Presence Of Tropolone Research Articles

The Dissolution of Amorphous Silica in the Presence of Tropolone Under Acidic Conditions

AbstractDissolution of amorphous silica or silicate is an important reaction to release silicic acid in natural water and this reaction is affected by several factors. The existence of a natural organic compound, tropolone, because of its abundance, is of particular importance. In the present study, the dissolution of amorphous silica in the presence of tropolone (HL) was investigated in an aqueous solution under acidic conditions. The dissolution is controlled by the reaction between silicic acid and tropolone (Si(OH)4 + 3HL + H+ ⇌ SiL3+ + 4H2O), where the conditional formation constant K = [SiL3+]/[Si(OH)4][HL]3[H+]). The solubility of amorphous silica in the presence of tropolone was significantly greater than that in pure water due to the formation of the Si-tropolonate complex in the solution. The acceleration of silica dissolution by tropolone depends on the reaction pH and tropolone concentration. The solubility of the amorphous silica in the tropolone solution at pH 1 was approximately ten times greater than in the 0.1 mol/dm3 HCl used as a reference. This increase in the solubility correlates to a K value of the Si-tropolone complex at each pH. From the solubility experiments, the conditional formation constants (log K) of the Si-tropolonate complex at each reaction pH 1, 2, and 3 were 6.39, 5.88, and 5.77, respectively. The significant acceleration of the dissolution of amorphous silica by tropolone at pH 1 can be attributed to the large formation constant of the Si-tropolonate complex.

Impact of Protein on Darkening in Yellow Alkaline Noodles

Darkening in yellow alkaline noodles (YAN) was examined over a 24 h period in noodles made from 4 wheat varieties, including varieties with different levels of polyphenol oxidase (PPO) activity, selected to cover a range of protein levels. Noodles were made in the presence and absence of the PPO inhibitor, tropolone. The darkening was divided into two time periods: 0-4 h and 4-24 h. The first four hours was described by a composite rate equation, and this period was subdivided into two stages. The rate of darkening in the first stage was independent of both protein concentration and PPO activity. The amount of darkening (c), however, was highly dependent on protein concentration during this stage (-tropolone, r = 0.902; +tropolone, r = 0.905), but independent of PPO activity. The first stage darkening was a zero order reaction where additional protein does not increase the reaction rate, but when the protein supply has been depleted, the reaction stops. The rate of darkening during the first stage (k'(1) = 5.6 +/- 1.0) was similar to the rate of change in the protein structure (k'(1) = 6.5 +/- 1.3) as measured using the amide II band by infrared spectroscopy. This suggested that the first stage of darkening represents changes in light reflectance and absorbance caused by changes in hydrogen bonding rather than changes in covalent bonding. During the second stage of darkening, both the rate (k'(2)) and amount of darkening (DeltaL*(4h-c)) were significantly correlated with protein concentration (-tropolone, r = 0.465; +tropolone, r = 0.813), and in the absence of tropolone the amount of darkening was increased by PPO activity. The amount of darkening (DeltaL*(24h-4h)) during the second time period (4-24 h) (or third stage) was significantly correlated in the presence of tropolone (r = 0.375) and in the absence of tropolone (r = 0.428) with protein concentration. However, compared with earlier stages the response of non-PPO darkening during the third stage to change in protein concentration was smaller. Protein oxidation, or more specifically oxidation of tyrosine groups within the protein, appears to be the main mechanism involved in non-PPO darkening in YAN during the second and third stages with glutenin being the main reactant. Albumin and globulin are important substrates for PPO. No differences in darkening were detected in YAN made from the four varieties in the presence of tropolone; however, differences in YAN darkening were observed for the second and third stages due to site and year variation.

Utilization of iron-catecholamine complexes involving ferric reductase activity in Listeria monocytogenes.

Listeria monocytogenes is a ubiquitous potentially pathogenic organism requiring iron for growth and virulence. Although it does not produce siderophores, L. monocytogenes is able to obtain iron by using either exogenous siderophores produced by various microorganisms or natural catechol compounds widespread in the environment. In the presence of tropolone, an iron-chelating agent, growth of L. monocytogenes is completely inhibited. However, the growth inhibition can be relieved by the addition of dopamine or norepinephrine under their different isomeric forms, while the catecholamine derivatives 4-hydroxy-3-methoxyphenylglycol and normetanephrine did not relieve the inhibitory effect of tropolone. Preincubation of L. monocytogenes with chlorpromazine and yohimbine did not antagonize the growth-promoting effect of catecholamines in iron-complexed medium. In addition, norepinephrine stimulated the growth-promoting effect induced by human transferrin in iron-limited medium. Furthermore, dopamine and norepinephrine allowed 55Fe uptake by iron-deprived bacterial cells. The uptake of iron was energy dependent, as indicated by inhibition of 55Fe uptake at 0 degrees C as well as by preincubating the bacteria with KCN. Inhibition of 55Fe uptake by L. monocytogenes was also observed in the presence of Pt(II). Moreover, when assessed by a whole-cell ferric reductase assay, reductase activity of L. monocytogenes was inhibited by Pt(II). These data demonstrate that dopamine and norepinephrine can function as siderophore-like compounds in L. monocytogenes owing to their ortho-diphenol function and that catecholamine-mediated iron acquisition does not involve specific catecholamine receptors but acts through a cell-bound ferrireductase activity.

Identification and determination of butyltin compounds in water by ion trap gas chromatography-mass spectrometry after conversion to methyl or hydride derivatives

Abstract Capillary column gas chromatography with ion trap mass spectrometric detection has been shown to be a powerful technique for the determination of trace and ultratrace quantities of tributyltin and its degradation products (di- and monosubstituted analogues) in water. Butyltins were extracted into hexane in the presence of tropolone (0.2%, w/v) followed by either Grignard methylation or NaBH4 reduction to corresponding butyltinhydrides to produce species of sufficient volatility. The wide linear dynamic range (over three orders of magnitute) and pg sensitivity obtained for the ion trap mass spectrometer operating in electron impact (EI) mode has demonstrated the ability of this GC-MS configuration to provide routinely trace and ultratrace analyses of organotins. Two derivatization routes are compared, in combination with GC-MS using classical electron impact or chemical ionization (CI). Hydride derivatization offers reduced labour effort and for most cases easier interpretation of observed spectra. Grignard methylation provides lower detection limits when using EI ionization and superior stability of standard calibration solutions. CI detection mode using CI reagent gases methane, isobutane, acetonitrile a methanol was studied. Methanol and acetonitrile CI provide simple mass spectra, yielding complementary spectral information to EI. The reported values of detection limits for acetonitrile CI are comparable to those using EI ionization mode. The acetonitrile CI mass spectra are characterized by the formation of [M( fragment )+]+ions.

Voltammetric speciation of butyltin compounds

A sensitive and selective procedure for the determination of tributyltin chloride (TBT), dibutyltin dichloride (DBT) and monobutyltin trichloride (MBT) based on solid phase extraction (SPE) with ENVI-Carb non-porous carbon as column material followed by adsorptive cathodic stripping voltammetry (AdSV) in the presence of tropolone is reported. The determination limits achieved using a 500 mL water sample were 210 ng L -1 (as Sn) for TBT, 30 ng L -1 (as Sn) for DBT and 40 ng L -1 (as Sn) for MBT. The method was used to determine the levels of butyltin species in surface water from the yacht harbour at Zewen on the Mosel River and in the tap water supply in Trier.

ＧＣ／ＭＳによるムラサキイガイ中の有機スズの代謝産物の同定

Metabolic products of organotin compounds in mussel were studied by using gas chromatography/mass spectrometry (GC/MS). Organotin compounds in mussels collected along Tokyo bay were extracted with 1 N HBr ethanol solution and benzene mixture in presence of tropolone. The extracts were propylated with Grignard reagent before GC and GC/MS analysis. The existence of butyltin, dibutyltin, tributyltin, phenyltin, diphenyltin, triphenyltin in the extracts was shown by FPD gas chromatography. Several unidentified compounds, which responded well to FPD detector, were subject to GC/MS analysis after fractionations by silica gel column chromatography, subsequent by high performance liquid chromatography. Compounds identified by GC/MS were as follows; dibutyl(3-oxobutyl)tin, butyl(3-oxobutyl)tin, dibutyl(3-hydroxybutyl)tin, and butyl(3-hydroxybutyl)tin. These identifications were confirmed by synthesis of authentic standards. Butyltin compounds, found in this study, are also known as metabolic products of tributyltin in mammals. Oxidation of tributyltin to dibutyl(3-oxobutyl)tin seems to be favored in mussel, while debutylation is favored in mammals. In summer, dibutyl(3-oxobutyl)tin becomes one of the major organotin compounds in mussel.

Possible activation of intracellular ?-adrenoceptors by extraneuronally accumulated isoprenaline in perfused rat heart

Two rat hearts were perfused in series by a modified Loewi's method. The recipient heart was perfused with the perfusate collected from the donor heart. 1. After perfusion with 3H-isoprenaline in the presence of tropolone, an inhibitor of catechol-O-methyltransferase, the donor heart was washed out with amine-free medium containing tropolone and corticosterone. The heart rate of the recipient heart increased after the change to the perfusate from the donor heart during the wash-out. After wash-out the heart rate of the donor heart (which had accumulated 43.4 pmol.g-1 3H-isoprenaline) was higher than that of the recipient heart (which had accumulated 0.44 pmol.g-1 3H-isoprenaline), and the rates of efflux of 3H-isoprenaline from both hearts were similar. 2. After perfusion with 3H-isoprenaline and corticosterone in the absence of tropolone, the enhanced heart rate of the donor heart decreased during wash-out with amine-free medium in the presence of corticosterone. The heart rate of the recipient heart increased after the medium change to the perfusate from the donor heart, and the heart rates in both hearts were similar after wash-out. Only small amounts of 3H-isoprenaline remained in both hearts after wash-out, and the rates of efflux of 3H-isoprenaline from both hearts were similar. 3. After perfusion with 3H-isoprenaline in the presence of tropolone, the effects of propranolol and atenolol on the heart rate during wash-out with amine-free medium containing tropolone and corticosterone were compared. The inhibitory effect of propranolol on the heart rate was significantly greater than that of atenolol.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of extraneuronal uptake inhibitors on the positive chronotropic response to isoprenaline and on the accumulation of isoprenaline in perfused rat heart after inhibition of catechol-O-methyl transferase.

Experiments were carried out in isolated perfused rat hearts. The presence of tropolone (100 mumol/l), an inhibitor of catechol-O-methyl transferase (COMT), significantly potentiated the positive chronotropic response to isoprenaline (0.1, 1, 3 and 10 nmol/l). Two uptake2 inhibitors, 3-O-methylisoprenaline (100 mumol/l) and normetanephrine (100 mumol/l), induced a positive chronotropic response, but corticosterone (100 mumol/l) and hydrocortisone (100 mumol/l) had no such effect. 3-O-methylisoprenaline (100 mumol/l) and normetanephrine (100 mumol/l) enhanced the positive chronotropic response to isoprenaline (0.1, 1, 3 and 10 nmol/l). Corticosterone (100 mumol/l) potentiated the positive chronotropic response to isoprenaline (0.1 and 1 nmol/l). Hydrocortisone (30 mumol/l) enhanced the response to 0.1 nmol/l isoprenaline but did not affect the positive chronotropic responses to 1, 3 or 10 nmol/l isoprenaline. The addition of uptake2 inhibitors (3-O-methylisoprenaline, 100 mumol/l; normetanephrine, 100 mumol/l; corticosterone, 100 mumol/l) to the perfusion medium significantly reduced the positive chronotropic response to the perfusion with isoprenaline (3 nmol/l) and tropolone (100 mumol/l). The accumulation of 3H-isoprenaline in the heart perfused with 3H-isoprenaline (1, 10 and 100 nmol/l) was significantly increased by the presence of tropolone (100 mumol/l): the accumulation for 1, 10 and 100 nmol/l of 3H-isoprenaline was 5.07, 47.0 and 500 pmol/g, respectively. The high accumulation observed during perfusion with 3H-isoprenaline (3 nmol/l) and tropolone (100 mumol/l) was significantly decreased by the addition of an uptake2 inhibitor, 3-O-methylisoprenaline (100 mumol/l), normetanephrine (100 mumol/l) or corticosterone (100 mumol/l), but not by hydrocortisone (30 mumol/l).(ABSTRACT TRUNCATED AT 250 WORDS)

A new model of ventricular fibrillation induced by isoprenaline and catechoi-o-methyl transferase inhibitor at a high perfusion temperature in isolated rat hearts

Isolated rat hearts were perfused with various concentrations of isoprenaline (0.01–10 μmol/liter) for 30 min at a constant flow rate (6.5 ml/min) at 37–44°C. The occurrence of ventricular fibrillations was isoprenaline concentration dependent and also perfusion temperature dependent in the combined treatment with various concentrations of isoprenaline and high perfusion temperatures. When the hearts were perfused with isoprenaline (1 μmol/liter) in the presence of tropolone (100 μmol/liter) at 40–41°C, the duration of ventricular fibrillations was significantly prolonged, but the incidence of ventricular fibrillations was similar to that produced with isoprenaline (1 μmol/liter) alone. The antiarrhythmic drugs such as quinidine sulfate, lidocaine hydrochloride, dl-propranolol hydrochloride, carteolol hydrochloride, atenolol, dl-verapamil hydrochloride, and diltiazem hydrochloride, given at a concentration of 10 μmol/liter, significantly suppressed the incidence and duration of such ventricular fibrillations. Bretylium tosylate (10 μmol/liter) significantly suppressed the duration of the ventricular fibrillations but not their incidence. These results indicate that ventricular fibrillation induced by combined treatment with a high concentration of isoprenaline and tropolone at a high perfusion temperature in isolated rat hearts is a more useful experimental model of arrhythmia than conventional models.

Equilibrium and structural studies of silicon(IV) and aluminium(III) in aqueous solution. 12. A potentiometric and 29Si-NMR study of silicon tropolonates

Complexation in the H +-Si(OH) 4-tropolone (HL) system was studied in 0.6 M (Na)Cl medium at 25° C. Speciation and formation constants were determined from potentiometric (glass electrode) and 29Si-NMR data. Experimental data cover the ranges 1.5 ⩽ - log[H +] ⩽ 8.4, 0.002 ⩽ B ⩽ 0.012 M, and 0 ⩽ C ⩽ 0.060 M ( B and C stand for the total concentration of Si and tropolone, respectively). In acid solutions (-log[H +] ⩽ 3) a hexacoordinated cationic complex, SiL 3 +, is formed with log K(Si(OH) 4 + 3HL + H + XXX SiL 3 + + 4H 2O) = 7.08 ± 0.03. Furthermore, the formation of a disilicic acid was established from 29Si-NMR data. The dimerization constant of Si(OH) 4 was found to be 10 exp (1.2 ± 0.1). In model calculations the solubility of quartz and amorphous SiO 2 in the presence of tropolone is demonstrated. Data were analyzed using the least-squares computer program LETAGROPVRID.

Changes in the incidence and duration of ventricular fibrillation in dependence on the extraneuronal accumulation of isoprenaline in the perfused rat heart.

The relationship between the accumulation of isoprenaline and the incidence and duration of ventricular fibrillation was investigated in the perfused rat heart. Isolated rat hearts were perfused with 3H-isoprenaline (1 mumol/l) for 30 min at a constant flow rate of 6.5 ml/min at a temperature between 40 and 41 degrees C. Electrocardiograms were recorded during the perfusion period and the isoprenaline content of the tissue was measured after the perfusion. The accumulation of isoprenaline was significantly increased and the duration of ventricular fibrillation was significantly prolonged by the presence of tropolone (100 mumol/l). When extraneuronal uptake inhibitors such as normetanephrine (100 mumol/l), 3-O-methylisoprenaline (100 mumol/l) or phenoxybenzamine (1 mumol/l) were added to the perfusion fluid containing 3H-isoprenaline (1 mumol/l) and tropolone (100 mumol/l), the accumulation of isoprenaline was significantly decreased, the incidence of ventricular fibrillation was significantly reduced and the duration of ventricular fibrillation was significantly shortened. There was a significant correlation for dependence of duration of ventricular fibrillation on the isoprenaline content of rat hearts perfused with various extraneuronal uptake inhibitors in the presence of tropolone (correlation coefficient [r] = 0.62, P less than 0.001). These results indicate that the accumulation of isoprenaline in perfused rat hearts relates to the occurrence and duration of ventricular fibrillation.

Decrease in glucose oxidation in isolated brown fat cells from rats due to tropolone and dimethoxybenzene

1. 1. Glucose conversion to carbon dioxide in control and insulin treated brown fat cells is reduced in the presence of tropolone and dimethoxybenzene. 2. 2. The effects of ortho-, meta- and para-dimethoxybenzene are similar to each other; all are more potent than monomethoxybenzene. 3. 3. The reduction in glucose oxidation with tropolone plus trimethoxybenzene is greater than that due to colchicine or to either agent alone. 4. 4. Since the methoxybenzenes and tropolone resemble the “A” and “C” rings of colchicine, their ability to reduce glucose oxidation is discussed in relationship to both the structure of the colchicine molecule and its effects on glucose oxidation.

Antibacterial activity of tropolone.

Tropolone was shown to be bacteriostatic and bactericidal for a wide range of bacterial species. This antibacterial activity was quantitated using standard methods. Tropolone treatment of whole cells resulted in cell lysis characterized by bleb formation and subsequent loss of cell contents after rupture of the bleb. Although bleb formation and lysis did not occur in the presence of 20% sucrose, cell viability was lost. Spheroplasts and protoplasts also lysed in the presence of tropolone. These results indicate that tropolone acts on the cell wall or envelope and on the plasma membrane.

Studies on the temperature-dependent sensitivity of mouse atria to adrenergic drugs

The sensitivity of mouse atria (chronotropic response) to β-adrenergic receptor antagonists was examined at 37 and 26°C under various experimental conditions. When isoproterenol was used as agonist, at 37°C, the pA 2 value (from pA 2 plots) for propranolol was 8.86 and the slope of the regression line was 0.54. At 26°C, the pA 2 value for propranolol was 9.2 and the slope was 0.7. In the presence of tropolone, 10 −5M, the values for pA 2 and slope of the regression lines were, respectively, 9.0 and 0.90 at 37°C and 9.17 and 0.98 at 26°C. In other words, decreasing antagonism was prevented by low temperature and tropolone. Isoproterenol was potentiated by tropolone and low temperature, but the effects of low temperature were reduced by tropolone. With sotalol as antagonist, there was greater blockade (dose ratios) of the effects of isoproterenol at 26 than at 37°C. When nylidrin, a non-catecholamine, was used as agonist there was no temperature-dependent sensitivity to sotalol. Furthermore, nylidrin was not potentiated by low temperature. The data show that the observed degree of β-receptor antagonism can be altered by changing the bath temperature and suggest that this effect is related to COMT activity or an influence of agonist disposition in the tissue.

Factors influencing observed β-adrenergic receptor antagonism in guinea-pig trachea

Antagonism of β-adrenergic receptors by (−)-sotalol has been examined in isolated guinea-pig trachea by the use of pA 2 plots. When (−)-isoproterenol was used as agonist, the slope value of the pA 2 plot was 0.82 and was increased to 0.98 when experiments were performed in the presence of tropolone, 10 −4 M, to inhibit COMT. When a COMT resistant compound, (−)-soterenol, was used as agonist, the slope value was 0.95. To test the hypothesis that high concentrations of agonists which are substrates for COMT saturate the enzymatic sites or access to these sites and thereby potentiate their own effects during competitive receptor antagonism, the ability of sotalol to block effects of (+)-isoproterenol was examined. Since a low slope value (0.80) of the pA 2 plot was still obtained under these experimental conditions, agonist saturation of either process does not appear to be operative in this tissue. This suggest that the β-receptor antagonist may impede the O-methylation process in concentration-dependent fashion. The apparent nonclassical antagonism of β-receptors produced by sotalol in guinea-pig trachea can be attributed to changes in agonist disposition in the tissue than deviations from currently accepted receptor theory.

Temperature-dependent supersensitivity to isoprenaline in mouse atria

The positive chronotropic effect of (−)-isoprenaline in mouse atria was determined at 37 and at 26°C under control conditions and in the presence of the catechol-O-methyltransferase (COMT) inhibitor tropolone. Under control conditions, the atria were markedly more sensitive at the lower bath temperature (ED 50 37 °C/ED 50 26°C = 16.61). However, in the presence of tropolone, there was little difference in the sensitivity (ED 50 37°C/ED 50 26°C = 2.18). These data suggest that decreased activity of COMT at 26°C is a major factor in temperature-dependent supersensitivity. Support for this concept comes from studies with (−)-soterenol and (±)-nylidrin at 37°C and 26°C. Temperature-dependent supersensitivity was not observed with these agonists which are not substrates for COMT.