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PubMed1988

Binding mode transitions of Escherichia coli single strand binding protein-single-stranded DNA complexes. Cation, anion, pH, and binding density effects.

We have extended our investigations of the multiple binding modes that form between the Escherichia coli single strand binding (SSB) protein and single-stranded DNA (Lohman, T. M. & Overman, L. B. (1985) J. Biol. Chem. 260, 3594-3603; Bujalowski, W. & Lohman, T. M. (1986) Biochemistry 25, 7799-7802) by examining the effects of anions, pH, BaCl2, and protein binding density on the transitions among these binding modes. "Reverse" titrations that monitor the quenching of the intrinsic tryptophan fluorescence of the SSB protein upon addition of poly(dT) have been used to measure the apparent site size of the complex at 25 degrees C in pH 8.1 and 6.9 as a function of NaF, NaCl, NaBr, and MgCl2 concentrations. Under all conditions in which "reverse" titrations were performed, we observe three distinct binding modes with site sizes of 35 +/- 2, 56 +/- 3, and 65 +/- 3 nucleotides/SSB tetramer; however, the transitions among the three binding modes are strongly dependent upon both the cation and anion valence, type, and concentration as well as the pH. A net uptake of both cations and anions accompanies the transitions from the (SSB)35 to the (SSB)56 binding mode at pH 6.9, whereas at pH 8.1 this transition is anion-independent, and only a net uptake of cations occurs. The transition from the (SSB)56 to the (SSB)65 binding mode is dependent upon both cations and anions at both pH 6.9 and 8.1 (25 degrees C), and a net uptake of both cations and anions accompanies this transition. We have also examined the transitions by monitoring the change in the sedimentation coefficient of the SSB protein-poly(dT) complex as a function of MgCl2 concentration (20 degrees C, pH 8.1) and observe an increase in s20,w, which coincides with the increase in apparent site size of the complex, as measured by fluorescence titrations. The frictional coefficient of the complex decreases by a factor of two in progressing from the (SSB)35 to the (SSB)65 binding mode, indicating a progressive compaction of the complex throughout the transition. The transition between the (SSB)35 and the (SSB)56 complex is dependent on the protein binding density, with the lower site size (SSB)35 complex favored at higher binding density. These results indicate that the transitions among the various SSB protein-single-stranded DNA binding modes are complex processes that depend on a number of solution variables that are thermodynamically linked.(ABSTRACT TRUNCATED AT 400 WORDS)

Anions↗
PubMed1988

Comparative effects of magnesium salts on reactivity of arterioles and venules to constrictor agents: an in situ study on microcirculation.

The influence of different magnesium salts (i.e., MgCl2, MgSO4, Mg aspartate HCl and Mg acetate) on reactivity of rat mesenteric arterioles (10-25 micron I.D.) and venules (15-30 micron I.D.) to standard constrictor doses of epinephrine and BaCl2 was examined utilizing perivascular, i.a. and i.v. administration of each Mg salt. Perivascular application (0.1, 1.0 and 10 mumol) of the four Mg salts on the microvessels attenuated the vasoconstrictor actions of both epinephrine and BaCl2, dose-dependently. With respect to arterioles, the vasoconstriction induced by BaCl2 was inhibited more potently by each Mg salt than that induced by epinephrine; the reverse was observed with respect to the venules. MgCl2 displayed the most potent antagonism to the constriction induced by BaCl2 in arterioles as well as by epinephrine in venules. Infusion of each Mg salt in very low doses (e.g., 0.1 mumol/min i.a.) resulted in significant attenuation of the arteriolar constrictions induced by both stimulants. However, the difference in the degree of attenuation on i.a. infusion of each Mg salt was significantly less than that observed by perivascular pretreatment. Arteriolar constrictions induced by epinephrine and BaCl2 were also attenuated by systemic i.v. infusion of each Mg salt, except for MgSO4, when low doses (e.g., 0.1 and 1.0 mumol/min.) were given; surprisingly, high dose i.v. infusion (10 and 20 mumol/min) often potentiated arteriolar constrictions induced by both stimulants, but the magnitude of this potentiation depended on the Mg salt utilized.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetates↗
PubMed1987

On chromosomal DNA modifications by chemical and physical treatment of C-bands.

Experiments were performed on fixed metaphase chromosomes using standard techniques for revealing paracentromeric heterochromatin (C bands) followed by staining with acridine orange with the aim of studying C-banding mechanism. Data obtained suggest that the specific resistance to the chemical-physical treatments of the heterochromatic areas is a consequence of the particular structural conditions that the C-positive material shows only after its early renaturation.

Acridine Orange↗
PubMed1987

Bronchodilator and other pharmacological activities of R-836 (2,5-diethyl-7-(4-thiomorpholino)-1,2,4-triazolo[1,5-c]pyrimidin e).

The bronchodilator activity of R-386 (2,5-diethyl-7-(4-thiomorpholino)-1,2,4-triazolo[1,5-c]pyrimidine) was demonstrated in isolated guinea-pig tracheal preparations and in vivo in dogs, guinea-pigs and rats. Guinea-pig tracheal preparations contracted by histamine, acetylcholine, BaCl2, leukotriene C4 or antigen were relaxed 50% by concentrations (IC-50 values) of R-836 of approximately 0.3 microgram/ml (10(-6) M) in all cases. In the conscious guinea-pig, oral or i.p. administration of R-836 prevented asphyxial collapse, death or dyspneic changes produced by histamine, antigen of LTC4. In anesthetized guinea-pigs, R-836 reduced bronchoconstriction produced by antigen or PAF (Konzett-Rössler preparation). In the dog, i.v. or intraduodenal administration of R-836 reduced bronchoconstriction produced by methacholine or histamine. In the rat, i.p. administration of R-836 reduced bronchoconstriction produced by 5-HT or antigenic challenge. In these in vivo models, when direct comparisons were made, R-836 was estimated to possess 2 to 3 times the potency of theophylline. R-836, at doses 80 times those necessary to produce bronchodilation, had no effect on blood pressure or heart rate of guinea-pigs. R-836 was not a CNS stimulant in mice, was not diuretic in rats, only marginally inhibited adenosine-induced responses in mice and guinea-pigs and was a weak inhibitor of phosphodiesterase in vitro.

Acetylcholine↗
PubMed1986

The time-course of contractions induced by acetylcholine and barium in the vas deferens of normal and castrated guinea-pigs.

1. The influence of castration on contraction of the guinea pig vas deferens induced by acetylcholine was investigated regarding facilitation of endogenous neurotransmitter release, changes in post-synaptic events and modification in acetylcholine metabolization. 2. Castration prolonged the duration of the isometric contraction of the vas deferens induced by acetylcholine (3 mM) but not the duration of that induced by barium chloride (10 mM). 3. Reserpinization (0.5 mg/kg) of normal and castrated guinea pigs did not change the time-course of acetylcholine-induced contraction in the vas deferens. 4. 4-Aminopyridine (0.05 mM) prolonged the contraction induced by acetylcholine and barium chloride. This effect was blocked by reserpine pretreatment, indicating that in the presence of 4-AP, both acetylcholine and barium release endogenous noradrenaline. Since there was no difference between the effects of 4-AP on organs from normal and castrated animals, prolongation of the acetylcholine-induced contraction is not related to an increase in neutransmitter release. 5. Total cholinesterase and acetylcholinesterase activities were reduced after castration and the time-course of carbachol contraction was not changed. Thus, this decrease in enzyme activity appears to play a relevant role in the prolongation of acetylcholine-induced contraction.

Acetylcholine↗
PubMed1987

Effects of sodium and calcium concentration on the barium chloride-induced electrical and contractile responses of the guinea pig vas deferens.

1. The mechanism of 10 mM barium chloride-induced electrical and contractile responses of the guinea pig vas deferens was investigated using calcium channel blockers and by modifying the Na+ and Ca2+ concentrations of the nutritional solution. Isometric contraction and membrane depolarization were measured simultaneously by the sucrose-gap technique. 2. In the absence of added Ca2+ there was a decay of the contractile but not of the depolarizing effect, which was independent of the frequency of 10 mM barium chloride administration. However, both barium-induced contraction and depolarization were reduced and the former more rapidly in a Ca2+-free solution (0.5 mM EGTA). 3. In low-Na+ solution (16 mM) there was a 3-fold increase in depolarization and no change in contraction, but in a low-Na+ Ca2+-free solution (0.5 mM EGTA), only contraction was reduced. 4. Nifedipine blocked both barium-induced contraction and depolarization in a dose-dependent manner when the organs were bathed in regular nutrient solution. In contrast, in low-Na+ solution only 50% of the depolarization was blocked by 10(-6) M nifedipine, which completely inhibited contraction. Both barium-induced contraction and depolarization in low-Na+ Ca2+-free solution were blocked by 10(-3) M LaCl3. 5. These data indicate that in the presence of calcium, barium mobilizes extracellular calcium through voltage-dependent channels and the contraction is due to the entry of calcium. In contrast, in the absence of added Ca2+ or in Ca2+-free solutions (0.5 mM EGTA), barium enters through the voltage-dependent channel and the contraction is reduced because the intracellular stores of calcium are limited.

Animals↗
PubMed1986

Identification and molecular characterization of the isoquinoline rat intestinal binding site using 6,7-dimethoxy-4-(4'-amino-3'-[125I]iodobenzyl) isoquinoline.

The mechanism of the relaxant action of isoquinolines on smooth muscle is conjectural. In order to gain further insight into the intestinal action of isoquinolines, we have synthesized an isoquinoline derivative which can be radioiodinated, resulting in the obtention of a ligand with a high specific activity. 6,7-Dimethoxy-4-(4'-aminobenzyl) isoquinoline (DMABI) is an arylamine analogue of the most relaxating isoquinoline derivative, i.e., 6,7-dimethoxy-4-(4'-chlorobenzyl) isoquinoline. Its iodinated derivative, 6,7-dimethoxy-4-(4'-amino-3'-[125I]iodobenzyl) isoquinoline (125I-DMABI) binds reversibly to rat intestinal membranes. Binding is rapid, saturable, and temperature dependent. The binding of 125I-DMABI to intestinal membranes is competitively inhibited by identical concentrations of unlabeled DMABI or iodo-DMABI in the range between 10(-8) and 10(-5)M. Scatchard analysis indicates the existence of two classes of binding sites: a class with a low capacity (14 +/- 2 pmol/mg of protein) and a Kd = 0.10 +/- 0.02 microM, and a class with a high capacity (240 +/- 31 pmol/mg of protein) and a Kd = 8.0 +/- 1.1 microM. Specific binding of the radioiodinated ligand is inhibited by a variety of 4-benzyl isoquinolines and 1-benzyl isoquinolines. Structure-activity relationship demonstrates the primordial role of C-6 and C-7 methoxy groups and the important role of 4-benzyl on configuration related to the isoquinoline nucleus. A high significant correlation between competitive binding (Ki) and relaxant effect in rat intestine (IC50) is observed and strongly suggests that the isoquinoline-binding site mediates the pharmacologic response. Upon photolysis, this ligand incorporates irreversibly into rat intestinal membranes. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis and autoradiography reveal a major 125I-DMABI-labeled protein with molecular weight of 36,000 and two minor proteins with molecular weights of 52,000 and 26,000. The labeling of these proteins is specific since it is completely abolished by 100 microM DMABI. Scanning of autoradiographs and integration of peaks show that the probe binds with the same apparent affinity to the three proteins. These findings indicate the utility of this novel high affinity radioiodinated probe as a tool for elucidating the mechanism of action of isoquinoline.

Animals↗
PubMed1986

[Comparative study of the toxicity of metal chlorides and a synthetic organic molluscacide, N-tritylmorpholine, in 2 fresh-water amphipods, Gammarus pulex and Echinogammarus berilloni].

The effects of three metal salts (BaCl2, CuCl2, ZnCl2) and of N-trityl-morpholine (Triphenmorph) were studied on two aquatic amphipod species, Gammarus pulex and Echinogammarus berilloni. Experiments were made up in eucalcic and oligocalcic waters for determining the LC50 at different exposure times. The order of toxicity was the same in eucalcic water with the two species: Triphenmorph greater than Cu2+ greater than Zn2+ greater than Ba2+. This order was the same in oligocalcic water with Echinogammarus berilloni; with Gammarus pulex, CuCl2 was more toxic than Triphenmorph.

Animals↗
PubMed1985

[Antiarrhythmic action of 3-carbethoxyamino-5-dimethylaminoacetyl-iminodibenzyl hydrochloride (Bonnecor, AWD 19-166, GS -15) on experimental arrhythmia induced by aconitin, ouabain, calcium chloride and barium chloride].

In comparison with detajmium, prajmalium, ajmaline, quinidine, lidocaine, disopyramide, propranolol, and Ethmozin the substance GS 015 is tested on the aconitin-induced arrhythmia of the rat, the auricular fibrillation by aconitin of the dog, the ventricular arrhythmia induced by ouabaine of the dog, the arrhythmia caused by calcium chloride of the rat, and the arrhythmia induced by barium chloride of the rabbit. The particular qualities of effect in the special forms of arrhythmia are discussed in connection with the study of the antiarrhythmic action in case of coronary occlusion, with the increase of the electric fibrillatory threshold, and with the electrophysiologic tests.

Aconitine↗
PubMed1985

Barium removes the ouabain-induced increase in the rod response to light.

The mass receptor potential of the excised, superfused retina of the bullfrog was isolated with aspartate. Rods were selectively stimulated by using very dim flashes of light. In the presence of 0.1 mM ouabain, the amplitude of the receptor response was found first to increase transiently and, subsequently, to decrease progressively. The ouabain-induced transient increase in receptor response was completely eliminated by 0.4 mM barium chloride. However, barium did not affect the rate at which the response decayed in the presence of ouabain. The ability of barium to remove the ouabain-induced transient increase in the amplitude of the receptor response is discussed in terms of reducing the coupling ratio of the postulated electrogenic sodium-potassium pump of rods.

Animals↗
PubMedDate not supplied

[Comparative characteristics of the activity of lithium preparations and anti-arrhythmia agents in strophanthin, calcium chloride and barium chloride arrhythmias in an experiment].

During disorders of cardiac rhythm induced by strophanthine K in anesthesized cats, by calcium chloride in mice and anesthesized rats, and by barium chloride in rabbits, lithium hydroxybutyrate (0.55-3.2 mg/kg according to cation) compares very favourably with lithium chloride, novocainamide, lidocaine, trimecaine, etmozine, quinidine and verapamil as regards antiarrhythmic activity and the range of therapeutic action.

Animals↗