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PubMed2001

Capture of gas-phase arsenic oxide by lime: kinetic and mechanistic studies.

Trace metal emission from coal combustion is a major concern for coal-burning utilities. Toxic compounds such as arsenic species are difficult to control because of their high volatility. Mineral sorbents such as lime and hydrated lime have been shown to be effective in capturing arsenic from the gas phase over a wide temperature range. In this study, the mechanism of interaction between arsenic oxide (As2O3) and lime (CaO) is studied over the range of 300-1000 degrees C. The interaction between these two components is found to depend on the temperature; tricalcium orthoarsenate (Ca3As2O8) is found to be the product of the reaction below 600 degrees C, whereas dicalcium pyroarsenate (Ca2As2O7) is found to be the reaction product in the range of 700-900 degrees C. Maximum capture of arsenic oxide is found to occur in the range of 500-600 degrees C. At 500 degrees C, a high reactivity calcium carbonate is found to capture arsenic oxide by a combination of physical and chemical adsorption. Intrinsic kinetics of the reaction between calcium oxide and arsenic oxide in the medium-temperature range of 300-500 degrees C is studied in a differential bed flow-through reactor. Using the shrinking core model, the order of reaction with respect to arsenic oxide concentration is found to be about 1, and the activation energy is calculated to be 5.1 kcal/mol. The effect of initial surface area of CaO sorbent is studied over a range of 2.7-45 m2/g using the grain model. The effect of other major acidic flue gas species (SO2 and HCl) on arsenic capture is found to be minimal under the conditions of the experiment.

Adsorption↗

PubMed2002

A population-based European cohort study of persistence in newly diagnosed hypertensive patients.

This study assessed the percentage of patients after 1 year who persisted on initially prescribed antihypertensive therapy. Medical records of 2416 patients with newly diagnosed hypertension who were prescribed initial antihypertensive monotherapy by general practitioners in Germany, France, and the United Kingdom were evaluated. Comparisons were made among the angiotensin II receptor antagonist (AIIRA) irbesartan, all other antihypertensive classes (including AIIRAs other than irbesartan), and the AIIRA losartan. Patients initiated on the AIIRA irbesartan scored highest with a persistence rate of 60.8%, followed by patients who received all other AIIRA agents with a persistence rate of 51.3%. Angiotensin-converting enzyme inhibitors, calcium channel blockers, beta-blockers, and losartan were associated with comparable persistence rates, between 42.0% and 49.7%. Patients who received diuretics scored lowest with a persistence rate of 34.4%. Persistence has emerged as an essential factor for blood pressure control. Prescribing an antihypertensive agent that provides a favourable efficacy and tolerability profile may provide greater persistence with therapy and hence a higher level of blood pressure control.

Adrenergic beta-Antagonists↗

PubMed1984

Hoe 263, a new substance with calcium channel antagonistic activity.

Hoe 263 inhibited the contraction of the potassium-depolarized pulmonary artery of the guinea pig. In this experiment it was slightly more active than verapamil. The calcium uptake of the potassium-depolarized pulmonary artery was inhibited by Hoe 263 more effectively than by prenylamine. The upstroke velocity of the potassium-depolarized papillary muscle of the guinea pig was depressed with similar concentrations of Hoe 263 and verapamil. In the (3H)-nitrendipine binding test, Hoe 263 was effective at similar concentrations as prenylamine and verapamil. The positive inotropic effect of K-strophanthin was depressed by Hoe 263 at concentrations which were comparable with those necessary for verapamil.

Animals↗

PubMed2002

Fortification: overcoming technical and practical barriers.

The main barriers to successful iron fortification are the following: 1) finding an iron compound that is adequately absorbed but causes no sensory changes to the food vehicle; and 2) overcoming the inhibitory effect on iron absorption of dietary components such as phytic acid, phenolic compounds and calcium. These barriers have been successfully overcome with some food vehicles but not with others. Iron-fortified fish sauce, soy sauce, curry powder, sugar, dried milk, infant formula and cereal based complementary foods have been demonstrated to improve iron status in targeted populations. The reasons for this success include the use of soluble iron such as ferrous sulfate, the addition of ascorbic acid as an absorption enhancer or the use of NaFeEDTA to overcome the negative effect of phytic acid. In contrast, at the present time, it is not possible to guarantee a similar successful fortification of cereal flours or salt. There is considerable doubt that the elemental iron powders currently used to fortify cereal flours are adequately absorbed, and there is an urgent need to investigate their potential for improving iron status. Better absorbed alternative compounds for cereal fortification include encapsulated ferrous sulfate and NaFeEDTA, which, unlike ferrous sulfate, do not provoke fat oxidation of cereals during storage. Encapsulated compounds also offer a possibility to fortify low grade salt without causing off-colors or iodine loss. Finally, a new and useful additional approach to ensuring adequate iron absorption from cereal based complementary foods is the complete degradation of phytic acid with added phytases or by activating native cereal phytases.

Biological Availability↗

PubMed1992

Powders, composed of chlorine-releasing agent acrylic resin mixtures or based on peroxygen compounds, for spills of body fluids.

The use of powders, composed of a mixture of a chlorine-releasing agent with highly absorbent acrylic resin, for disinfecting body fluid spills was evaluated by laboratory tests. 'Encap' and 'Red Z' were found to absorb rapidly up to 200 ml of water to form a semi-solid gel. When experimental formulations containing 1%, 5% and 10% available chlorine were evaluated by a standardized surface test, those containing 10% gave the best results. The ease and rate of absorption of fluids by these formulations decreased as the fluid consistency increased and they seem more suitable for watery spills than for blood. The use of a powder based on peroxygen compounds ('Virkon') for disinfecting contaminated spills was evaluated by laboratory tests and hospital trials. Laboratory tests showed that 'Virkon' is strongly and rapidly bactericidal. In hospital ward trials by nurses using 'Virkon' on both natural and artificial spills, 60 of 62 contact plates pressed on to decontaminated surfaces proved negative, and no unpleasant fumes were generated when 'Virkon' was applied to urine. In another trial, 1% 'Virkon' solution proved very effective in decontaminating mortuary tables. Antiviral activity was not tested.

Absorption↗

PubMed1998

Stimulation of phospholipase D via alpha1-adrenergic receptors in Madin-Darby canine kidney cells is independent of PKCalpha and -epsilon activation.

We have demonstrated previously that protein kinase Calpha (PKCalpha) plays a key role in regulating phospholipase D (PLD) activation by nucleotides and the phorbol ester phorbol-12-myristate-13-acetate in Madin-Darby canine kidney (MDCK-D1) cells. In the current work, we investigated PLD activation in MDCK-D1 cells triggered by the adrenergic receptor agonist epinephrine and its mechanism of activation. Epinephrine, acting through the alpha1-adrenergic receptor subtype, promoted transient translocation of PKCalpha and more prolonged translocation of PKCepsilon to the membrane fraction, indicating activation of these two isoforms. In addition, epinephrine promoted activation of PLD, as shown by a sustained accumulation of phosphatidylethanol. All of these events were blocked by pretreatment of cells with the alpha1-adrenergic antagonist prazosin. D609, an inhibitor of phosphatidylcholine hydrolysis, blocked translocation of PKCalpha and PKCepsilon but did not inhibit PLD activation. Unlike results with PMA, or with the P2 purinergic receptor agonist ATP, epinephrine-stimulated PLD activity was not inhibited in MDCK-D1 cells in which PKCalpha expression is attenuated by an antisense cDNA construct or in cells in which PKC activity was inhibited by 1 microM GF 109203X. However, PLD activation by epinephrine was abolished by concomitant incubation of cells with the calcium chelator EGTA. These data, together with previous results, are consistent with the hypothesis that in MDCK-D1 cells, epinephrine acting on alpha1-adrenergic receptors, promotes a rapid increase in cytosolic Ca2+ that promotes activation of PLD through an as-yet poorly defined mechanism. The data demonstrate that different types of G protein-linked receptors that activate PLD can mediate this activation in either a PKC activation-dependent or -independent manner within a single cell type.

Adenosine Triphosphate↗

PubMed2004

Activation of phospholipase C-gamma1 in human keratinocytes by hyperosmolar shock without enzyme phosphorylation.

Human keratinocytes are exposed to strong physical changes, and have the potentiality to react to external stimuli by switching on adaptation mechanisms. In hyperosmotically shocked keratinocytes a rapid and strong increase in calcium has been observed. We showed that this increase could not be prevented by growing the cells in medium devoid of calcium and in the presence of EGTA, indicating that the intracellular calcium increase was due to delivery from internal stores. Further, we observed an increased synthesis of dyacylglycerol and inositol trisphosphates after shock, suggesting that phospholipase C mediates both events. Our experiments demonstrated that osmotic shock in human keratinocytes leads to activation of phospholipase C-gamma1, as measured using an in vitro assay system. This activation is independent of protein tyrosine phosphorylation and corresponded to a relocation of the enzyme to perinuclear membranes as shown by immunofluorescence.

Arachidonic Acid↗

PubMed2005

Flux and turnover of fixed carbon in soil microbial biomass of limed and unlimed plots of an upland grassland ecosystem.

The influence of liming on rhizosphere microbial biomass C and incorporation of root exudates was studied in the field by in situ pulse labelling of temperate grassland vegetation with (13)CO(2) for a 3-day period. In plots that had been limed (CaCO(3) amended) annually for 3 years, incorporation into shoots and roots was, respectively, greater and lower than in unlimed plots. Analysis of chloroform-labile C demonstrated lower levels of (13)C incorporation into microbial biomass in limed soils compared to unlimed soils. The turnover of the recently assimilated (13)C compounds was faster in microbial biomass from limed than that from unlimed soils, suggesting that liming increases incorporation by microbial communities of root exudates. An exponential decay model of (13)C in total microbial biomass in limed soils indicated that the half-life of the tracer within this carbon pool was 4.7 days. Results are presented and discussed in relation to the absolute values of (13)C fixed and allocated within the plant-soil system.

Biomass↗

PubMed2006

Viscolin, a new chalcone from Viscum coloratum, inhibits human neutrophil superoxide anion and elastase release via a cAMP-dependent pathway.

The mistletoe Viscum coloratum is used in traditional Chinese medicine to treat inflammatory diseases. In this study, a cellular model in isolated human neutrophils, which are important in the pathogenesis of rheumatoid arthritis, chronic obstructive pulmonary disease, and other inflammatory diseases, was established to elucidate the anti-inflammatory functions of V. coloratum. The partially purified extract of V. coloratum (PPE-SVC) potently inhibited formyl-L-methionyl-L-leucyl-L-phenylalanine (FMLP)-induced superoxide anion generation and elastase release in a concentration-dependent manner with IC(50) values of 0.58+/-0.03 and 4.93+/-0.54 microg/ml, respectively. Furthermore, a new chalcone derivative, viscolin (4',4''-dihydroxy-2',3',6',3''-tetramethoxy-1,3-diphenylpropane), was isolated from PPE-SVC. Viscolin was demonstrated to inhibit superoxide anion generation and elastase release, as well as to accelerate resequestration of cytosolic calcium in FMLP-activated human neutrophils. Furthermore, the inhibitory effects of viscolin were reversed by protein kinase A (PKA) inhibitor, suggesting that PKA mediates the viscolin-caused inhibitions. Viscolin induced a substantial increase in cAMP levels, and that occurred through the inhibition of phosphodiesterase (PDE) activity but not an increase in adenylate cyclase function. Consistent with this, viscolin potentiated the PGE(1)-caused inhibition of superoxide anion release and calcium mobilization, as well as elevation of cAMP formation. These results demonstrate that inhibition of inflammatory responses in human neutrophils by viscolin is associated with an elevation of cellular cAMP through inhibition of PDE. Comparable results were also observed by PPE-SVC, indicating that the effect of PPE-SVC is at least partly mediated by viscolin. In summary, viscolin is a novel inhibitor of PDE and might be useful for treatment of neutrophilic inflammation.

Biphenyl Compounds↗

PubMed2004

The blocking of capacitative calcium entry by 2-aminoethyl diphenylborate (2-APB) and carboxyamidotriazole (CAI) inhibits proliferation in Hep G2 and Huh-7 human hepatoma cells.

Calcium entry is a component of the processes regulating the proliferative phenotype of some types of cancer. In non-excitable cells, capacitative calcium entry (CCE) and non-capacitative calcium entry (NCCE) are thought to be the main pathways of Ca2+ influx into cells. Thus, blocking calcium entry may prevent normal and pathological cell proliferation and there is evidence to suggest that molecules blocking calcium entry also have antiproliferative properties. Carboxyamidotriazole (CAI), a novel inhibitor of the non-voltage-dependent calcium entry has been shown to have such properties in model systems in vitro and in vivo. We used Hep G2 and Huh-7 human hepatoma cells to investigate the effects of calcium entry blockers on cell proliferation. CAI (10 microM) and 2-APB (20 microM) completely blocked CCE in thapsigargin-treated Huh-7, and CAI and 2-APB inhibited cell proliferation with IC50 of 4.5 and 43 microM, respectively. The plateau phase of the [Ca2+]i increases triggered by 10% FCS were abolished in the absence of external Ca2+ and in the presence of CAI or 2-APB. We, therefore, suggest that CCE is the main pathway involved in regulation of the processes leading to cell proliferation.

Antineoplastic Agents↗

PubMed1990

Purification and characterization of acidolysin, an acidic metalloprotease produced by Clostridium acetobutylicum ATCC 824.

Acidolysin an extracellular protease produced by Clostridium acetobutylicum ATCC 824 was purified to homogeneity by anion-exchange chromatography with a recovery of 91%. The enzyme was a monomeric protein with a molecular weight of 44,000 as estimated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and an acidic isoelectric point of 3.3. Acidolysin was very sensitive to metal-chelating agents and phosphoramidon and was unaffected by sulfhydryl reagents. It was shown to be a calcium- and zinc-containing protease. It exhibited optimal activity against Azocoll at pH 5 and 45 degrees C. It was stable at low pH and heat labile above 50 degrees C. It exhibited specificity toward peptide bonds formed by the amino group of hydrophobic amino acids (isoleucine, leucine, and phenylalanine) and its NH2-terminal amino acid sequence showed a high degree of similarity with that of Bacillus subtilis neutral metalloprotease A. Acidolysin is the first phosphoramidon-sensitive, acidic zinc metalloprotease reported.

Amino Acid Sequence↗

PubMed2004

2APB- and JTV519(K201)-sensitive micro Ca2+ waves in arrhythmogenic Purkinje cells that survive in infarcted canine heart.

OBJECTIVES/BACKGROUND: Studies from several laboratories have implicated intracellular Ca(2+) dynamics in the modulation of electrical activity. We have reported that abnormal Ca(2+) wave activity is the underlying cause of afterdepolarization-induced electrical activity in subendocardial Purkinje cells that survive in the 48-hour infarcted canine heart. These cells form the focus of arrhythmias at this time postcoronary artery occlusion. METHODS: We studied the effects of agonists and antagonists on the abnormal Ca(2+) release activity of Purkinje cell aggregates dispersed from the subendocardium 48 hours postcoronary artery occlusion (IZPCs). Studies were completed using epifluorescent microscopy of Fluo-3 loaded Purkinje cells. RESULTS: Similar to our previous report, highly frequent traveling micro Ca(2+) transients (muCaiTs) and cell-wide Ca(2+) waves were seen in IZPCs in the absence of any drug. Isoproterenol (ISO) increased muCaiTs and cell-wide Ca(2+) waves in Purkinje cells dispersed from the normal heart (NZPCs). In IZPCs, ISO increased cell-wide wave frequency but had no effect on the already highly frequent micro Ca(2+) wave transient activity, suggesting that ISO lowers the threshold of cell-wide generators responding to micro Ca(2+) transients. Drugs that block inward sodium or calcium currents (verapamil, tetrodotoxin) had no effect on Ca(2+) activity in Purkinje cells. Antagonists of intracellular Ca(2+) release channels [ryanodine, JTV519(K201)] greatly suppressed spontaneous Ca(2+) release events in IZPCs. 2APB, an agent that blocks IP(3) receptors, greatly reduced the frequency of Ca(2+) events in IZPCs. CONCLUSIONS: In arrhythmogenic Purkinje cells that survive in the infarcted heart, agents that block or inhibit intracellular Ca(2+) release channel activity reduced Ca(2+) waves and could be antiarrhythmic.

Adrenergic beta-Agonists↗

PubMed2003

Besides affecting intracellular calcium signaling, 2-APB reversibly blocks gap junctional coupling in confluent monolayers, thereby allowing measurement of single-cell membrane currents in undissociated cells.

2-aminoethoxydiphenyl borate (2-APB) has been widely used as a blocker of the IP3 receptor and TRP channels, including store-operated calcium channels. We now show in monolayers of normal rat kidney cells (NRK/49F) that 2-APB completely and reversibly blocks gap junctional intercellular communication at concentrations similar to that required for inhibition of PGF2alpha-induced increases in intracellular calcium. Gap junctional conductances between NRK cells were estimated with single-electrode patch-clamp measurements and were fully blocked by 2-APB (50 microM), when applied extracellularly but not via the patch pipette. Half maximal inhibition (IC50) of electrical coupling in NRK cells was achieved at 5.7 microM. Similar results were obtained for human embryonic kidney epithelial cells (HEK293/tsA201) with an IC50 of 10.3 microM. Using 2-APB as an electrical uncoupler of monolayer cells, we could thus measure inward rectifier potassium, L-type calcium, and calcium-dependent chloride membrane currents in confluent NRK monolayers, with properties similar to those in dissociated NRK cells in the absence of 2-APB. The electrical uncoupling action described here is a new 2-APB property that promises to provide a powerful pharmacological tool to study single-cell properties in cultured confluent monolayers and intact tissues by electrical and chemical uncoupling of the cells without the need of prior dissociation.

Animals↗

PubMed1985

Evidence for multiple sources of calcium involved on the contractile effects of agonists in the dog uterus. Influence of ovarian sexual hormones.

We compared the characteristics of Ca2+ pools involved in the contractile effect of acetylcholine (Ach), histamine (Hist), oxytocin (Oxy) and barium (Ba2+) in prepuberal untreated or estrogen plus progesterone dominated uteri. After Ca2+ (0.2 mM) withdrawal different rates of decay for cited agonists were observed. If Ca2+ concentration was increased to 2.0 mM before the Ca2+ withdrawal, the t 1/2 for Ach and Hist were markedly increased. Hormonal treatment significantly increase the rate of decay for all agonists except for Ba2+ independent of the initial Ca2+ concentration, suggesting that in this condition the tightly bound Ca2+ is absent.

Acetylcholine↗

PubMed1982

Local anaesthetics including benzyl alcohol activate the adenylate cyclase in Trypanosoma brucei by a calcium-dependent mechanism.

1. The adenylate cyclase of Trypanosoma brucei is activated by local anaesthetics. 2. Activation of adenylate cyclase by the local anaesthetic, benzyl alcohol, requires Ca2+. 3. The kinetics of the presteady state reveal that the activation step occurs prior to and is separate from the catalytic step. 4. The activation step in the presence of Ca2+ can be stimulated some 200-fold and is highly co-operative with respect to benzyl alcohol concentration. 5. The mechanism by which local anaesthetics activate may be by exposing the Ca2+ -binding site of the Ca2+ receptor which is oriented towards the hydrophobic regions of the plasma membrane in the basal state.

Adenylyl Cyclases↗

PubMed2006

The L-type calcium channel blockers, hantzsch 1,4-dihydropyridines, are not peroxyl radical-trapping, chain-breaking antioxidants.

The antioxidant properties of Hantzsch 1,4-dihydropyridine esters and two dibenzo-1,4-dihydropyridines, 9,10-dihydroacridine (DHAC) and N-methyl-9,10-dihydroacridine (N-Me-DHAC), have been explored by determining whether they retard the autoxidation of styrene or cumene at 30 degrees C. Despite a claim to the contrary [(2003) Chem. Res. Toxicol. 16, 208-215], the Hantsch esters were found to be virtually inactive as chain-breaking antioxidants (CBAs), their reactivity toward peroxyl radicals being some 5 orders of magnitude lower than that of the excellent CBA, 2,2,5,7,8-pentamethyl-6-hydroxy-chroman (PMHC). DHAC was found to be about a factor of 10 less reactive than PMHC. From kinetic measurements using DHAC, N-deuterio-DHAC, and N-Me-DHAC, it is concluded that it is the N--H hydrogen in DHAC that is abstracted by peroxyl radicals, despite the fact that in DHAC the calculated C-H bond dissociation enthalpy (BDE) is about 11 kcal/mol lower than the N-H BDE. The rates of hydrogen atom abstraction by the 2,2-diphenyl-1-picrylhydrazyl radical (dpph*) have also been determined for the same series of compounds. The trends in the peroxyl and dpph* rate constants are similar.

Acridines↗

PubMed1999

Reaction of rat connective tissue to implanted dentin tubes filled with mineral trioxide aggregate or calcium hydroxide.

This study was conducted to observe the rat subcutaneous connective tissue reaction to the implanted dentin tubes filled with calcium hydroxide or mineral trioxide aggregate. The animals were sacrificed after 7 and 30 days, and the specimens were prepared for morphological study. Some undecalcified specimens were prepared for histological analysis with polarized light and Von Kossa technique for calcium. The results were similar for both studied materials. At the tube openings, there were Von Kossa-positive granules that were birefringent to polarized light. Next to these granulations, there was an irregular tissue like a bridge that was Von Kossa-positive. The dentin walls of the tubes exhibited in the tubules a structure highly birefringent to polarized light, usually like a layer and at different depths. It is possible that the mechanism of action of both materials has some similarity.

Aluminum Compounds↗

PubMedDate not supplied

Detection of intracellular Ca2+ transients in sympathetic neurones using arsenazo III.

Changes in cytosolic calcium ion concentration ([Ca2+]i) have been implicated in a wide variety of cellular stimulus--transduction roles. In nerve cells, it is believed that electrical activity raises [Ca2+]i by allowing influx of Ca2+ through voltage-dependent channels in the surface membrane. Elevation of neuronal [Ca2+]i may also occur due to release of Ca2+ from intracellular storage sites. Transient increases in [Ca2+]i are thought to trigger neurotransmitter release, and to modulate axonal transport, energy metabolism and growth cone movement. Intracellular Ca2+ also appears to regulate membrane potassium channels and thereby to regulate electrical excitability. Although [Ca2+]i transients have been measured in a few giant invertebrate neurones, detection of such transients in a vertebrate neurone has not been previously reported. We have measured [Ca2+]i in bullfrog sympathetic neurones by photometry of a microinjected calcium indicator dye, arsenazo III (refs 14-16), and report here that action potentials and voltage-clamped depolarizations cause long-lasting increases in [Ca2+]i. Aslo, exposure to the drug theophylline can cause spontaneous periodic increases in [Ca2+]i. Comparisons of [Ca2+]i signals with simultaneous intracellular recordings of membrane potential suggest that the kinetics of the post-tetanic hyperpolarization (PTH) following a series of action potentials or the spontaneous hyperpolarizations induced by theophylline directly reflect the kinetics of the [Ca2+]i transient.

Action Potentials↗