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At least 127 records · Page 7Linked to original sources
PubMed1983

Purification of new calcium activated protease (low calcium requiring form) and comparison to high calcium requiring form.

A new calcium activated protease which requires low concentration of calcium was purified to almost homogeneity from porcine heart muscle. The protease was composed of two polypeptide chains of approximately 90 K and 30 K. The 90 K subunit was larger than the large subunit of the high calcium requiring form of calcium activated protease, therefore we concluded that the low calcium requiring form is different from the high calcium requiring form and its auto-digested protease. The low calcium requiring form of calcium activated protease was also activated by manganese and balium, and was very stable even at pH 9.0.

Animals↗
PubMed1999

In vitro release modulation from crosslinked pellets for site-specific drug delivery to the gastrointestinal tract. II. Physicochemical characterization of calcium-alginate, calcium-pectinate and calcium-alginate-pectinate pellets.

Pellets of calcium-alginate, calcium-pectinate and calcium-alginate-pectinate were produced via crosslinking in an aqueous medium for site-specific drug delivery in the gastrointestinal tract. A comparative study of their physicochemical characteristics by means of texture analysis, modulated temperature differential scanning calorimetry (MTDSC), scanning electron microscopy and swelling dynamics under different pH conditions was undertaken. It was found that the incorporation of low methoxylated pectin (i.e., degree of methoxylation approximately 35%) together with alginate appears to influence the degree of crosslinking and subsequently the physical, mechanical and resilience behavior. In general, texture analysis of various pellets indicated that both strength and resilience profiles were in the order of calcium-alginate>/=calcium-alginate-pectinate>calcium-pectinate. Calcium-alginate pellets were found to be viscoelastic, while calcium-pectinate was highly brittle. Through the application of MTDSC, depolymerization transitions, reversing and non-reversing heat flow were determined and interpreted for each formulation. Scanning electron microscopy and micro-thermal analysis revealed distinct morphological differences in each case. The influence of and nature of crosslinking, and textural properties of such pellets on drug release rate modulation is discussed.

Administration, Oral↗
PubMed1999

Biphasic Effect of Calcium Influx on Tau Phosphorylation: Phosphorylation: Biphasic Effect of Calcium Influx on Tau Phosphorylation: Involvement of Calcium-Dependent Phosphatase and Kinase Activities.

Conflicting data has emerged documenting decreased and increased levels of phospho-tau following calcium influx. Calcium influx achieved by treatment of SH-SY-5Y human neuroblastoma with 1 micro M calcium ionophore A23187 in the presence of 0.1 mM extracellular calcium depleted phospho-tau levels within 30 min. However, extending ionophore treatment to 60 min raised phospho-tau levels beyond that of control levels. Total tau levels were unchanged throughout these treatments, indicating that the reduction in PHF-1 reflected sequential alterations in tau phosphorylation rather than total tau. More rapid accumulation of phospho-tau accompanied treatment with increased concentrations of ionophore (3 micro M) and extracellular calcium (0.9 mM). An inhibitor active against calcium-dependent kinase(s) prevented the increase in phospho-tau following calcium influx. These data underscore that phospho-tau levels represent the summation of kinase and phosphatase activities and indicate that net dephosphorylation or phosphorylation is dependent upon the extent and/or rate of calcium influx

Journal Article↗
PubMed1999

Modulation of calcium mobilization in aortic rings of pregnant rats: Contribution of extracellular calcium and of voltage-operated calcium channels.

Pregnancy is associated with decreased vascular responsiveness to vasopressor stimuli. We have tested the involvement of Ca2+ mobilization in myotropic responses of aortic rings obtained from pregnant and virgin rats. Contractions of the rings to phenylephrine, in the absence of calcium in the bathing medium, were lower in tissues from virgin than from pregnant rats. Concentration-response curves to CaCl2 that were measured after stimulation by phenylephrine in the absence of Ca2+ were shifted to higher levels of contraction. This was not observed when KCl was used to prestimulate the aorta. D-600, a phenylalkylamine calcium channel blocker, similarly inhibited these responses to CaCl2 in tissues from both pregnant and virgin animals. D-600 exerted a concentration-dependent inhibition of responses to phenylephrine and KCl. However, the calcium antagonist was less effective in aortic rings of pregnant than of virgin rats. Basal 45Ca2+ uptake was lower in aortic rings from pregnant than from virgin rats, and Bay K 8644 was unable to reverse this difference. The time course of basal and stimulated (KCl) 45Ca2+ influx was lower in aorta of pregnant rats at all times studied. Moreover, when the intracellular calcium pools were emptied with phenylephrine, the refilling of these pools was delayed in aortic rings of pregnant rats. These results indicate an altered extracellular calcium mobilization of aortic rings from pregnant rats. These changes may be due to a functional alteration of the voltage-operated calcium channels during pregnancy.

Animals↗
PubMedDate not supplied

Lack of voltage-dependent calcium channel opening during the calcium influx induced by progesterone in human sperm. Effect of calcium channel deactivation and inactivation.

Progesterone induces calcium influx and acrosomal exocytosis in human sperm. Pharmacologic evidence suggests that voltage-dependent calcium channels (VDCCs) are involved. In this study, membrane potential (Vm) and intracellular calcium concentration ([Ca(2+)](i)) were monitored simultaneously to assess the effect of VDCC gating on the calcium influx triggered by progesterone. Holding the Vm to values that maintained VDCCs in a deactivated (-71 mV) closed state inhibited the calcium influx induced by progesterone by approximately 40%. At this Vm, the acrosomal reaction induced by progesterone, but not by A23187, was inhibited. However, when the Vm was held at -15 mV (which maintains VDCCs in an inactivated closed state), the progesterone-induced calcium influx was stimulated. Furthermore, the progesterone and voltage-dependent calcium influxes were additive. These findings indicate that progesterone does not produce VDCC gating in human sperm.

Acrosome Reaction↗
PubMed2000

Effects of phosphorus-containing calcium preparation (bone meal powder) and calcium carbonate on serum calcium and phosphorus in young and old healthy volunteers: a double-blinded crossover study.

To evaluate the effects of bone meal powder (BEC) on calcium and phosphorus metabolism, a calcium absorption test was conducted using a preparation of calcium carbonate (CAC) as the control drug. A total of 12 healthy volunteers, consisting of 6 younger (aged 20-29 years, 3 men and 3 women) and 6 older (aged 60-69 years, 3 men and 3 women) persons, were subjected to a double-blinded crossover study. Serum calcium (s-Ca) level significantly increased to 105.3% +/- 1.9% (P < 0.01 vs the basal value; mean +/- SD) from the basal value in the BEC group and to 104.4% +/- 2.7% (P < 0.01) in the CAC group at 3h post load. Urinary excretions of calcium (u-Ca/glomerular filtration rate, u-Ca/GF) after BEC and CAC load rose to 226.6% +/- 154.5% (P < 0.05) and 211.1% +/- 148.0% (P < 0.05), respectively. Serum phosphorus (s-P) levels after BEC load increased to 110.0% +/- 15.1% (P < 0.05), whereas that after CAC load showed no significant change (99.3% +/- 7.9%). On the other hand, urinary excretion of phosphorus (u-P/GF) after CAC load decreased to 60.0% +/- 32.4% (P < 0.01) and that in the BEC group showed no significant change (92.5% +/- 49.5%). The increase in s-Ca led to decrease in serum intact parathyroid hormone (i-PTH) level [77.3% +/- 33.4% (P < 0.05) for BEC and 69.5% +/- 20.3% (P < 0.01) for CAC] although s-P was increased by the BEC load. The responses to BEC and CAC administration were compared in the younger and the older groups. The responses in the younger and the older group showed fundamentally the same trends and to the same extent. However, the changes in serum ionized calcium (i-Ca) and i-PTH levels at 1.5 h post load were significantly smaller in the older group than in the younger group (P < 0.01; P < 0.05). The increment in s-P level after BEC load in the older group was larger than that in the younger group. In conclusion, BEC can modulate not only calcium but also phosphorus metabolism in both younger and older subjects. Further investigations are required to evaluate the effects of BEC on bone density and safety for renal function in long-term observations.

Adult↗
PubMed2000

Effects of mutations in the calcium-binding sites of recoverin on its calcium affinity: evidence for successive filling of the calcium binding sites.

A molecule of the photoreceptor Ca(2+)-binding protein recoverin contains four potential EF-hand Ca(2+)-binding sites, of which only two, the second and the third, are capable of binding calcium ions. We have studied the effects of substitutions in the second, third and fourth EF-hand sites of recoverin on its Ca(2+)-binding properties and some other characteristics, using intrinsic fluorescence, circular dichroism spectroscopy and differential scanning microcalorimetry. The interaction of the two operating binding sites of wild-type recoverin with calcium increases the protein's thermal stability, but makes the environment around the tryptophan residues more flexible. The amino acid substitution in the EF-hand 3 (E121Q) totally abolishes the high calcium affinity of recoverin, while the mutation in the EF-hand 2 (E85Q) causes only a moderate decrease in calcium binding. Based on this evidence, we suggest that the binding of calcium ions to recoverin is a sequential process with the EF-hand 3 being filled first. Estimation of Ca(2+)-binding constants according to the sequential binding scheme gave the values 3.7 x 10(6) and 3.1 x 10(5) M(-1) for third and second EF-hands, respectively. The substitutions in the EF-hand 2 or 3 (or in both the sites simultaneously) do not disturb significantly either tertiary or secondary structure of the apo-protein. Amino acid substitutions, which have been designed to restore the calcium affinity of the EF-hand 4 (G160D, K161E, K162N, D165G and K166Q), increase the calcium capacity and affinity of recoverin but also perturb the protein structure and decrease the thermostability of its apo-form.

Calcium↗
PubMed1986

1,25-Dihydroxyvitamin D3-mediated intestinal calcium transport. Biochemical identification of lysosomes containing calcium and calcium-binding protein (calbindin-D28K).

A variety of intestinal cell organelles and proteins have been proposed to mediate 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3)-stimulated calcium absorption. In the present study biochemical analyses were undertaken to determine the subcellular localization of 45Ca after calcium transport in vivo in ligated duodenal loops of vitamin D-deficient chicks injected with 1.3 nmol of 1,25-(OH)2D3 or vehicle 15 h prior to experimentation. Separation of Golgi, mitochondria, basal lateral membrane, and lysosome fractions in the epithelial homogenates was achieved by differential sedimentation followed by centrifugation in Percoll gradients and evaluation of appropriate marker enzyme activities. Both vitamin D-deficient and 1,25-(OH)2D3-treated chicks had the highest levels of 45Ca-specific activity in lysosomal fractions. The lysosomes were also the only organelles to exhibit a 1,25-(OH)2D3-mediated difference in calcium content, increasing to 138% of controls. Lysosomes prepared from 1,25-(OH)2D3-treated chicks also contained the greatest levels of immunoreactive calbindin-D28k (calcium-binding protein). Chloroquine, a drug known to interfere with lysosomal function, was tested and found to inhibit 1,25-(OH)2D3-stimulated intestinal calcium absorption. Neither 1,25-(OH)2D3 nor chloroquine affected [3H]2O transport. In additional experiments, microsomal membranes (105,000 X g pellets) were subjected to gradient centrifugation. The highest levels of 45Ca-specific activity and calcium-binding protein in material from 1,25-(OH)2D3-treated chicks were found in fractions denser than endoplasmic reticulum and may represent endocytic vesicles. In studies on intestinal mucosa of 1,25-(OH)2D3-treated birds fractionated after 30 min of exposure to lumenal Ca2+ or Ca2+ plus chloroquine, 45Ca was found to accumulate in lysosomes and putative endocytic vesicles, relative to controls. A mechanism involving vesicular flow is proposed for 1,25-(OH)2D3-mediated intestinal calcium transport. Endocytic internalization of Ca2+, fusion of the vesicles with lysosomes, and exocytosis at the basal lateral membrane complete the transport process.

Acid Phosphatase↗
PubMed2006

Estimation of ionized calcium, total calcium and albumin corrected calcium for the diagnosis of hypercalcaemia of malignancy.

OBJECTIVE: To measure levels of ionized calcium, total calcium and albumin corrected calcium in patients with different malignant disorders for the diagnosis of hypercalcaemia of malignancy. DESIGN: A case control comparative study. PLACE AND DURATION OF STUDY: The study was carried out in the Department of Pathology, Army Medical College Rawalpindi, Armed Forces Institute of Pathology and Department of Oncology CMH, Rawalpindi from March 2003 to December 2003. SUBJECTS AND METHODS: Ninetyseven patients of various malignant disorders, admitted in the Department of Oncology, CMH, Rawalpindi, and 39 age and gender-matched disease-free persons (as control) were included in the study. Blood ionized calcium (Ca++), pH, sodium (Na+) and potassium (K+) were analysed by Ion selective electrode (ISE) on Easylyte auto analyser. Other related parameters were measured by colourimetric methods. RESULTS: Blood Ca(++) levels in patients suffering from malignant disorders were found significantly high (mean +/- SD: 1.30+017 mmol/L) as compared to control subjects (mean +/- SD 1.23+0.03 mmol/L) (p<0.001). The number of patients with hypercalcaemia of malignancy detected by Ca(++) estimation was significantly higher (38%) as compared to total calcium (8.4%) and albumin corrected calcium ACC (10.6%) (p<0.001). There was no statistically significant difference in other parameters e.g. phosphate, urea, creatinine, pH, Na+ and K+ levels in study subjects and controls. CONCLUSION: Detection of hypercalcaemia can be markedly improved if ionized calcium estimation is used in patients with malignant disorders.

Adolescent↗
PubMed1994

Relationships between amplitudes and kinetics of rapid cytosolic free calcium fluctuations in GH4C1 rat pituitary cells: roles for diffusion and calcium-induced calcium release.

We have examined statistical relationships between the amplitudes and the kinetics (rise times, fall times, and decay constants) of cytosolic free calcium fluctuations (spikes) in a population of 353 individual GH4C1 rat pituitary cells. The fast falling phase was approximated by a single exponential decay, and the decay time constant, tau, increased linearly with spike amplitude in 80% of the cells studied. The slope of the tau versus amplitude plot for each cell was inversely related to the cell's mean spike amplitude. Thus, some process responsible for prolonging the decay phase of spikes appeared to operate strongly in cells with spikes of low amplitude, but to become less prominent in cells with high amplitude spikes. Mean tau correlated more strongly with mean rise and fall times than with mean spike amplitude, indicating that the kinetic properties of spikes were not tightly coupled to spike amplitude. These findings are consistent with a model wherein the rise phase corresponds to entry of extracellular calcium via L-type calcium channels into localized sub-plasmalemmal domains, followed by diffusion of subplasmalemmal calcium into the cell interior; and the falling phase corresponds to further calcium diffusion combined with activation of cytoplasmic calcium-induced calcium release, which prolongs the falling phase.

Aniline Compounds↗
PubMed1997

Intracellular calcium chelator BAPTA protects cells against toxic calcium overload but also alters physiological calcium responses.

The effect of the membrane-permeant calcium chelator 1,2-bis-(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid tetra(acetoxymethyl) ester (BAPTA/AM) on ionomycin-induced cellular calcium overload was studied in single differentiated NH15-CA2 neuroblastoma x glioma hybrid cells. To monitor [Ca2+]i we used the fluorescent indicator Fura-2. Preincubation of the cells with 3 microM BAPTA/AM reduced the number of cells showing deregulation of [Ca2+]i during ionomycin-induced calcium influx. The calcium transients elicited by application of KCl were also severely affected by the chelator. These transients, although varying from cell to cell in shape, amplitude and duration, are well reproducible in individual cells. After incubation of cells for 1 h with 0.3-30 microM BAPTA/AM the time course of these cellular transients was markedly slowed. At 1 microM BAPTA/AM, the time constant of decline of [Ca2+]i was increased by a factor of 4.1 +/- 2.4 (n = 14) and the amplitude was reduced to about 50%. With 30 microM BAPTA/AM, the K(+)-induced calcium transients were almost completely inhibited. We conclude that intracellularly loaded calcium chelators may be used for the prevention of [Ca2+]i-induced cell damage, however, at the expense of a disturbed calcium signalling.

Animals↗
PubMed1995

Interaction of calcium with Bordetella pertussis adenylate cyclase toxin. Characterization of multiple calcium-binding sites and calcium-induced conformational changes.

The adenylate cyclase (CyaA) secreted by Bordetella pertussis is a toxin that is able to enter eukaryotic cells and cause a dramatic increase in cAMP level. In addition, the toxin also exhibits an intrinsic hemolytic activity that is independent from the ATP cycling catalytic activity of the toxin. Both the cytotoxic and hemolytic activities are calcium-dependent. In this work, we have analyzed the calcium interacting properties of CyaA. We have shown that CyaA exposed to CaCl2 could retain membrane binding capability and hemolytic activity when it was further assayed in the presence of an excess of EGTA. Determination of the calcium content of CyaA exposed first to calcium and subsequently to EGTA indicated that some (3-5) calcium ions remained bound to the protein, suggesting the existence of Ca2+ binding sites of high affinity. Binding of Ca2+ to these sites might be necessary for both the membrane binding capability and the hemolytic activity of the toxin. In addition, CyaA possesses a large number (about 45) of low affinity (KD = 0.5-0.8 mM) Ca2+ binding sites that are located in the C terminus of the toxin, between amino acids 1007 and 1706. This region mainly consists of about 45 repeated sequences of the type GGXGXDXLX (where X represents any amino acid) that are characteristic of the RTX (Repeat in ToXin) bacterial protein family. Our data suggest that each one can bind one calcium ion. Circular dichroism spectroscopy analysis showed that calcium binding to the low affinity sites induces a large conformational change of CyaA, as revealed by an important increase in the content of alpha-helical structures. This conformational change might be directly involved in the Ca(2+)-dependent translocation of the catalytic domain of CyaA through the plasma membrane of target cells.

Adenylate Cyclase Toxin↗
PubMed1992

Control of predialytic hyperphosphatemia by oral calcium acetate and calcium carbonate. Comparable efficacy for half the dose of elemental calcium given as acetate without lower incidence of hypercalcemia.

Since Mai et al. found, with the intestinal lavage technique, that the same dose of elemental calcium given as acetate (Ca Ac) complexed in the gut of uremic patients twice as much phosphate as calcium carbonate (CaCO3) while inducing a rather low calcium absorption, we wanted to see if half the dose of elemental calcium given as Ca Ac could control, on medium term, the predialysis plasma phosphate as well as CaCO3 while inducing less frequent hypercalcemia. This was evaluated in a cross-over study of 3 periods of 10 weeks according to the sequence Ca Ac, CaCO3 and Ca Ac, in 12 compliant patients on chronic dialysis previously treated by CaCO3. Because of poor tolerance of Ca Ac during the first period, 4 patients were excluded and the results were assessed only on the 8 patients who completed the study. For half the doses of elemental calcium (620 +/- 250 mg versus 1,310 +/- 560 mg versus 710 +/- 200 mg/day), Ca Ac allowed the same control of predialytic hyperphosphatemia (1.67 +/- 0.34; 1.74 +/- 0.32; 1.75 +/- 0.38) with paradoxically comparable normal mean plasma calcium concentration (2.61 +/- 0.14; 2.56 +/- 0.13; 2.55 +/- 0.14 mmol/l). Plasma alkaline phosphatases and intact PTH concentrations remained also stable during the 3 periods. The frequency of hypercalcemia greater than 2.75 mmol/l (12; 9; 20%) and of hyperphosphatemia greater than 2 mmol/l (17; 22; 27%) were comparable with the 2 treatments. In conclusion, Ca Ac controls predialytic hyperphosphatemia as efficiently as CaCO3 for half the dose of elemental calcium without, however, decreasing the frequency of hypercalcemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetates↗
PubMed1975

Calcium uptake and calcium release by subcellular fractions of smooth muscle. II. Kinetics of calcium uptake by microsomes and mitochondria from pig coronary artery and guinea pig ileum.

Calcium uptake by the microsomal and mitochondrial fractions of pig coronary artery and guinea pig ileum was studied in the presence of ATP, ATP plus oxalate and without ATP and oxalate. Microsomes and mitochondria of both smooth muscles were found to be unable to accumulate appreciable amounts of calcium in the absence of ATP. Oxalate noticeably stimulated the calcium uptake of the mitochondrial fraction from pig coronary artery but had little effect on calcium uptake by the microsomal fraction of this smooth muscle. The calcium uptake of microsomes and mitochondria from guinea pig ileum was not or only slightly enhanced by oxalate. There are typical kinetics regarding the time course and the extent of calcium uptake by microsomes and mitochondria from pig coronary artery and guinea pig ileum. In comparison, considerable qualitative and quantitative differences between both smooth muscles are observed. The high ATP-dependent calcium uptake capacity of the mitochondria from pig coronary artery and guinea pig ileum are a further argument for the hypothesis that these organelles may play an important role in the contraction-relaxation mechanism of smooth muscle.

Adenosine Triphosphate↗
PubMed1994

Regulation of intracellular calcium in the mouse egg: evidence for inositol trisphosphate-induced calcium release, but not calcium-induced calcium release.

Fertilization of the mammalian egg initiates transient and repetitive release of Ca2+ from intracellular stores. The mechanism by which these Ca2+ transients are produced is not completely known. We examined the role of two principal Ca2+ release mechanisms, inositol trisphosphate-induced Ca2+ release and Ca(2+)-induced Ca2+ release, in altering intracellular Ca2+ in the mouse egg. Microinjection of inositol 1,4,5-trisphosphate (IP3) transiently elevated intracellular Ca2+ and, at higher concentrations, produced repetitive Ca2+ transients. Addition of 100 microM thimerosal, a sulfhydryl reagent, caused repetitive Ca2+ transients. IP3 and thimerosal responses were inhibited by prior injection of heparin, a competitive antagonist of IP3-induced Ca2+ release. Addition of caffeine or injection of caffeine, ryanodine, or cyclic ADP-ribose, which are known to initiate or modulate Ca(2+)-induced Ca2+ release in sea urchin eggs and other cells, produced no change in intracellular Ca2+. The response to injection of Ca2+ was not altered by prior injection of ryanodine. The magnitude of the Ca2+ transients produced by injection of IP3 was not changed by prior injection of cyclic ADP-ribose or external caffeine. We found no evidence of Ca(2+)-induced Ca2+ release from ryanodine- or caffeine-sensitive stores. It is most likely that release of Ca2+ from intracellular stores in the mouse egg is dependent on IP3-induced Ca2+ release.

Adenosine Diphosphate Ribose↗
PubMed1991

Direct measurement of intracellular free calcium in cultured human puerperal myometrial cells stimulated by oxytocin: effects of extracellular calcium and calcium channel blockers.

The changes in intracellular free calcium concentration ([Ca2+]i) induced by oxytocin in single cells of cultured human puerperal myometrium were measured with the calcium-sensitive fluorescent dye fura 2 in a digital imaging fluorescence microscopic system. Oxytocin at concentrations of 30-300 nmol/L induced a dose-dependent increase in [Ca2+]i with a peak at 20 seconds. This increase depended mainly on extracellular calcium ([Ca2+]ex) at concentrations of 0.6-4.8 mmol/L. In the absence of [Ca2+]ex, the increase was only 16% of that in its presence. The voltage-sensitive calcium channel blockers nicardipine, nifedipine, and nitrendipine had similar effects, causing significant suppression of the increase in [Ca2+]i induced by oxytocin. Diltiazem also suppressed the increase in [Ca2+]i, though less than the other calcium channel blockers. These data indicate that the increase in [Ca2+]i induced by oxytocin is predominantly dependent upon [Ca2+]ex. Furthermore, the data explain why calcium channel blockers are effective for weakening uterine muscle contractions and indicate which type of blocker is most effective.

Calcium↗