Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: CAS:7440-70-2 (calcium)
 333,191 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Calsequestrin is a Ca2+ binding protein expressed by a few cell types (mostly muscle fibers). In these cells the distribution of the protein is within the endoplasmic/sarcoplasmic reticulum, however, not uniformly throughout but at discrete sites of the lumen. In order to investigate the mechanisms of this unusual intracellular distribution together with the possible functions of the protein, we have studied stable transfected clones of epithelial HeLa cells. Treatment of these cells with butyric acid induced a rapid (24 h) and massive (approx. 10-fold) increase of the transfected protein, whereas the other lumenal and membrane proteins of the endoplasmic reticulum were either modified slightly or unchanged. When butyric acid treatment was interrupted the calsequestrin levels returned rapidly (within 24 h) to the pre-treatment level. Such a rapid turnover was due in part to secretion, sustained by both spontaneous and Ca(2+)-dependent release of calsequestrin to the extracellular medium. From the physiological point of view, the transfected cells exhibited only moderate increases of the Ca2+ release responses triggered by either ATP (a ligand addressed to the P2u receptor and working through IP3 generation) or thapsigargin (a blocker of the endoplasmic reticulum Ca2+ ATPase), with no further increase after butyric acid induction of calsequestrin. This result appears to correlate with the occurrence of only small amounts of calsequestrin within the endoplasmic reticulum lumen of all transfected cells. The bulk of calsequestrin, in contrast, was found sequestered within large vacuoles distributed both near the cell surface and, after butyric acid treatment, also in the deep cytoplasm. These vacuoles (possibly a lysosomal subcompartment) appear to contain no Ca2+ as no difference in 45Ca release from transfected cells was observed without or with butyric acid pretreatment when exposed to ionomycin, alone or combined with monensin. We conclude that HeLa cells possess no adequate mechanisms to keep calsequestrin in its physiologically relevant location, the endoplasmic reticulum. In the transfected cell the protein seems therefore to be diverted (possibly by default) to vacuoles destined to be rapidly eliminated by the cell.
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PMID:Expression of muscle calsequestrin in epithelial HeLa cells: distribution and functional role. 791 67

1. Weak excitation to rat hippocampal CA1 neurons via Schaffer collaterals at a frequency of 0.1 or 0.2 Hz accompanied by repeated brief exposures to the inhibitory transmitter gamma-amino-butyric acid (GABA) causes a long-term depression (LTD, up to 90% of the control) of the stimulated pathway. This depression can be reversed by high-frequency stimulation. 2. Although inhibition is necessary for the induction of this LTD, the depression can be produced with either the GABAA or the GABAB receptor agonists. 3. This conjunctive LTD could not be blocked by the N-methyl-D-aspartate receptor antagonist, 2-amino-5-phosphonovaleric acid. 4. It was, however, blocked by the metabotropic glutamate receptor antagonist L-2-amino-3-phosphonopropionic acid and (RS)-alpha-methyl-4-carboxyphenylglycine, indicating that activation of a metabotropic glutamate receptor is necessary for the LTD. Induction also appeared to require an intracellular Ca2+ increase. 5. Because GABAergic inhibition often modulates glutamatergic transmission in the brain, we propose that this form of synaptic modification is of potential importance for neural plasticity.
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PMID:Weak excitation and simultaneous inhibition induce long-term depression in hippocampal CA1 neurons. 803 37

We studied the effect of fatty acids and their acyl-CoA esters on protein kinase C (PK-C) activity in human skin fibroblasts. Butyrate, octanoate, palmitate and oleate did not alter PK-C activity in either cytosolic or particulate fraction. In the presence of calcium, phosphatidylserine and diacylglycerol, both palmitoyl-CoA (Pal-CoA) and oleoyl-CoA (Ole-CoA) enhanced particulate PK-C activity by approx. 70% and octanoyl-CoA (Oct-CoA) by approx. 35%. Partially purified cytosolic PK-C activity was enhanced by 60-70% by 13.5 microM of either Pal-CoA or Ole-CoA. Basal histone phosphorylation (i.e., PK-C-independent phosphorylation) was decreased in the particulate fraction in the presence of these esters in a concentration-dependent manner. Both Pal-CoA and Ole-CoA fully substituted diacylglycerol in activating the kinase in both the cytosolic and particulate fractions, whereas Oct-CoA had a moderate effect. The pattern of endogenous cytosolic and particulate protein phosphorylation was altered in the presence of either Pal-CoA or Ole-CoA. We conclude that long-chain fatty acyl-CoA esters may activate PK-C in non-stimulated fibroblasts, i.e., in the absence of physiological diacylglycerol formation. Activation of PK-C in stimulated fibroblasts, i.e., in the presence of an elevated diacylglycerol concentration, is less pronounced. These results support the hypothesis that activation of PK-C and alteration of endogenous protein phosphorylation may play a role in the pathogenesis of diseases in which there is intracellular accumulation of fatty acyl-CoA esters, such as in inborn fatty-acid oxidation defects.
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PMID:Effect of fatty acids and their acyl-CoA esters on protein kinase C activity in fibroblasts: possible implications in fatty acid oxidation defects. 813 Feb 78

A high-fat/high-protein diet has been reported to promote colon cancer by increasing luminal bile acid and ammonia concentrations, whereas butyrate, calcium, and low colonic pH may have protective effects. In this study, bromodeoxyuridine labeling of colonic epithelium was investigated after incubating biopsies from the ascending colon of 70 patients with HCl (20 mM, pH 6.0), butyric acid (H-BUT, 20 mM, pH 6.0), sodium butyrate (Na-BUT, 10 mM, pH 8.0), CaCl2 (10 mM), calcium butyrate (Ca-BUT, 10 mM), ammonium butyrate (NH4-BUT, 10 mM), deoxycholic acid (DCA, 5 microM), and a combination of DCA and Na-BUT (DCA/Na-BUT, 5 microM/10 mM). Compared to NaCl, H-BUT and Na-BUT increased the whole crypt-labeling index significantly, whereas HCl and CaCl2 had no effect. Reduced labeling, however, occurred with Ca-BUT in comparison to equimolar Na-BUT. No differences in the labeling indexes were found for NH4-BUT compared to Na-BUT, but increased labeling with expansion of the proliferative zone to the upper 40% of the crypt was seen with DCA compared to NaCl. DCA-induced hyperproliferation was abolished by coincubation with DCA/Na-BUT. These data suggest that butyrate, calcium, and DCA have complex influences on mucosal proliferation. Since luminal concentrations of these compounds are influenced by dietary interventions, the findings of this study may be of particular interest with regard to colon cancer development and prevention.
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PMID:Proliferation of human colonic mucosa as an intermediate biomarker of carcinogenesis: effects of butyrate, deoxycholate, calcium, ammonia, and pH. 832 39

The ability of isolated human chondrocytes to produce active oxygen species has been investigated. The two methods for determining H2O2 and hydroxyl radicals (.OH) production were, by a fluorimetric method (production of dichlorofluorescein from a precursor in the presence of horseradish peroxidase and H2O2) and by a chromatographic method (measurement of ethylene production from gamma-methiol-keto-butyric acid after .OH attack). Chondrocytes were tested, both with and without activation by phorbol myristate acetate (PMA: 10(-6) M), in the presence of Ca2+ (1 x 10(-4) M) and Mg2+ (2 x 10(-4) M) or after variable periods of anoxia under nitrogen (4 to 12 h) followed by reoxygenation (with 95% O2, 5% CO2). Under these experimental conditions, the PMA-excited chondrocytes produced from 80 to 180 nmol of hydrogen peroxide per 1 x 10(6) cells and chondrocytes subjected to anoxia-reoxygenation produced up to 1700 nmol H2O2 per 1 x 10(6) cells. The hydroxyl radical production by PMA or anoxia-reoxygenation excited cells reached 600% of the production of non-excited cells and 1300% when they were subjected to successive stimulations by PMA and anoxia-reoxygenation. The possible pathological significance of these observations is discussed. The results indicate that stimulated human chondrocytes are capable of producing active oxygen species which could play a major role in joint inflammation and cartilage damage.
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PMID:Production of active oxygen species by isolated human chondrocytes. 839 61

Butyric acid has many strong effects on gene expression in mammalian and viral systems, as well as in increasing the expression of recombinant DNAs artificially introduced into cultured cells. We screened 14 analogues of butyric acid for their ability to upregulate expression from 3 different recombinant chloramphenicol acetyltransferase expression vectors stably integrated into NIH 3T3 cells that had been transformed by calcium phosphate transfection or electroporation. Butyric acid, 2-bromobutyric acid, 3-bromopropionic acid, 3-mercaptopropionic acid, vinylacetic acid, and butyraldehyde were found to upregulate human immunodeficiency viral long terminal repeat-, SV40 early gene promoter-, and glucocerebrosidase promoter-directed expression of heterologous genes in cultured cells. Three other analogues had lesser effects; and 6 additional analogues had very little, if any, effect.
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PMID:Analogues of butyric acid that increase the expression of transfected DNAs. 848 74

A microbial biosensor based on thick film technology was developed. The microorganisms, Arthrobacter nicotianae, were immobilized in Ca-alginate directly on the electrode surface. For the stability of the calcium alginate gel the addition of 0.5 mM CaCl2 to the assay buffer was necessary. The respiratory activity of the microorganisms was monitored by oxygen consumption at -600 mV vs. Ag/AgCl reference electrode. The sensor was used in a batch system and was applied to the determination of free fatty acids in milk. Short-chain fatty acids (C4:0-C12:0) were the preferential substrates, with butyric acid being the main substrate. Consequently, the concentration of free short-chain fatty acids was represented as the butyric acid equivalent. The sensor showed linearity over the concentration range 9.5-165.5 microM (correlation coefficient, r = 0.99920). The response time of the sensor was approximately 3 min. No additional dialysis membrane was necessary, which led to a high sensitivity of the sensor and fast response times. Recovery rates of 98-113% were found for butyric acid in milk samples using the sensor without any additional membrane and a sample dilution of 200 by the assay. Two widespread disadvantages of microbial sensors, long response times and long times to return to the baseline signal after use, could be overcome.
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PMID:Microbial biosensor for free fatty acids using an oxygen electrode based on thick film technology. 882 65

1. Depolarization-induced suppression of inhibition (DSI) is a form of plasticity of gamma-amino-butyric acid (GABAA)-mediated (henceforth 'GABAergic') responses in the CNS. We made whole-cell recordings from CA1 pyramidal neurons to investigate the effects of DSI on excitatory synaptic transmission in the hippocampal slice preparation. 2. Significant enhancement of the voltage-clamped excitatory postsynaptic current (EPSC) occurs during DSI of the temporally overlapping inhibitory postsynaptic current. With high levels of calcium chelators in the pipette solution, or bath application of bicuculline, EPSC enhancement is blocked, suggesting that it results from DSI and that the DSI process selectively affects GABAergic, but not glutamatergic, transmission. 3. The probability of synaptically evoked action potential firing is increased during DSI under current clamp. DSI could influence other excitatory phenomena as well.
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PMID:Increased neuronal excitability during depolarization-induced suppression of inhibition in rat hippocampus. 886 55

We carried out a balance study to examine the effects of isomaltulose, lactose, isomalt, and isomaltulose-based oligomers (IBOs) on mineral (calcium, magnesium, phosphorus, and iron) absorption and retention. Four-week-old male Wistar rats were divided into five groups of six rats each and fed a basal diet or diet the containing either 5% isomaltulose, 5% lactose, 5% isomalts or isomaltulose-based oligomers (IBOs) ad libitum for 16 d. After 1 wk, the animals were subjected to a 5-d mineral (calcium, magnesium, phosphorus, and iron) balance study. The isomalt feeding, as well as the IBOs feeding, led to significantly elevated mineral absorption and retention. On the other hand, lactose feeding, widely known to enhance calcium absorption, increased only calcium absorption and isomaltulose feeding did not affect mineral absorption or retention. The organic acids in cecum contents were increased by IBOs or isomalt feeding. Succinic and acetic acids in cecum contents were significantly increased by IBOs feeding. Similarly, succinic, acetic, and i-valeric acids and total amount of organic acid in cecum content were significantly increased by isomalt feeding. Although the organic acids in cecum contents were increased by IBOs or isomalt feeding, the pH values and acidity in cecum contents were not changed by IBOs or isomalt feeding. The effect of addition of various organic acids to the mucosal fluid was examined with in vitro study using a hindgut segment. By the addition of acetic acid, and butyric acid, the mineral (calcium, magnesium, and phosphorus) uptake was increased.
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PMID:The effects of isomaltulose, isomalt, and isomaltulose-based oligomers on mineral absorption and retention. 890 97

Extracellular gamma amino butyric acid (GABA) levels were measured in the caudate nucleus and the prefrontal cortex of the rhesus monkey brain using in vivo microdialysis under isofluorane gas anesthesia. Evoked GABA release was investigated for voltage sensitivity and calcium (Ca2+) dependency. There was a multifold increase in extracellular GABA levels following local perfusion with: (1) high potassium (50 mM, KCI), (2) veratridine (10 microM), and (3) the GABA releasing agent and uptake blocker, (-) nipecotic acid (1 mM). Release of GABA was significantly reduced when veratridine or (-) nipecotic acid were coinfused in Ca(2+)-free cerebrospinal fluid (CSF). Coinfusion of nipecotic acid with TTX (10 microM) also resulted in attenuation of evoked GABA release. These results suggest that GABA levels recovered using in vivo microdialysis, from the caudate nucleus and the prefrontal cortex in the rhesus monkey, derive in significant part from vesicular pools and the exocytotic process is both Ca(2+)-dependent and voltage-sensitive.
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PMID:In vivo characterization of extracellular GABA release in the caudate nucleus and prefrontal cortex of the rhesus monkey. 906 27


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