Production of experimental encephalomyelitis with calcium acetate compound extracted from brain tissue.
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Acetates↗
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Multiple types of sensory neurons respond to irritating volatile organic compounds (VOCs): calcium fluorimetry of trigeminal ganglion neurons.
Many volatile organic compounds (VOCs) are significant environmental irritants that stimulate somatosensory nerve endings to produce pain and irritation. We measured intracellular calcium in cultured trigeminal ganglion neurons to characterize the cellular mechanisms and chemical structural determinants underlying sensitivity to VOCs. Trigeminal neurons responded to homologous series of alcohols (C4-C7) as well as saturated and unsaturated aldehydes in a concentration dependent manner. Ranked in terms of threshold to recruit neurons by compounds of the same carbon chain length, enaldehyde<aldehyde<alcohol. Unlike aldehydes and alcohols that displayed ascending concentration curves, recruitment of neurons by enaldehydes (C4-C7) appeared to saturate, consistent with a mechanism that is restricted in its neural distribution. Using pentanol, pentanal and pentenal as model compounds, we found that many but not all cool/cold-sensitive and capsaicin-sensitive neurons responded with increases in intracellular calcium. These VOCs also stimulated other neurons that were insensitive to cooling and capsaicin. Because not all cooling- and all capsaicin-sensitive neurons responded to the model VOCs, it is highly unlikely that known nociceptive ion channels such as TRPV1 or TRPA1 mediate sensitivity to these compounds. For pentanol, pentanal and pentenal, induced calcium influx was dependent on the presence of extracellular calcium. Responses of all neurons to pentanal and pentenal were also dependent upon extracellular sodium. Responses to pentanol were variably dependent on sodium. The distribution of sensitivity suggests that VOC irritation may be mediated by an as yet unidentified mechanism(s) that is/are distributed across different modalities of neurons.
Aldehydes↗
Interactions between calcium channel compounds and adenosine systems in brain of rat.
A number of organic ligands of calcium channels were investigated for possible actions on several aspects of adenosine systems in the cerebral cortex of rat. The principle findings of the present study were that a number of antagonists of calcium channels and the agonist compound Bay K 8644 inhibited binding to adenosine receptors, binding to nucleoside transporters, and the accumulation of [3H]adenosine with a low microM potency. 2-Nitrophenyl dihydropyridine derivatives were more potent than 3-nitrophenyl dihydropyridine or non-dihydropyridine ligands of calcium channels at inhibiting binding to adenosine receptors. Dihydropyridine ligands of calcium channels were more potent than non-dihydropyridine ligands of calcium channel in inhibiting the binding of [3H]nitrobenzylthioinosine to cortical membranes or inhibiting the accumulation of [3H]adenosine into synaptoneurosomes. However, unlike the case of adenosine receptors, no distinction between 2-nitrophenyl and 3-nitrophenyl dihydropyridine derivatives was observed. In addition, the non-dihydropyridine ligand of calcium channels, diltiazem was a weak inhibitor of the accumulation of [3H]adenosine. These results demonstrate that organic ligands of calcium channels, particularly dihydropyridine compounds, can interact with several aspects of adenosine systems.
Adenosine↗
Accumulation of technetium-99m methylene diphosphonate. Conditions affecting adsorption to hydroxyapatite.
Experiments were carried out to explore the mechanism of technetium-99m methylene diphosphonate (99mTc-MDP) adsorption with various calcium compounds including hydroxyapatite powder. 99mTc-MDP adsorption to hydroxyapatite was markedly inhibited by the addition of either pyrophosphate or methylene diphosphonate (MDP). Moreover, adsorbed 99mTc-MDP was partly removed by rinsing with pyrophosphate solution. Adsorption was pH-dependent and was inhibited by univalent cations, adenosine triphosphate solution, and guanosine triphosphate. Adsorption was most apparent to hydroxyapatite and calcium pyrophosphate and was less marked for the other calcium compounds tested. It is suggested that 99mTc-MDP adsorption is affected by the hydroxyapatite crystalline structure and environmental factors such as pH and the presence of phosphates, calcium compounds, and various cations.
Adsorption↗
Extracellular effect of calcium on compound 48/80 stimulated mast cells.
The effects of changes in the extracellular concentration of calcium on activation of rat mast cells by compound 48/80 were studied. The intracellular exchangeable Ca2+ pools at various concentrations of extracellular Ca2+ were determined by equilibration of the cells with 45Ca2+. The cells stimulated by compound 48/80 in the presence of 2.5 microM and 1.6 mM extracellular Ca2+ released comparable amounts of histamine. However, the intracellular Ca2+ pool was doubled in 2.5 microM Ca2+ and was increased sixfold in 1.6 mM Ca2+. In 14.4 mM extracellular Ca2+, there was neither release of histamine nor uptake of Ca2+ which suggested an impairment in activation. The kinetics of Ca2+ influx in the presence of 2.5 microM Ca2+ did not reveal intracellular mobilization of calcium. The cells activated in 1.6 mM Ca2+ at 0 degrees C when allowed to stand in 14.4 mM extracellular Ca2+ released decreased amounts of histamine upon warming to 37 degrees C. The inhibition of the release progressively increased with time of standing at 0 degrees C. The decrease in histamine release was not seen with the cells standing in 1.6 mM Ca2+ at 0 degrees C. The effect of 14.4 mM Ca2+ added prior to tha challenge with compound 48/80 did not depend on the time of incubation. The data presented in this paper suggest that the high concentration of Ca2+ inhibits the histamine release from mast cells by interfering with membrane-associated phenomena.
Animals↗
[Clinical investigations on the action of a compound of calcium, vitamin C and phosphorus in certain vegetative syndromes, especially in migraine].
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Ascorbic Acid↗
Proceedings: Quantification of isoproterenol-induced myocardial necroses and the protective effect of calcium-antagonistic compounds by point counting.
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Animals↗
Effect of calcium antagonist compound nisoldipine on transepithelial electrical parameters in the isolated frog cornea.
The new calcium antagonist, nisoldipine, inhibited short circuit current and transcorneal potential difference in the isolated frog cornea (a chloride transporting epithelium). Transepithelial resistance increased. The effects of nisoldipine were dose-dependent. Nisoldipine did not change the stimulation of short circuit current induced by epinephrine. Intracellular membrane potential across both the apical and basolateral cell membrane were decreased by nisoldipine. The data indicate that intracellular calcium seemed to modulate chloride transport of the cornea by changing cell membrane permeability.
Animals↗
Comparison of two hydrated sodium calcium aluminosilicate compounds to experimentally protect growing barrows from aflatoxicosis.
Two formulations of hydrated sodium calcium aluminosilicate (HSCAS-1 and HSCAS-3), anti-caking agents for mixed feed, were added to the diets of growing barrows and were evaluated for their potential to diminish the clinical signs of aflatoxicosis. The experimental design consisted of 8 barrows (2 replicates of 4 each/treatment) assigned to 1 of the following 6 treatment diets (total of 48): 1) 0 g of HSCAS-1 or HSCAS-3 and 0 mg of aflatoxin (AF)/kg of feed (control); 2) 5 g HSCAS-1/kg of feed; 3) 5 g HSCAS-3/kg of feed; 4) 3 mg AF/kg of feed; 5) 3 mg AF plus 5 g HSCAS-1/kg of feed; or 6) 3 mg AF plus 5 g HSCAS-3/kg of feed. Barrows were maintained in indoor concrete-floored pens, with feed and water available for 28 days (from 8 to 12 weeks of age). Barrows were observed twice daily and weighed weekly, and blood samples were collected at day 28 for hematologic, immunologic, and serum biochemical measurements. At the termination of the study, barrows were euthanized and necropsied. Barrow body weight gains were diminished, compared to those of controls, by consumption of AF alone and both of the AF plus HSCAS diets; however, the AF plus HSCAS-1 and AF plus HSCAS-3 barrow body weight gains were significantly greater (P < 0.05) than those of the AF-alone barrows.(ABSTRACT TRUNCATED AT 250 WORDS)
Aflatoxins↗
Influence of some lysosomotropic compounds on calcium ion desorption process from liposome membrane.
The effect of a group of model lysosomotropic compounds on the process of Ca2+ ion desorption from lecithin liposome membranes was studied. The compounds studied were: hydrochlorides of fatty acids 2-dimethylaminoethyl esters (DM-n) for n = 9, 11, 13 and 15 carbon atoms in the fatty acid alkyl chain and methochloride of 2-dimethylaminoethyl laurate (DMS-11). It was found that all the compounds studied caused increased desorption with increasing concentration of the compound. Most effective was the quaternary ammonium salt, DMS-11. Moreover, it was found that the process of Ca2+ desorption from the membrane depended on pH of the medium. Compound DM-11 was more active at pH 8 than at pH 5. The action of DM-n compounds depended on the alkyl chain length, DM-11 and DM-13 being the most active. Apparently free amines penetrate the phospholipid membranes and incorporate into its hydrophobic core causing structural deformations. Hydrochlorides of fatty acids and the quaternary ammonium salt induce desorption of calcium ions mostly as a result of competitive electrostatic interactions. By quantum chemistry, PM3 method, and methods of molecular modelling we established the higher hydrophilicity of the polar head of DM-n series with respect to the polar head of the DMS-n compounds. DM-n compounds possess both acceptor and donor properties for hydrogen bonding while DMS-n are instrumental as acceptors only. It should be noted, that the results obtained in this paper for model membranes are in accordance with those for biological ones.
Calcium↗
Cardiovascular effects of NPK-1886, a new dihydropyridine compound with calcium entry blocking activity.
The cardiovascular effect of NPK-1886 (NPK), a novel photostable dihydropyridine compound, was studied by comparing it with that of nifedipine (Nif). In normal Wistar rats (NWR), systolic blood pressure was only slightly depressed by NPK or Nif, while in three types of hypertensive rats (i.e., spontaneously hypertensive rats (SHR), renal hypertensive rats (RHR) and DOCA-saline-induced hypertensive rats (DOC-Na-R)), the hypotensive potency of NPK was more than or equal to that of Nif. The effectiveness of NPK on the normal and hypertensive models was in the following order: DOC-Na-R, RHR, SHR, NWR. Coronary perfusion flow in Langendorff's heart was increased almost the same extent by NPK and Nif. On isolated rabbit aortic strips, the antagonistic potencies of NPK, like those of Nif, were greater for calcium than for norepinephrine, serotonin and angiotensin II. The negative ino- and chronotropic potency of NPK in isolated guinea-pig right atria was less than that of Nif. The slow membrane action potentials of guinea-pig papillary muscle were suppressed by NPK, but less than by Nif, with manifestations of a reduction of Vmax and AP-duration. These results indicate that NPK has a potent hypotensive effect on hypertensive models and a weaker cardiac inhibition. The general toxicity of NPK was lower than that of Nif.
Action Potentials↗
Organotin compounds induce calcium overload and apoptosis in PC12 cells.
We examined the effects of four tri-substituted organotin compounds on intracellular Ca2+ and survival in PC12 cells. Treatment with micromolar concentrations of tributyltin and triphenyltin caused a rapid increase in the cytosolic free Ca2+ concentration ([Ca2+]i). This was due to enhanced Ca2+ influx and release from intracellular stores. When the [Ca2+]i elevation was maintained for over 30 min, internucleosomal DNA cleavage typical of apoptotic cell death followed. In contrast, when the increase in [Ca2+]i was transient, cells did not show internucleosomal DNA cleavage and retained their viability. Triethyltin modified [Ca2+]i only slightly, whereas trimethyltin had no effect. The latter two agents did not modify cell viability. Our data suggest that the toxicity of organotins in PC12 cells is linked to their ability to promote intracellular Ca2+ overload, which triggers apoptosis.
Animals↗
Effect of lignans isolated from Hernandia nymphaeifolia on estrogenic compounds-induced calcium mobilization in human neutrophils.
The effect of five lignans isolated from Hernandia nymphaeifolia on estrogenic compounds (17beta-estradiol, tamoxifen and clomiphene)-induced Ca(2+) mobilization in human neutrophils was investigated. The five lignans were epi-yangambin, epi-magnolin, epi-aschantin, deoxypodophyllotoxin and yatein. In Ca(2+)-containing medium, the lignans (50-100 microM) inhibited 10 microM 17beta-estradiol- and 5 microM tamoxifen-induced increases in intracellular free Ca(2+) levels ([Ca(2+)](i)) without changing 25 microM clomiphene-induced [Ca(2+)](i) increase. 17beta-estradiol and tamoxifen increased [Ca(2+)](i) by causing Ca(2+) influx and Ca(2+) release because their responses were partly reduced by removing extracellular Ca(2+). In contrast, clomiphene solely induced Ca(2+) release. The effect of the lignans on these two Ca(2+) movement pathways underlying 17beta-estradiol- and tamoxifen-induced [Ca(2+)](i) increases was explored. All the lignans (50-100 microM) inhibited 10 microM 17beta-estradiol-and 5 microM tamoxifen-induced Ca(2+) release, and 17beta-estradiol-induced Ca(2+) influx. However, only 100 microM epi-aschantin was able to reduce tamoxifen-induced Ca(2+) influx while the other lignans had no effect. Collectively, this study shows that the lignans altered estrogenic compounds-induced Ca(2+) signaling in human neutrophils in a multiple manner.
Calcium↗
The effect of dietary supplementation with calcium salts on skeletal calcium in suckling rats.
This study aimed at identifying a calcium compound which could serve as an effective and safe dietary supplement in suckling rats over the period of intense growth and development. The main objective was to assess the effect of additional calcium intake on skeletal calcium in suckling pups. Suckling Wistar rats were fed using a pipettor with one of the following calcium salts from day 6 to 14 after the birth: gluconate, hydrogenphosphate, carbonate (each suspended in cow's milk), or chloride (in demineralized water). Control rats received only cow's milk. Calcium in the carcass (body without organs and skin) was analysed by atomic absorption spectrometry. The only effective dietary supplement that produced no risk for the suckling pups' growth was calcium hydrogenphosphate in cow's milk in the total amount of 340 mg. That dose increased the daily calcium intake 3 to 4 times compared to non-supplemented controls, increasing carcass calcium content by about 16 per cent. Other calcium compounds were either inefficient (carbonate) or had adverse effects on pups' growth (chloride and gluconate).
Animals↗
Impact of halogenated compounds on calcium homeostasis in hepatocytes.
Halocarbons (CCl4, 1,1-dichlorethylene) cause a wide spectrum of effects and injury in hepatocytes. One early effect of these compounds is the inhibition and destruction of the endoplasmic reticulum (ER) calcium pump. Subsequent to inhibition of this pump, the ER calcium pool is depleted and cytosolic levels of calcium are increased for a prolonged period of time. This effect of halocarbons has been characterized and is similar in vivo and in vitro. The importance of this redistribution of cell calcium in expression of halocarbon injury of hepatocytes has not been fully resolved. Several degradative enzymes (phospholipases, proteases) have been implicated as calcium-dependent mediators in toxicity. Our preliminary studies of the effect of calcium redistribution suggest that activation of a calcium-sensitive endonuclease in liver does not play a central role in initiating the lethal effect of halocarbons on hepatocytes.
Animals↗
Effect of a membrane-stabilizing compound on calcium binding to the plasma membrane of Acanthamoeba castellanii.
Binding of calcium ions at the plasma membrane was studied in Acanthamoeba cells pretreated with ZIMET 3164, a benzimidazole nitrogen mustard derivative, which is known to show a potent immunosuppressive action combined with a membrane-stabilizing effect in mice. For reference, 2 compounds were applied: ZIMET 3393 (Cytostasan¿), another benzimidazole mustard derivative, which exerts only a moderate membrane effect and acts as a strong cytostatic, and ZIMET 176/68, a barbituric acid derivative, which acts as an inhibitor of humoral immune responses but without membrane-stabilizing effect. Application of any of the 3 compounds does not reduce the appearance of calcium binding sites, visualized by means of ultracytochemical reaction, notwithstanding their different action in the mammalian organism. On the contrary, it was estimated by morphometric analysis that the number of Ca-dependent deposits was augmented after treatment with low doses of any of the 3 compounds, what seems to be connected with the induced metabolic disturbances in low molecular phosphates level. High doses and/or prolongation of treatment of the cells resulted in diminution of the number of deposits and induces profound disturbances in cell ultrastructure, probably due to the toxic action of the applied doses. In these cases, band-like structures crosslinking the two leaflets of the plasma membrane may be observed; it is suggested that they represent integral membrane proteins.
Amoeba↗
Effects of drug serum of anti-fibrosis I herbal compound on calcium in hepatic stellate cell and its molecular mechanism.
AIM: To investigate the effects of anti-fibrosis I herbal compound on intracellular Ca(2+) in activated hepatic stellate cell (HSC) and to try to survey its molecular mechanism in treatment and prevention of hepatic fibrosis and portal hypertension. METHODS: The activated HSC line was plated on small glass cover slips in 24 wells culture dishes at a density of 5X10(6) /mL, and incubated in RPMI-1640 media for 24 h. After the cells were loaded with Fluo-3/AM, intracellular Ca(2+) was measured with laser scanning confocal microscopy (LSCM). The dynamic changes of intracellular Ca(2+), stimulated by carbon tetrachloride, TGF-beta(1) antibody and the drug serum of anti-fibrosis I herbal compound and under orthogonal design were determined by LSCM. The effect of anti-fibrosis I herbal compound on intracellular Ca(2+) was observed before and after the addition of TGF-(1) antibody. RESULTS: The intracellular Ca(2+) were significantly different in different dosage of carbon tetrachloride anti-fibrosis I formula drug serum, TGF-beta(1) antibody and different turn of these substance, but their interval time between CCl(4) and TGF-beta(1) antibody, CCl(4) and anti-fibrosis I drug serum had no influence on intracellular Ca(2+). The result showed intracellular Ca(2+) wasn't significantly different between rat serum without anti-fibrosis I and untreated group. After carbon tetrachloride stimulation, intracellular Ca(2+) of activated HSC increased significantly when the dosage of CCl(4) from 5 to 15 mmol/L, however, decreased significantly after stimulation by 5-20 microg/mL TGF-beta(1) antibody or 5-20 mL/L drug serum. Moreover, before and after the addition of TGF-beta(1) antibody, intracellular Ca(2+) was significantly different. These results suggested that the molecular mechanism was independent of blocking TGF-beta(1) effects. CONCLUSION: Anti-fibrosis I herbal compound may treat hepatic fibrosis and decrease portal hypertension by inhibiting activated HSC contractility through decrease of intracellular Ca(2+).
Animals↗
Different mechanisms for suppression of apoptosis by cytokines and calcium mobilizing compounds.
Overexpression of wild-type p53 in M1 myeloid leukemia cells induces apoptotic cell death that was suppressed by the calcium ionophore A23187 and the calcium ATPase inhibitor thapsigargin (TG). This suppression of apoptosis by A23187 or TG was associated with suppression of caspase activation but not with suppression of wild-type-p53-induced expression of WAF-1, mdm-2, or FAS. In contrast to suppression of apoptosis by the cytokines interleukin 6 (IL-6) and interferon gamma, a protease inhibitor, or an antioxidant, suppression of apoptosis by A23187 or TG required extracellular Ca2+ and was specifically abolished by the calcineurin inhibitor cyclosporin A. IL-6 induced immediate early activation of junB and zif/268 (Egr-1) but A23187 and TG did not. A23187 and TG also suppressed induction of apoptosis by doxorubicin or vincristine in M1 cells that did not express p53 by a cyclosporin A-sensitive mechanism. Suppression of apoptosis by A23187 or TG was not associated with autocrine production of IL-6. Apoptosis induced in IL-6-primed M1 cells after IL-6 withdrawal was not suppressed by A23187 or TG but was suppressed by the cytokines IL-6, IL-3, or interferon gamma. The results indicate that these Ca2+-mobilizing compounds can suppress some pathways of apoptosis suppressed by cytokines but do so by a different mechanism.
Animals↗