STUDIES ON THE NEURAMINIDASE OF INFLUENZA VIRUS. II. ADDITIONAL PROPERTIES OF THE ENZYMES FROM THE ASIAN AND PR 8 STRAINS.
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Calcium↗
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Estrogen and bisphenol A disrupt spontaneous [Ca(2+)](i) oscillations in mouse oocytes.
The present work aims to study the effects of estrogen or endocrine disrupters (EDs) on the dynamic changes in intracellular Ca(2+) concentration of mouse immature oocytes (IOs) loaded with Ca(2+)-sensitive dye Fura-2 using an image analyzer. The majority of IOs isolated from the ovary exhibited spontaneous Ca(2+) oscillations at regular intervals. Entry of external Ca(2+), probably through gap junctions, contributes to Ca(2+) oscillations since they were reversibly inhibited by removing Ca(2+) from the bathing medium or by the application of a gap-junction inhibitor carbenoxolone (CBX, 30 microM). Both 17beta-estradiol (E2) and E2-BSA, a membrane impermeable estrogen, shortened the duration of Ca(2+) oscillations in a dose-dependent manner (1-1000 nM), and produced an irregular pattern of the oscillations, strongly suggesting that E2 acts on the plasma membrane of the oocyte. For bisphenol A (BPA), one of the estrogen-mimicking EDs, a 10,000-fold higher concentration (100 microM) was necessary to exert similar inhibitory action to that of E2.
Animals↗
Honokiol and magnolol induce Ca2+ mobilization in rat cortical neurons and human neuroblastoma SH-SY5Y cells.
We examined the intracellular Ca(2+) response in primary cultured rat cortical neurons and human neuroblastoma SH-SY5Y cells by Fluo 3 fluorescence imaging analysis. In these two kinds of neuronal cells, honokiol and magnolol increased cytoplasmic free Ca(2+) with a characteristic lag phase. The cytoplasmic free Ca(2+) increase was independent of extracellular Ca(2+), but dependent on activation of phospholipase C and inositol 1,4,5-triphosphate (IP(3)) receptors. These results suggest that honokiol and magnolol increase cytoplasmic free Ca(2+) through a phospholipase C-mediated pathway, and that the release of Ca(2+) from intracellular stores mainly contributes to the increase in cytoplasmic free Ca(2+). Thus, honokiol and magnolol may be involved in a new activation mechanism closely associated with intracellular Ca(2+) mobilization.
Animals↗
Effect of wood ash treatment on improving the fermentability of wood hydrolysate.
Softwood hydrolysates were overlimed with wood ash to improve the fermentability of hydrolysates. It could be demonstrated in fermentation tests that wood ash treatment increases fermentability compared to the hydrolysates untreated and treated with alkaline compounds such as Ca(OH)(2), NaOH, and KOH, which are commonly used for overliming. The enhanced fermentability of the hydrolysate treated with wood ash is due to the reduction of the inhibitors of the fermentation such as furan and phenolic compounds and to nutrient effects of some inorganic components from the wood ash on the fermentation.
Bioreactors↗
Bethanechol inhibition of chicken intestinal brush border Na/H exchange: role of protein kinase C and other calcium-dependent processes.
Bethanechol, a muscarinic agonist, inhibits the initial rate of amiloride-sensitive Na uptake by intact mucosa of avian small intestine as well as by isolated chicken villus enterocytes, an effect that is maximal at 90 seconds and reverses by 6 minutes. Bethanechol similarly decreases intracellular pH in isolated cells suspended in bicarbonate-free buffer in a time course similar to inhibition of enterocyte Na uptake, suggesting inhibition of Na/H exchange. In brush border membrane vesicles rapidly prepared from cells stimulated with bethanechol, proton-dependent 22Na uptake is transiently inhibited in a time course similar to inhibition of cell Na uptake. Bethanechol also stimulates transient translocation of protein kinase C from the cytosol to the particulate fraction, a portion of this activity translocating to the brush border membrane. To determine the calcium dependence of bethanechol's action, enterocytes were loaded with varying concentrations of the calcium buffering agent quin-2. Inhibition of cell Na uptake by the calcium ionophore ionomycin could be completely reversed by quin-2 buffering in a concentration-dependent manner. In contrast, quin-2 buffering had little or no effect on the inhibition of Na uptake caused by the protein kinase C activators phorbol esters and oleoylacetylglycerol. Bethanechol's inhibitory effects were partially, but not completely reversed by quin-2 buffering. These data suggest that the effects of bethanechol on chicken villus enterocyte brush border Na/H exchange are mediated by calcium-dependent process(es) as well as by protein kinase C.
Animals↗
Hypoxia alters the subcellular distribution of protein kinase C isoforms in neonatal rat ventricular myocytes.
Cardiac myocytes coexpress multiple protein kinase C (PKC) isoforms which likely play distinct roles in signaling pathways leading to changes in contractility, hypertrophy, and ischemic preconditioning. Although PKC has been reported to be activated during myocardial ischemia, the effect of ischemia/hypoxia on individual PKC isoforms has not been determined. This study examines the effect of hypoxia on the subcellular distribution of individual PKC isoforms in cultured neonatal rat ventricular myocytes. Hypoxia induces the redistribution of PKC alpha and PKC epsilon from the soluble to the particulate compartment. This effect (which is presumed to represent activation of PKC alpha and PKC epsilon) is detectable by 1 h, sustained for up to 24 h, and reversible within 1 h of reoxygenation. Inhibition of phospholipase C with tricyclodecan-9-yl-xanthogenate (D609) prevents the hypoxia-induced redistribution of PKC alpha and PKC epsilon, whereas chelation of intracellular calcium with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA) blocks the redistribution of PKC alpha, but not PKC epsilon; D609 and BAPTA do not influence the partitioning of PKC alpha and PKC epsilon in normoxic myocytes. Hypoxia, in contrast, decreases the membrane association of PKC delta via a mechanism that is distinct from the hypoxia-induced translocation/activation of PKC alpha/PKC epsilon, since the response is slower in onset, slowly reversible upon reoxygenation, and not blocked by D609 or BAPTA. The hypoxia-induced shift of PKC delta to the soluble compartment does not prevent subsequent 4-beta phorbol 12-myristate-13-acetate-dependent translocation/activation of PKC delta. Hypoxia does not alter the abundance of any PKC isoform nor does it alter the subcellular distribution of PKC lambda. The selective hypoxia-induced activation of PKC isoforms through a pathway involving phospholipase C (PKC alpha/PKC epsilon) and intracellular calcium (PKC alpha) may critically influence cardiac myocyte contractility, gene expression, and/or tolerance to ischemia.
Animals↗
Enantiomeric resolution of the calcium channel antagonist 8-benzylamino-8,11-oxapentacyclo[5.4.0.0(2,6).0(3,10).0(5,9)]unde cane (NGP 1-01).
We report the enantiomeric resolution and results of studies designed to probe possible enantiospecific calcium channel activity of 8-benzylamino-8,11-oxapentacyclo[5.4.0.0(2,6).0(3,10).0(5,9)]undec ane (NGP 1-01), a known polycyclic benzylamino calcium channel antagonist. R-(-)-acetylmandeloylchloride was used to generate the two diastereomers which were separated by conventional column-chromatography. Hydrolysis of the separated amide diastereomers was achieved in 10% oxalic acid/dichloromethane with silica gel as catalyst and yielded the resolved enantiomers of NGP 1-01. Enantiomeric purity was assessed by in situ derivatization of the individual enantiomers with 2,3,4,6-tetra-O-acetyl-beta-D-glucopyranosyl isothiocyanate (TAGIT) and HPLC analysis. A standard C18 column was used and the enantiomeric purity was found to be 98.5% and 96.63% for the (+)- and (-)-enantiomer, respectively. The enantiomers exhibited similar activity profiles, for calcium channel antagonism and also did not differ from the racemic mixture, suggesting that NGP 1-01 has very weak or no stereo-selectivity in the calcium channel assay used.
Animals↗
Fc epsilon RI-mediated chloride uptake by rat mast cells: modulation by chloride transport inhibitors in relation to histamine secretion.
1. We have examined the role of extracellular chloride in the mast cell secretion process. The immunologically-directed ligand, antibody to IgE (anti-IgE) required extracellular chloride ions for optimum secretion from rat peritoneal mast cells. In contrast, replacement of extracellular chloride did not alter the mast cell secretory response to compound 48/80, calcium ionophore A23187 or substance P. 2. Anti-IgE-stimulation of mast cells evoked a significant uptake of chloride ions compared to non-stimulated cells. The magnitude of chloride uptake correlated with the magnitude of stimulated histamine secretion. 3. Compound 48/80, substance P and A23187 did not alter the rate of chloride ion uptake, although these agents caused significant histamine secretion. 4. The Na+/K+/2Cl- cotransport inhibitor, furosemide, reduced the rate of anti-IgE-stimulated chloride uptake at a relatively high concentration (700 microM). However, the more potent Na+/K+/2Cl- cotransport inhibitors, bumetanide (100 microM) and piretanide (100 microM) had no effect on the stimulated chloride uptake. 5. Furosemide inhibited anti-IgE-induced histamine secretion, bumetanide potentiated the response and piretanide had no effect. This suggests that their respective action on histamine secretion are unrelated to inhibition of the Na+/K+/2Cl- carrier. 6. The chloride channel blocker, 5-nitro-2-((3-phenylpropyl)-amino)-benzoic acid (NPPB), reduced both anti-IgE-stimulated chloride uptake and the corresponding histamine secretion in a dose-dependent manner. The magnitude of the inhibitory action of the drug on these two cellular processes was comparable, implying that chloride channel activity is related to the mechanism of histamine secretion. 7. It is concluded that chloride uptake has a role in the control of Fc epsilon RI-mediated histamine secretion from rodent mast cells.
Animals↗
Binding of a calcium antagonist, [3H]nitrendipine, to high affinity sites in bovine aortic smooth muscle and canine cardiac membranes.
[(3)H]Nitrendipine, a potent calcium channel antagonist [3-ethyl-5-methyl-1-1,4-dihydro-2,6 - dimethyl - 4 - (3 - nitrophenyl) - 3,5 - pyridine carboxylate], was used to label high affinity binding sites on membranes prepared from bovine aortic smooth muscle. The binding of [(3)H]nitrendipine is rapid (t(1/2) < 5 min) and reversible at 37 degrees C. The binding sites have a high affinity for [(3)H]nitrendipine with an equilibrium dissociation constant of 2.1 nM. The density of sites is 40-60 fmol/mg of membrane protein. Analogues of nitrendipine compete for the binding sites with affinities consistent with their known biological effects as calcium antagonists. Nisoldipine, [isobutyl methyl 1,4-dihydro-2,6-dimethyl-4-(2-nitrophenyl)-3,5-pyridine carboxylate], a calcium antagonist more potent than nifedipine [2,6-dimethyl-3,5-dicarbomethoxy-4-(2-nitrophenyl)-1,4-dihydropyridine] in relaxing vascular smooth muscle, has an affinity three-fold higher than that of nifedipine in competing for the binding sites. A biologically inactive derivative of nifedipine does not compete for [(3)H]nitrendipine binding. Verapamil (alpha-isopropyl-alpha[(N-methyl - N-homoveratryl) -alpha-aminopropyl]-3,4-dimethyoxyphenyl acetonitrile), a structurally different calcium antagonist, only partially (25%) inhibits binding at high concentrations (1 muM). Prazosin, an alpha adrenergic antagonist does not compete for [(3)H]nitrendipine binding sites. The binding of [(3)H]nitrendipine is not affected by 1.5 mM calcium. Canine cardiac membranes also have high affinity [(3)H]nitrendipine binding sites, (K(D) = 6 nM) but bovine erythrocytes do not. The relative affinities of nisoldipine and nifedipine for the cardiac membrane binding sites reflect the relative activities of these compounds as calcium channel antagonists. These results suggest that the [(3)H]nitrendipine binding sites are the sites through which dihydropyridines act as calcium channel antagonists.
Animals↗
Relationship of intracellular calcium and oxygen radicals to Cisplatin-related renal cell injury.
We investigated the involvement of reactive oxygen species (ROS) and intracellular calcium in nephrotoxicity related to an antitumor agent, cisplatin. In this study, we employed cultured renal epithelial cells (LLC-PK1). Cisplatin at 500 microM significantly increased the production of ROS 5 h and caused cell injury. This agent significantly increased the intracellular calcium level ([Ca2+]i) in a dose-dependent manner 1 h or more after exposure. DPPD (N,N'-diphenyl-p-phenylenediamine), an antioxidant, inhibited a cisplatin-related increase in active oxygen production and cell injury but did not inhibit an early increase in the [Ca2+]i level. An intracellular calcium-chelating compound BAPTA-AM (1,2-bis(O-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid tetra(acetoxymethyl) ester) inhibited an increase in ROS production and cell injury induced by cisplatin. Furthermore, BAPTA-AM suppressed the rise of [Ca2+]i level in 1 h after exposure; however, an extracellular calcium chelator EGTA and a calcium antagonist nicardipine did not inhibit the rise in [Ca2+]i level in the early phase. An NADPH oxidase inhibitor inhibited a cisplatin-related increase in ROS production and cell disorder. These results suggest that cisplatin-related calcium release from the site of intracellular calcium storage in the early phase causes oxidative stress in renal tubular epithelial cells. Cisplatin may increase the intracellular production of ROS via NADPH oxidase.
Animals↗
Subsurface demineralization in dental enamel and other permeable solids during acid dissolution.
Subsurface demineralization of dental enamel during acid dissolution has been reported many times, but its cause remains obscure. At first, the phenomenon was thought to result from the physical structure of enamel. More recent studies have shown that subsurface demineralization occurs in other permeable solids, indicating that there must be more fundamental factors involved in this curious effect. In order for this phenomenon to be investigated, dissolution experiments were carried out by means of real-time scanning microradiography in various systems, including enamel, or aggregates of hydroxyapatite (calcium, strontium, or barium), or hydroxides (calcium or magnesium). These were chosen to discriminate between effects of structure and composition. It was found that it was not possible for the demineralization observed in these systems to be attributed to a common feature. From this, it is concluded that subsurface demineralization in enamel and other mineralized tissues should not be ascribed to a single cause.
Acetates↗
Electroporation loading and photoactivation of caged InsP3: tools to investigate the relation between cellular ATP release in response to intracellular InsP3 elevation.
Photolytic liberation of InsP(3) in single cells triggers cell-to-cell propagating calcium changes that are communicated by a gap junctional and a paracrine purinergic pathway involving InsP(3)-triggered ATP release. We investigated the relation between the InsP(3) stimulus and the resulting ATP release in ECV304 cells using UV photolysis of caged compounds and bioluminescent ATP measurements. Careful consideration of all steps, starting from caged InsP(3) loading into the cells by electroporation, up to photoliberation upon UV exposure, allowed to derive a dose-response relation that revealed a first part with a flattening ATP release response in the below 10microM InsP(3) concentration range and a second phase of steeply increasing ATP release in response to above 10microM InsP(3) stimulation. ATP release triggered by below 10microM InsP(3) concentrations attained a level in the order of 30% above baseline ATP release, while the steeply increasing response to high InsP(3) concentrations attained values in the order of 150% above baseline. Our data indicate the involvement of low affinity InsP(3) receptor sites in the pathway leading to triggered ATP release, with activation of these receptors causing the release of 1-2% of the total cellular ATP pool.
Adenosine Triphosphate↗
Dry soda lime markedly degrades sevoflurane during simulated inhalation induction.
We have investigated gas composition during simulated inhalation induction with sevoflurane to elucidate possible mechanisms of incidental prolonged induction times and airway irritation. Using a circle system, 8% sevoflurane in oxygen 6 litre min-1 was washed into an absorbing canister filled with fresh soda lime containing 2.9% KOH (Draegersorb, 'D') or no KOH (< 0.01%, Sofnolime, 'S'). The absorbent was dried by oxygen 20,000 litre before every second experiment. Maximum soda lime temperatures attained after 4-6 min were 107 degrees C using dry D and 62 degrees C (61 degrees C) with dry S. Temperature did not increase with fresh soda lime. With dry soda lime, sevoflurane was not detected at the T-piece for 3 min and reached 6-7% within 6-10 min. After 1 min, we detected methanol and compound A (CH2F-O-C(= CF2) (CF3)). Total amounts over 20 min were: methanol 1125 mg (D dry), 334 mg (S dry) and < 5 mg (fresh soda lime); compound A 148 mg (D dry), 13 mg (S dry) and 3-8 mg (fresh); and fluoride 8.5 mg (D dry), 3.3 mg (S dry) and 1 mg (fresh). Formaldehyde was detected only with dry lime (D > 2.5 mg, S > 0.6 mg). In summary, the use of moist soda lime is of crucial importance during inhalation induction. With dry soda lime, the patient may inhale potentially toxic degradation products in significant amounts. Sevoflurane degradation is aggravated by a high KOH content of the lime. The observed airway irritation may be caused by formic acid, which is generated in isomolar concentrations with methanol (Cannizzaro reaction). The amount of compound A found with dry KOH-containing lime is unlikely to be noxious.
Anesthesia, Closed-Circuit↗
Protection of TRPC7 cation channels from calcium inhibition by closely associated SERCA pumps.
Numerous studies have demonstrated that members of the transient receptor potential (TRP) superfamily of channels are involved in regulated Ca2+ entry. Additionally, most Ca2+-permeable channels are themselves regulated by Ca2+, often in complex ways. In the current study, we have investigated the regulation of TRPC7, a channel known to be potentially activated by both store-operated mechanisms and non-store-operated mechanisms involving diacylglycerols. Surprisingly, we found that activation of TRPC7 channels by diacylglycerol was blocked by the SERCA pump inhibitor thapsigargin. The structurally related channel, TRPC3, was similarly inhibited. This effect depended on extracellular calcium and on the driving force for Ca2+ entry. The inhibition is not due to calcium entry through store-operated channels but rather results from calcium entry through TRPC7 channels themselves. The effect of thapsigargin was prevented by inhibition of calmodulin and was mimicked by pharmacological disruption of the actin cytoskeleton. Our results suggest the presence of a novel mechanism involving negative regulation of TRPC channels by calcium entering through the channels. Under physiological conditions, this negative feedback by calcium is attenuated by the presence of closely associated SERCA pumps.
Adenosine Triphosphate↗
Histological and scanning electron microscopy assessment of various vital pulp-therapy materials.
Pulp capping and pulpotomy procedures were performed on 15 male mongrel dogs. Three materials were used: calcium hydroxide, acid-etched dentin bonding, and mineral trioxide aggregate. Six of the animals were killed at 50 days and nine were killed at 150 days. Samples from 11 dogs were used for histological evaluation, and the remaining dog samples were used for scanning electron microscopy evaluation. Each slide was graded histologically according to previously published criteria. Scanning electron microscopy analysis was performed, and the weight percentage of elements found in the dentin of a nontreated tooth versus the bridge formed in the exposed specimen was established. By evaluating pulp inflammation in vital pulp-therapy treatments, it was found that mineral trioxide aggregate was not significantly different from the untreated control group, both in pulp-capping procedures at 50 days (p = 0.357) or 150 days (p = 0.198) and pulpotomy procedures at 50 days (p = 0.357) or 150 days (p = 0.198). Moreover, histologically mineral trioxide aggregate was a considerably better material than calcium hydroxide or acid-etched dentin bonding in maintaining the integrity of the pulp.
Aluminum Compounds↗
A new colorimetric method for the measurement of serum calcium using a zinc-zincon indicator.
A new method is described for the measurement of serum calcium. Calcium in the sample displaces zinc from an EGTA complex, the zinc then forming a blue-coloured complex with a zincon indicator. The method is rapid, sensitive and linear; it may be applied directly to serum and is readily automated. No compound tested gave rise to any interference at physiological concentration, although excessive haemolysis leads to low results being obtained. To avoid interference from endogenous zinc a serum blank is required for each sample; this also avoids errors introduced by turbidity of the sample. The results obtained correlate well with atomic absorption spectroscopy (r = 0.935, y = 1.12x-0.28, n = 68).
Azo Compounds↗
[Calcium antagonism by papaverine in isolated rat gastric fundus strips in a model system].
Examining isolated strips of gastric fundus tissue of rats the authors observed that papaverin up to 7.8 X 10(-8) to 6.25 X 10(-7) mol/l increased the intensity of convulsions induced by constant amounts of barium chloride (9.5 X 10(-4); with further increase of the concentration the intensity of convulsions gradually sank under the initial value. An increased proneness to cramping was also observed when the calcium content of the Tyrode solution was reduced. In this case the proneness to cramping was highest between 1 and 1.3 mmol/l calcium content. When the calcium content was 1 mmol/l, papaverin increased the proneness to cramping only to a smaller degree, in agreement with the effect measured when the calcium content of the organ bath was reduced below 1 mmol/l. In model experiments, calcium antagonized the potential difference-increasing effect of papaverin at the ether/NaCl (0.1 mol/l) phase boundary. From this the authors infer an interaction (complex formation) between papaverin and calcium at the phase boundary, which is independent of the biological medium. Their findings and the papaverin -calcium antagonism first observed by Benigni [2] can be interpreted in this way.
Animals↗
Removal of terephthalic acid in alkalized wastewater by ferric chloride.
Terephthalic acid, which is a main component in alkali-decrement wastewater, is efficiently removed using ferric chloride in high pH solutions. About 90% removal of terephthalic acid is achieved at pH between 8 and 11. Especially, the removal reached 94.3% at pH 11. However, as the pH increased from pH 12 and 13, the low removal of terephthalic acid were found. The increasing ferric chloride dosage had a dramatic positive impact on the achieved removal of terephthalic acid. Further increase in the ferric chloride dosage did not produce better removal rate. The increase of terephthalic acid concentration also led to the increase of ferric chloride dosage in order to get the same removal of terephthalic acid. There was approximately a negative linear relationship between terephthalic acid concentration and removal of terephthalic acid. Compared with other coagulants, it can be seen that ferric chloride is more effective in a high pH solution and the amount of ferric chloride required is also less as compared with aluminum chloride, magnesium chloride and calcium chloride. Our results clearly showed that terephthalate anions strongly binds to positive Fe(OH)(3) flocs and forms insoluble complexes, probably through a mechanism involving electrostatic attraction. The electrostatic attraction may be particularly useful means of purifying wastewater in high pH solutions.
Adsorption↗