt was almost the same for both drugs. The difference in the time course of the bronchodilation was also significant. The rise in PEF after 4 h following ipratropiumbromide was similarly highly significant (p less than 0.001); as for Rt the time course for both drugs ran nearly parallel. Neither substance caused a significant rise in pulse rate at the dosages used.

Airway Resistance

Intoxication of cattle with sodium bromide-contaminated feed.

Five concentrations of bromide ion, sodium bromide, were incorporated into a pelleted ration and fed to 5 groups of cattle for 49 days. Another group of cattle was fed volunteer oat hay cut from a field that had been fumigated with methyl bromide. On analysis, the hay contained between 6,800 and 8,400 parts per million of bromide ion. Groups fed the pelleted ration containing the highest concentration of bromide and those eating the contaminated hay developed signs of motor incoordination between the 10th and 12th days. The sign of incoordination correlated with serum bromide concentrations of 30 mEq/L or more. Serum bromide concentrations and associated neurologic signs subsided markedly 14 days after feeding of the toxic feeds was discontinued.

Animal Feed

Factors affecting petite induction and the recovery of respiratory competence in yeast cells exposed to ethidium bromide.

When growing cultures of S. cerevisiae are treated with high concentrations of ethidium bromide (greater than 50 mug/ml), three phases of petite induction may be observed: I. the majority of cells are rapidly converted to petite, II. subsequently a large proportion of cells recover the ability to form respiratory competent clones, and III. slow, irreversible conversion of all cells to petite. The extent of recovery of respiratory competence observed is dependent on the strain of S. cerevisiae employed and the temperature and the carbon source used in the growth medium. The effects of 100 mug/ml ethidium bromide are also produced by 10 mug/ml ethidium bromide in the presence of the detergent, sodium dodecyl sulphate, and recovery is also observed when cells are treated with 10 mug/ml ethidium bromide under starvation conditions. Genetic analysis of strain differences indicates that a number of nuclear genes influence petite induction by ethidium bromide. In one strain, S288C, petite induction by 100 mug/ml ethidium bromide is extremely slow under certain conditions. Mitochondria isolated from from S288C lack the ethidium bromide stimulated nuclease activity found in D243-4A, a strain which shows triphasic kinetics of petite formation. This enzyme may, therefore, be responsible for the initial phase of rapid petite formation.

Acriflavine

Dependence of mammalian DNA replication on DNA supercoiling. I. Effects of ethidium bromide on DNA synthesis in permeable Chinese hamster ovary cells.

Chinese hamster ovary cells labelled with [14C]thymidine were made permeable, incubated with various concentrations of the intercalating dye ethidium bromide, and centrifuged through neutral sucrose gradients. The gradient profiles of these cells were qualitatively similar to those obtained by centrifuging DNA from untreated, lysed permeable cells through gradients containing ethidium bromide. The sedimentation distance of DNA had a biphasic dependence on the concentration of ethidium bromide, suggesting that the dye altered the amount of DNA supercoiling in situ. The effect of ethidium bromide intercalation on incorporation of [3H]dTMP into acid-precipitable material in an in vitro DNA synthesis mixture was measured. The incorporation of [3H]dTMP was unaffected by less than 1 microgram/ml of ethidium bromide, enhanced up to two-fold by 1--10 microgram/ml, and inhibited by concentrations greater than 10 micrograms/ml. Alkaline sucrose gradient analysis revealed a higher percentage of small DNA fragments (6--20 S) in the cells treated with 2 micrograms/ml ethidium bromide than in control cells. These fragments attained parental size within the same time as the fragments in control cells. In cells treated with 2 micrograms/ml ethidium bromide, a significant fraction of newly synthesized DNA resulted from new starts, whereas in untreated cells practically none of the newly synthesized DNA resulted from new starts. These results suggest that relaxation of DNA supercoiled structures ahead of the replication fork generates spurious initiations of DNA synthesis and that in intact cells the rate of chain elongation is limited by supercoiled regions ahead of the growing point.

Animals

Characterization of the cyanogen bromide fragments of the beta chain of human haptoglobin.

Characterization of the cyanogen bromide (CNBr) fragments of the beta chain of human haptoglobin revealed five major fragments resulting from cleavage of four methionyl residues. The fragments were isolated by gel filtration in guanidine-HCl on Sepharose 6B and Bio-Gel P10 and P60. Compositional analyses of the five cyanogen bromide fragments accounted for 248-253 amino acid residues in agreement with the number of residues determined for the intact beta chain. Most of the carbohydrate was attached to CNBr II. Automated amino-terminal sequence analysis and carboxyl-terminal hydrolysis with carboxypeptidase of the haptoglobin beta chain and cyanogen bromide fragments identified 139 residues, or about 55% of the beta-chain molecule. The placement of the fragments within the beta-chain molecule was established by sequence analysis of whole beta chain and a plasmin cleavage fragment. The position of CNBr V was confirmed by the absence of homoserine or homoserine lactone. Cyanogen bromide reaction of intact haptoglobin 1-1 resulted in the isolation of a beta-chain fragment, CNBr III, covalently attached to the intact alpha1 chain by a single disulfide bond. The beta chain was shown to have primary structural similarities to the chymotrypsin family of serin eproteases. Partial sequence analysis of CNBr V established the region which is comparable to the serine-195 active-site region: /Asp-Thr-Cys-Tyr-Gly-Asp-Ala-Gly-Ser-Ala-Phe/ (residues 189-199, chymotrypsinogen A numbering). The active-site serine-195 is replaced by alanine; however, the specificity residue of the trypsin-like enzymes, Asp-189, is preserved. Several minor cyanogen bromide cleavage products were also identified in yields of up to 15%. These minor cleavage products give evidence that tryptophanyl residues in proteins, or glycoproteins, are also susceptible to cyanogen bromide cleavage.

Amino Acid Sequence

Sodium cromoglycate and ipratropium bromide in exercise-induced asthma.

In thirteen patients with extrinsic asthma the effects of placebo, sodium cromoglycate, ipratropium bromide, and ipratropium bromide plus sodium cromoglycate were studied in a random double-blind fashion to assess their inhibitory action in exercise-induced asthma (EIA). Exercise testing consisted of steady state running on an inclined treadmill for up to eight minutes. In eight of the 13 patients studied the baseline ratio of expiratory flow at 50% vital capacity (VC) breathing helium-oxygen (V50He) to V50air was over 1.20 and they were called responders; the remaining five patients were called non-responders. There was a significantly lower baseline maximum mid-expiratory flow rate (MMEF) in non-responders (P less than 0.02) as compared to responders but no difference in forced expiratory volume in one second (FEV1) or forced vital capacity (FVC). Sodium cromoglycate (P less than 0.02), ipratropium bromide (P less than 0.01), and ipratropium bromide plus spdium cromoglycate (P less than 0.01) all significantly inhibited the percentage fall in FEV1 after exercise in the responders. Ipratropium bromide had no preventive action on non-responders, unlike sodium cromoglycate (P less than 0.05) and ipratropium bromide plus sodium cromoglycate (P less than 0.02). It is postulated that mediator release is an important factor in development of EIA in most extrinsic asthmatics, whereas cholinergic mechanisms are relevant only in those patients in whom the main site of airflow obstruction is in the large central airways.

Adolescent

Effects of ethidium bromide on the respiratory chain and oligomycin-sensitive adenosine triphosphatase in purified mitochondria from the cellular slime mold Dicyostelium discoideum.

Mitochondria were isolated from the cellular slime mold. Dictyoostelium discoideum, and partially purified by sucrose density gradient fractionation. The most purified mitochondrial fraction from the gradient contained essentially no contaminating lysosomes and minimal amounts of contaminating peroxisomes as determined by the marker enzymes N-acetyl-glucosaminidase and catalase. A mitochondrial fraction with the same amount of lysosomal and peroxisomal contamination was also isolated from cells which had been treated with ethidium bromide for 5 days. The most purified mitochondrial fraction from control and ethidium bromide-treated cells had an identical buoyant density of 1.181 to 1.182 g per ml, suggesting that treatment with the drug does not result in any drastic structural changes in the mitochondrial membrane which would affect its density. In the purified mitochondria from ethidium bromide-treated cells, the content of cytochromes a-a3 was decreased over 80% and that of cytochrome oxidase and oligomycin sensitive ATPase were reduced approximately 50%. By contrast, the specific activities of NADH and succinate dehydrogenases were identical in the purified mitochondria from control and ethidium bromide-treated cells. Previously, we had reported that the specific activities of these two enzymes had nearly doubled in whole cells maintained in ethidium bromide for a time equivalent to six or seven generations after growth had stopped (Stuchell, R. N., Weinstein, B. I., and Beattie, D. S. (1973) Fed. Eur. Biochem. Coc Lett. 37, 23-26). These results suggest that continued formation of new mitochondrial membranes, with an identical complement of succinate and NADH dehydrogenases, must occur despite the cessation of cell growth which occurs as a result of the ethidium bromide induced loss of mitochondrial enzymes. Consequently, the amount of mitochondria, or mitochondrial protein per cell, calculated from the activity of NADH and succinate dehydrogenases has increased nearly 50%. Possible models to explain the control of mitochondrial biogenesis are discussed to explain these results.

Adenosine Triphosphatases

Accelerated fall in serum bromide level after administration of perchlorate to man.

Five patients intoxicated with bromoureide showed accelerated elimination of bromide from serum after a single dose of perchlorate. It was probably due to increased renal excretion of bromide. Perchlorate has been reported to increase the renal clearance of other monovalent anions by inhibiting their tubular reabsorption and a similar interaction between perchlorate and bromide is suggested. Although perchlorate effectively eliminates bromide it should not replace chloride in the treatment of bromide intoxication, because of the side effects of its repeated administration.

Adult