A voltage clamp study of the sodium, calcium and chloride spikes of chick skeletal muscle cells grown in tissue culture.
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Animals↗
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Identification and quantification of polar naphthalene derivatives in contaminated groundwater of a former gas plant site by liquid chromatography-electrospray ionization tandem mass spectrometry.
A liquid chromatography (LC) method followed by electrospray ionization (ESI) and tandem mass spectrometry (MS-MS) was developed for the quantification of acidic naphthalene derivatives in the concentration range 0.1 to 100 microg/l without excessive sample preparation. For optimal sensitivity the LC-MS-MS measurements were performed recording mass fragmentation by collision induced dissociation in the multiple reaction mode. The collision energy was optimized for every analyte. The matrix effects of the sample were investigated by spiking standards of 1-naphthoic acid with humic acid (HA) and with calcium chloride. While HA decreased the signal intensity an increase was observed in the presence of calcium chloride. For the investigated groundwater samples of a tar oil contaminated site a complete separation of the analytes from the sample matrix by reversed-phase separation could be obtained. The absence of matrix effects on quantification results was confirmed by comparison of results based on external calibration with those based on standard addition of the analytes to a groundwater sample. In four groundwater samples of the contaminated site naphthalene derivatives like 1-naphthoic acid, 2-naphthoic acid, 1-naphthylacetic acid, 2-naphthylacetic acid, 1-hydroxy-2-naphthoic acid, 2-hydroxy-3-naphthoic acid, and naphthyl-2-methylenesuccinic acid have been detected.
Chromatography, Liquid↗
Effects of chronic norepinephrine administration on cardiac function in rats.
We assessed the changes in the contractile response of rat hearts in vivo after chronic exposure to a range of doses of norepinephrine (NE) and determined whether free radical production played a role in these changes. Osmotic minipumps were implanted subcutaneously (s.c.) in male rats and delivered either NE (0.15-0.35 mg/kg/h) or acid saline for 10-28 days. The animals were then anaesthetised and prepared for haemodynamic measurement, and dose-response curves to acutely administered NE and calcium chloride were constructed. We analysed plasma for evidence of free radical activity by measuring the levels of thiobarbituric acid-reactive substances (TBARS). All doses of NE studied produced left, but not right, ventricular hypertrophy. Treatment with 0.25 mg/kg/h NE for 28 days produced signs of distress and, by 10 days, treatment with 0.35 mg/kg/h resulted in 33% mortality. Treatment with the two lower doses, but not the highest dose, of NE resulted in increases in basal left ventricular (LV) maximum rate of pressure generation and a marked increase in systolic, but not diastolic, arterial blood pressure (SBP, DBP). All doses of NE caused reduced responses to acutely administered NE but no marked change in the response to calcium chloride. Levels of plasma free radicals were increased only with the highest dose of NE. Over the concentration range studied, chronic administration of NE to rats causes beta-adrenoceptor downregulation and free radical production was associated only with the administration of a dose of NE that resulted in high mortality.
Analysis of Variance↗
Dose response dependency in regulation of acute PTH (1-84) release and suppression in normal humans: a citrate and calcium infusion study.
The aim of the present study was to investigate the possible dose response dependency of the very early changes in intact parathyroid hormone concentrations (PTH) on different rates of blood ionized calcium (B-Ca2+) lowering and raising. On 8 different days, four healthy volunteers received trisodium-citrate infusions at five different rates and calcium chloride infusions at three different rates, all of 10 min duration. S-PTH and B-Ca2+ were measured twice before each infusion and after 1, 2, 3, 4, 5, 7, and 10 min of infusion. The decrements of B-Ca2+ expressed as area under the curve (AUC) correlated with the rate of trisodium-citrate infusions (r = 0.97, p < 0.001) and furthermore, these B-Ca2+ decrements were matched by S-PTH increments expressed as AUC (r = 0.96, p < 0001). Multigroup comparisons on the results of protocol A showed statistical significant (p < 0.02). The increments of B-Ca2+ expressed as AUC correlated with the rate of calcium chloride infusions (r = 0.92, p < 0.001) and furthermore, these B-Ca2+ increments were matched by S-PTH decrements measured as AUC (r = 0.95, p > 0.001). Multigroup comparisons on the results of protocol B showed statistical significant (p < 0.05). In conclusion, acute B-Ca2+ lowering and raising at different rates promotes stimulation and inhibition of the acute PTH release in rate dependent manner. For this mechanism being distinctly different from the steady state control of PTH secretion, we suggest the term 'delta regulation' (delta, i.e. the sign for change).
Adult↗
Usefulness as guided bone regeneration membrane of the alginate membrane.
Alginate membrane is a new bioabsorbable, guided bone regeneration (GBR) membrane, which is placed directly on the surface of the bone defect. It is designed to drop a calcium chloride aqueous solution into the bone defect, which is filled with sodium alginate aqueous solution. Alginate membrane is an excellent agent for this procedure due to its close assimilation to the surface of the bone. In this study, we evaluated the short-term biocompatibility of alginate membrane in the bone defects of rat tibiae. GBR membrane availability was also examined. Consequently, we found that the healing process in bone defects covered with an alginate membrane was delayed in comparison with that of controls, however, the defect was restored to nearly original condition. In contrast, in the controls, bone defect repairs exhibited partitioning as a result of connective tissue involvement. Furthermore, we observed a relation between the sodium alginate concentration and the rate of absorption of the sodium alginate membrane. Absorption of a 1.5% sodium alginate membrane was slow. As a result, the compound was not absorbed completely and bone repairs resembled an hourglass. Moreover, the inflammatory response was absent surrounding the alginate membrane. The present findings suggested that the alginate membrane functions effectively as a GBR membrane. In addition, the alginate membrane derived from 3% calcium chloride and 1% sodium alginate was most suitable as a GBR membrane.
Absorption↗
Granulosa cells have calcium-dependent action potentials and a calcium-dependent chloride conductance.
We have found chicken granulosa cells to be excitable. Experiments using the whole-cell patch-clamp technique showed that they had membrane resting potentials of -62 +/- 3 mV (n = 8) and generated action potentials, either in response to 10-ms depolarizing current pulses or, on occasion, spontaneously. The action potentials persisted in a Na(+)-free bath and were reversibly blocked by 4 mM Co2+. They lasted 0.9-3.0s with 64 mM Cl- in the pipette, were shortened 67 +/- 8% by the Cl- channel blocker 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB; 20 microM), and lengthened to 8.7 +/- 2.2 when the Cl- equilibrium potential (Vcl) was changed from -20 mV to -2 mV by using 134 mM Cl- in the pipette. With conventional whole-cell voltage-clamp, slowly activating and inactivating currents, which reached maximum amplitude after 0.35-1.40 s, were evoked by depolarizing voltage steps. These slow currents activated between voltage steps of -60 mV and -50 mV and reached a maximum inward amplitude at about -40 mV. Changing the Cl- concentration in the pipette (VCl of -2MV or -20 mV) or bath (VCl of -2 mV or + 18 mV) shifted their reversal potential in a direction consistent with a Cl- electrode. They were inhibited by the Cl- channel antagonists 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS; 0.5 mM), NPPB (20 microM), and 4-acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic acid (SITS; 0.5 mM). The slow currents were blocked by Ca2+ deprivation, or by CO2+ (4 mM), or by replacing external Ca2+ with Ba2+.(ABSTRACT TRUNCATED AT 250 WORDS)
Action Potentials↗
Reversal of dantrolene sodium-induced depression of skeletal muscle in the cat.
Dantrolene sodium, a muscle relaxant, does not have a clinically useful antagonist. The present study was undertaken to test the efficacies of germine monoacetate, 4-aminopyridine, neostigmine, and calcium chloride as possible agents for the reversal of the direct skeletal muscle depression produced by dantrolene sodium in the cat anesthetized with alpha-chloralose. Depression of the indirectly elicited twitch responses (0.1 Hz) of the tibialis anterior muscle by 25, 50, 75 and 84 per cent was produced by dantrolene, 0.16, 0.36, 0.88 and 1.13 mg/kg respectively; spontaneous recovery of twitch tension during the subsequent 30 min was negligible. After the 30-min observation period had elapsed, one of the reversal agents under study was given (iv) in divided doses at intervals of 10 min (five cats for each agent). Germine monoacetate (2 X 0.5 mg/kg) immediately reversed the dantrolene-induced twitch depression, with an over-shoot that persisted for an hour. 4-Aminopyridine (4 X 0.5 mg/kg) caused a steady but incomplete reversal to 17 per cent depression, 30 min after the last dose. Neostigmine (4 X 0.04 mg/kg) caused an immediate, but transient, reversal of the twitch depression, with overshoot. Calcium chloride (4 X 10 mg/kg) was without effect. It is concluded that germine monoacetate is the drug of choice for reversal of the muscle depression produced by dantrolene sodium in the cat.
4-Aminopyridine↗
Comparison study of intraosseous, central intravenous, and peripheral intravenous infusions of emergency drugs.
Intraosseous infusion of emergency drugs is a lifesaving alternative to intravenous administration when intravenous access cannot be rapidly established. We studied the comparative pharmacokinetics of the following six emergency drugs and solutions: epinephrine hydrochloride, 0.01 mg/kg; sodium bicarbonate, 1 mEq/kg; calcium chloride, 10 mg/kg; hydroxyethyl starch, 10 mL/kg; 50% dextrose in water, 250 mg/kg; and lidocaine hydrochloride, 1 mg/kg. Studies were conducted in normotensive, anesthetized dogs, with three animals studied with each of the drugs or solutions and each animal being treated with all three routes of administration (central intravenous, peripheral intravenous, and intraosseous) in randomized sequence. The effects of epinephrine were also assessed in a shock model. The intraosseous route of administration was comparable with the central and peripheral intravenous routes for all of the emergency drugs and solutions studied, with equivalent magnitudes of peak effect or drug level and equal or longer durations of action. Time to placement of the intraosseous needle varied from 15 seconds to 5 minutes, with a mean of 60 seconds. Time to placement of the needle varies with the skill and experience of the individual. With experience, all individuals could place the intraosseous needle in 60 seconds or less. The intraosseous route is comparable in effect to the central and peripheral intravenous routes of drug administration for epinephrine, sodium bicarbonate, hydroxyethyl starch, calcium chloride, 50% dextrose in water, and lidocaine and is a clinically feasible alternative when intravenous access will be critically delayed.
Animals↗
Bilirubin inhibits calcium carbonate precipitation in gallbladder bile.
BACKGROUND: Previous studies have shown that human bile contains one or more factors that inhibit the precipitation of calcium carbonate from supersaturated solutions of calcium chloride and sodium bicarbonate. Lower concentrations of this factor have been observed in the gallbladder bile of patients with calcified gallstones. We hypothesized that gallbladder bile contains factors that inhibit calcium carbonate and these factors are present in varying concentrations in normal persons and in patients with cholesterol gallstones with and without calcium carbonate. METHODS: Gallbladder bile of patients without gallstones (n = 8) and of patients with cholesterol gallstones containing either calcium carbonate (n = 8) or other calcium salts (n = 8) was assayed for calcium carbonate inhibition. Individual components of bile (bilirubin, phospholipid, bile salts, and albumin) were tested in different concentrations in the same assay system. In addition, samples of model bile were tested. RESULTS: An inhibitory factor for calcium carbonate precipitation was present within all human gallbladder bile, irrespective of the absence, presence, or type of gallstones. The addition of a bilirubin-albumin solution to a supersaturated solution of calcium chloride and sodium bicarbonate entirely blocked precipitation of calcium carbonate from solution. In addition, serial dilutions of bilirubin exhibited a linear response between bilirubin concentration and inhibitory effect. Model bile and phospholipid dissolved in sodium taurocholate also exhibited a modest inhibitory effect on calcium carbonate precipitation. CONCLUSIONS: We conclude that bilirubin, cholesterol, and phospholipids incrementally interfere with calcium carbonate precipitation in supersaturated solutions through the preferential formation of a soluble calcium complex.
Bile↗
The calcium-dependent chloride conductance mediator pCLCA1.
The regulatory behavior, inhibitor sensitivity, and properties of the whole cell chloride conductance observed in cells expressing the cDNA coding for a chloride conductance mediator isoform of the CLCA gene family, pCLCA1, have been studied. Common C-kinase consensus phosphorylation sites between pCLCA1 and the closely related human isoform hCLCA1 are consistent with a role for calcium in channel activation. Both channels are activated rapidly on exposure to the calcium ionophore ionomycin. Direct involvement of calcium in the activation of pCLCA1 was supported by the finding that treatment with the intracellular calcium chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-AM reduced the rate of chloride efflux from NIH/3T3 cells expressing the pCLCA1 channel. No combination of A-kinase activators used was effective in activating chloride efflux via this channel despite the presence of a unique strong A-kinase consensus site in pCLCA1. Notable differences of pCLCA1 from the reported properties of CLCA family members include the failure of phorbol 12-myristate 13-acetate to activate chloride efflux in cells expressing pCLCA1 and a lack of inhibition of chloride efflux from these cells after treatment with DIDS or dithiothreitol. However, selected inhibitors of anionic conductance inhibited pCLCA1-dependent anion efflux. The electrogenic nature of the ionomycin-dependent efflux of chloride from cells expressing pCLCA1 was confirmed by detection of outwardly rectifying chloride current and inhibition of this current by chloride conductance inhibitors in a whole cell patch-clamp study.
3T3 Cells↗
Presence of Ca2+ is obligatory for the cytotoxic activity of dengue virus-induced cytotoxic factor.
The present study was undertaken to investigate the role of calcium ions (Ca2+) in the cytotoxic activity of the cytotoxic factor (CF) produced by T lymphocytes of the dengue type 2 virus (DV)-infected mouse spleen. It was observed that CF prepared in Ca2(+)-free medium had no cytotoxic activity on normal mouse spleen cells suspended in Ca2(+)-free medium but had activity on cells suspended in medium having Ca2+. The cytotoxic activity of CF was restored by substitution with calcium chloride, the optimal dose being 10(-7) M. CF induced influx of Ca2+ as measured by uptake of radiolabelled calcium chloride (45Ca), in the susceptible target cells, macrophages (M phi) and T lymphocytes, but had no effect on CF-resistant B lymphocytes. Calcium channel blocking drugs, like verapamil, nifedipine and diltiazem, inhibited the cytotoxic activity of CF and also the CF-induced influx of 45Ca in M phi and T cells. Thus, presence of Ca2+ is obligatory for the cytotoxic activity of CF and the cell death is associated with increased intracellular Ca2+.
Animals↗
Calcium-sensitive chloride channels in vascular smooth muscle cells.
Chloride (Cl-) channels were characterized in vascular smooth muscle cells (VSMC) using radioisotope flux and patch-clamp electrophysiological techniques. Transmembrane 125iodine (125I) efflux from subcultured (Passage 1-5) rat aortic VSMCs was used as an indicator of Cl- movements to study the relationship between intracellular calcium concentration ([Ca2+]i) and Cl- channel activity. Angiotensin II (Ang II) (10(-7) M) and adenosine 5'-triphosphate (ATP) (10(-4) M) induced rapid increases (9.7- and 14.9-fold, respectively) in 125I efflux rates. We found that both Ang II- and ATP-stimulated 125I efflux and [Ca2+]i increases were completely abolished after brief incubation (20 microM, 20 min) with the acetoxymethyl ester of 1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA-AM), a membrane-permeable Ca2+ chelator. However, when external EGTA was used to blunt agonist-stimulated Ca2+ influx, 125I efflux was still increased in response to Ang II and ATP. These data suggest that Ca2+ release from intracellular sites is sufficient to activate Cl- channels in response to Ang II and ATP. Using standard patch-clamp electrophysiological techniques, we found that Ang II, a Ca(2+)-mobilizing agonist, stimulated outward Cl- currents (gCl = 75 pS) in cell-attached (C/A) patches of primary and subcultured VSMCs. Collectively, these data suggest that Ang II and other vasoconstrictor agents stimulate Cl- channel activity via increases in [Ca2+]i. Cl- channel activation may help to depolarize the VSMC membrane leading to increased Ca2+ influx during agonist stimulation.
Animals↗
Dependence of the flash-induced oxygen evolution pattern on the chemically and far red light-modulated redox condition in cyanobacterial photosynthetic electron transport.
Flash-induced photosynthetic oxygen evolution was measured in cells and thylakoid preparations from the coccoid cyanobacteria Synechocystis sp. PCC 6803 and Synechococcus sp. PCC 7942 and from the filamentous cyanobacterium Oscillatoria chalybea. The resulting characteristic flash patterns from these cyanobacteria can be chemically altered by addition of exogenously added substances like CCCP, DCPiP and inorganic salts. Potassium chloride, manganese sulfate and calcium chloride affected the sequences by specific increases in the flash yield and/or effects on the transition parameters. Chloride appeared to exert the strongest stimulatory effect on the oxygen yield. In comparison to chloride, both manganese and calcium did not significantly stimulate the flash amplitudes as such, but improved the functioning of the oxygen evolving complex by decreasing the miss parameter alpha. Particular effects were observed with respect to the time constants of the relaxation kinetics of the first two flash signals Y1/Y2 of the cyanobacterial patterns. In the presence of the investigated chemicals the amplitudes of the first two flash signals (Y2 in particular) were increased and the relaxation kinetics were enhanced so that the time constant became about identical to the conditions of steady state oxygen flash amplitudes. The results provide further evidence against a possible participation of either PS I or respiratory processes to Y1/Y2 of cyanobacterial flash patterns. Dramatic effects were observed when protoplasts from Oscillatoria chalybea or cells from Synechocystis sp. PCC 6803 and Synechococcus sp. PCC 7942 were exposed to weak far red background illumination. Under these conditions, Y2 (and to a smaller extent Y1) of otherwise unchanged flash sequences were specifically modified. Y2 was substantially increased and again the relaxation kinetics were accelerated making the signal indistinguishable from a Y(SS) signal. From the mathematical fit of the sequences we conclude that S2 contributes to 10-20% of the S-state distribution (in comparison to 0% in the control). Thus, far red background illumination might represent a valuable means for photosynthetic investigations where high amounts of S2 are required like e. g. EPR measurements. In such experiments the corresponding EPR signals appeared substantially enhanced following far red preillumination (Ahrling and Bader, unpublished observations). Our results clearly show that the 'controversial results' from parts of the literature suggesting the participation of different mechanisms (net oxygen evolution, inhibited uptake processes etc.) are not required to explain the flash-induced oxygen evolution in cyanobacteria: the seemingly 'incompatible' conditions and conformations can be perfectly interconverted by different modulation techniques (chemicals, far red) of the respective redox condition within the water oxidation complex of photosynthesis.
2,4-Dinitrophenol↗
Role of protein phosphatase 2A in calcium-dependent chloride secretion by human colonic epithelial cells.
EGF inhibits carbachol-induced chloride secretion by regulating a basolateral potassium channel via phosphatidylinositol 3-kinase (PI 3-kinase) and PKCepsilon activation. Although both EGF and carbachol cause tyrosine phosphorylation of p85 of PI 3-kinase, only EGF activates the enzyme. Serine phosphorylation of p85 is thought to suppress the lipid kinase of PI 3-kinase. Our present study examined whether the differential effects of carbachol and EGF on PI 3-kinase activity correspond to varying phosphorylation of p85, and the mechanisms and consequences. T(84) colonic epithelial cells were treated with either EGF or carbachol. Cell lysates were immunoprecipitated with p85 antibody and blotted with either phosphotyrosine or phosphoserine antibodies. Protein phosphatase (PP) 1 and 2A activities were also measured. Both tyrosine and serine residues of p85 were phosphorylated by carbachol, whereas EGF induced only tyrosine phosphorylation. Moreover, EGF abolished carbachol-induced serine phosphorylation of p85 and activated PP2A without affecting PP1. Carbachol did not affect either phosphatase. Calyculin A or okadaic acid pretreatment reversed the inhibitory action of EGF on carbachol-induced chloride secretion and restored serine phosphorylation of p85. Although carbachol recruits p85, it phosphorylates both serine and tyrosine residues so that the lipid kinase of PI 3-kinase is inhibited. EGF results in p85 tyrosine phosphorylation as well as dephosphorylation of serine residues via the activation of PP2A. This explains the differential induction of PI 3-kinase enzyme activity in response to EGF and/or carbachol and has functional implications. Our data provide further insights into negative signals that regulate chloride secretion and into the molecular basis of signaling diversification in the intestinal epithelium.
Calcium↗
Amsorb: a new carbon dioxide absorbent for use in anesthetic breathing systems.
BACKGROUND: This article describes a carbon dioxide absorbent for use in anesthesia. The absorbent consists of calcium hydroxide with a compatible humectant, namely, calcium chloride. The absorbent mixture does not contain sodium or potassium hydroxide but includes two setting agents (calcium sulphate and polyvinylpyrrolidine) to improve hardness and porosity. METHODS: The resultant mixture was formulated and subjected to standardized tests for hardness, porosity, and carbon dioxide absorption. Additionally, the new absorbent was exposed in vitro to sevoflurane, desflurane, isoflurane, and enflurane to determine whether these anesthetics were degraded to either compound A or carbon monoxide. The performance data and inertness of the absorbent were compared with two currently available brands of soda lime: Intersorb (Intersurgical Ltd., Berkshire, United Kingdom) and Dragersorb (Drager, Lubeck, Germany). RESULTS: The new carbon dioxide absorbent conformed to United States Pharmacopeia specifications in terms of carbon dioxide absorption, granule hardness, and porosity. When the new material was exposed to sevoflurane (2%) in oxygen at a flow rate of 1 l/min, concentrations of compound A did not increase above those found in the parent drug (1.3-3.3 ppm). In the same experiment, mean +/-SD concentrations of compound A (32.5 +/- 4.5 ppm) were observed when both traditional brands of soda lime were used. After dehydration of the traditional soda limes, immediate exposure to desflurane (60%), enflurane (2%), and isoflurane (2%) produced concentrations of carbon monoxide of 600.0 +/- 10.0 ppm, 580.0 +/- 9.8 ppm, and 620.0 +/-10.1 ppm, respectively. In contrast, concentrations of carbon monoxide were negligible (1-3 ppm) when the anhydrous new absorbent was exposed to the same anesthetics. CONCLUSIONS: The new material is an effective carbon dioxide absorbent and is chemically unreactive with sevoflurane, enflurane, isoflurane, and desflurane.
Absorption↗
Effect of ondansetron on the contractile responses to positive inotropic agents in electrically driven left atria of rats.
We studied the interaction of ondansetron with positive inotropic agents, including serotonin (5-hydroxytryptophane, 5-HT), noradrenaline, 4-aminopyridine (4-AP), calcium chloride, or with reserpine in isolated electrically driven rat atria. Concentrations of 5-HT ranging from 1 to 64 microg/ml increased atrial contractions in a dose-dependent manner. The inotropic effect of 5-HT in the right atria appeared to be weaker than that in the left atria. Ondansetron (30 microg/ml) depressed the positive inotropic effect of lower 5-HT concentrations . This effect was thought to be due to the local anesthetic action of ondansetron or its agonistic interaction with inhibitory imidazoline receptors on the sympathetic nerve endings that reduce noradrenaline release. The positive inotropic effect of 5-HT was abolished almost completely by cyproheptadine (2 microg/ml) and was reversed only partially by pretreatment with reserpine (1 or 3 mg/kg). This result was considered as evidence for the participation of pre- and post-junctional 5-HT2A receptors and the involvement of the sympathetic nervous system in the positive inotropic action of 5-HT in rat atria. Experiments with atropine (1 microg/ml) in atria from reserpine-pretreated rats revealed that the parasympathetic component of the autonomic nervous system is not involved in the inotropic action of 5-HT. Ondansetron (30 microg/ml) tended to increase the positive inotropic effects of noradrenaline, 4-AP, and calcium chloride, which were partially significant at certain concentrations. This result might be due to the activation of both pre- and post-junctional 5-HT2A receptors or due to the inhibition of noradrenaline reuptake into the sympathetic nerve endings through the activation of imidazoline receptors. From these findings, we conclude that the positive inotropic effect of 5-HT in the electrically driven rat atria seems to be mediated primarily by its interaction with 5-HT2A receptors, which are likely to be found on the pre- and post-junctional structures. Other mechanisms that might be involved in this relation are also discussed.
4-Aminopyridine↗
Calcium: effect of different amounts on nonheme- and heme-iron absorption in humans.
We investigated the effect of calcium on iron absorption in 126 human subjects. Addition of calcium chloride to wheat rolls significantly reduced iron absorption. Doses between 40 and 600 mg Ca were studied. The inhibition was clearly dose related up to 300 mg Ca. Calcium added to the dough when making the rolls reduced phytate degradation during fermentation and baking. As little as 40 mg Ca added to 80 g flour reduced phytate degradation by 50%, thus increasing the phytate content of the rolls to levels interfering with iron absorption. Calcium also had a direct dose-related inhibiting effect on iron absorption, noted by adding calcium to the rolls after they had been baked instead of to the dough. Iron absorption was reduced by 50-60% at doses of 300-600 mg Ca. Giving 165 mg Ca as milk, cheese, or calcium chloride reduced absorption by 50-60%. The same amount of calcium also significantly reduced heme-iron absorption, suggesting that the effect of calcium is related to the mucosal transfer of iron. The observed marked inhibitory effect on iron absorption of calcium in amounts frequently encountered in normal meals has important nutritional implications.
Absorption↗
Calpains mediate calcium and chloride influx during the late phase of cell injury.
The role of Ca++ in cell death is controversial. Extracellular Ca++ influx and calpain activation occurred during the late phase of renal proximal tubule cell injury produced by the mitochondrial inhibitor antimycin A. Chelation of intracellular Ca++, extracellular Ca++, the calcium channel blocker nifedipine, calpain inhibitor 1 and the dissimilar calpain inhibitor PD150606 blocked antimycin A-induced influx of extracellular Ca++ and cell death. The calcium channel blocker verapamil was ineffective. Calpain inhibitor 1 and PD150606 were cytoprotective also against tetrafluoroethyl-L-cysteine-, bromohydroquinone-, oxidant (t-butylhydroperoxide)- and calcium ionophore (ionomycin)-induced cell death. Extracellular Ca++ influx was associated with the translocation of calpain activity from the cytosol to the membrane and was prevented by calpain inhibitor 1, PD150606 and nifedipine. Finally, nifedipine, calpain inhibitor 1, PD150606 and the Cl- channel inhibitors [5-nitro-2-(3-phenylpropylamino)-benzoate, niflumic acid, diphenylamine-2-carboxylate, and indanyloxyacetic acid] blocked the increase in Cl- influx that occurs during the late phase of cell injury and triggers terminal cell swelling and death. These data suggest that Ca++ and calpains play a common and critical role in renal proximal tubule cell death produced by diverse agents. In addition, calpain activation appears to play a dual role during the late phase of cell injury. Initial calpain activation elicits extracellular Ca++ influx through a nifedipine-sensitive pathway, resulting in calpain translocation to the membrane and in turn Cl- influx.
Acrylates↗