Rate Of Ca Uptake Research Articles

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Bioavailability of waterborne strontium to the common carp, Cyprinus carpio, in complexing environments

The uptake of strontium (Sr) and calcium (Ca) in the common carp, Cyprinus carpio, was studied in chemically defined freshwater in the presence of the complexing ligands, ethylenediaminetetraacetic acid (EDTA), and nitrilotriacetic acid (NTA). The uptake rates were measured in the whole body, gills, and blood of the fish after an exposure period of 3 h. The uptake rates were determined by using the radiotracers 85Sr and 45Ca, and analyzed as a function of the free-ion activity of Sr and Ca in water. Although Sr 2+ activity decreased, the uptake of Sr showed an increase at relatively low concentrations of EDTA and NTA, and a decrease at relatively high concentrations. This can be explained by the decreased competition between Sr 2+ and Ca 2+ at the gill uptake sites due to ∼30–140-fold higher affinity of EDTA and NTA for Ca 2+ than Sr 2+. With decreasing Ca 2+ activity, Ca uptake rates decreased in the presence of EDTA and NTA, but the effect of NTA was less pronounced. A Michaelis–Menten type competitive inhibition model was derived that could predict the whole-body Sr and Ca uptake rates, taking into account the ambient Sr 2+ and Ca 2+ activities in the presence of EDTA. In case of NTA, the uptake rates were found to be 1.5–3.2 times higher than what was predicted by the model. When the fish were exposed to complexing environments in the complete absence of Ca, an increased uptake of Sr was still observed in case of NTA, but not EDTA. The increased uptake in the presence of NTA is attributed to the direct uptake of SrNTA − and CaNTA − complexes from water. The results reveal that the uptake of Sr and Ca in carp is not merely a function of the free metal-ion activity but that certain complex species may contribute significantly to overall uptake.

Glycogen and glycogen phosphorylase associated with sarcoplasmic reticulum: effects of fatiguing activity.

The purpose of the present study was to investigate the effects of fatiguing muscular activity on glycogen, glycogen phosphorylase (GP), and Ca(2+) uptake associated with the sarcoplasmic reticulum (SR). Tetanic contractions (100 ms, 75 Hz) of the gastrocnemius and plantaris muscles, elicited once per second for 15 min, significantly reduced force to 26.5 +/- 4.0% and whole muscle glycogen to 23% of rested levels. SR glycogen levels were 415.4 +/- 76.6 and 20.4 +/- 2.1 microg/mg SR protein in rested and fatigued samples, respectively. The optical density of GP from SDS-PAGE was reduced to 21% of control, whereas pyridoxal 5'-phosphate concentration, a quantitative indicator of GP content, was significantly reduced to 3% of control. GP activity after exercise, in the direction of glycogen breakdown, was reduced to 4% of control. Maximum SR Ca(2+) uptake rate was also significantly reduced to 81% of control. These data demonstrate that glycogen and GP associated with skeletal muscle SR are reduced after fatiguing activity.

Potentiation of Ca(2+) release by cADP-ribose in the heart is mediated by enhanced SR Ca(2+) uptake into the sarcoplasmic reticulum.

cADP-Ribose (cADPR) is a novel endogenous messenger that is believed to mobilize Ca(2+) from ryanodine-sensitive Ca(2+) stores. Despite intense research, the precise mechanism of action of cADPR remains uncertain, and experimental findings are contradictory. To elucidate the mechanism of cADPR action, we performed confocal Ca(2+) imaging in saponin-permeabilized rat ventricular myocytes. Exposure of the cells to cADPR resulted in a slow (>2 minutes) and steady increase in the frequency of Ca(2+) sparks. These effects on local release events were accompanied by a significant increase in sarcoplasmic reticulum (SR) Ca(2+) content. In comparison, sensitization of ryanodine receptors (RyRs) by caffeine, a true RyR agonist, caused a rapid (<1 second) and transient potentiation of Ca(2+) sparks followed by a decrease in SR Ca(2+) content. When the increase in the SR load was prevented by partial inhibition of the SR Ca(2+) with thapsigargin, cADPR failed to produce any increase in sparking activity. cADPR had no significant impact on activity of single cardiac RyRs incorporated into lipid bilayers. However, it caused a significant increase in the rate of Ca(2+) uptake by cardiac SR microsomes. Our results suggest that the primary target of cADPR is the SR Ca(2+) uptake mechanism. Potentiation of Ca(2+) release by cADPR is mediated by increased accumulation of Ca(2+) in the SR and subsequent luminal Ca(2+)-dependent activation of RyRs.

Specific proteolysis of the NR2 subunit at multiple sites by calpain

The NMDA subtype of glutamate receptor plays an important role in the molecular mechanisms of learning, memory and excitotoxicity. NMDA receptors are highly permeable to calcium, which can lead to the activation of the calcium-dependent protease, calpain. In the present study, the ability of calpain to modulate NMDA receptor function through direct proteolytic digestion of the individual NMDA receptor subunits was examined. HEK293t cells were cotransfected with the NR1a/2A, NR1a/2B or NR1a/2C receptor combinations. Cellular homogenates of these receptor combinations were prepared and digested by purified calpain I in vitro. All three NR2 subunits could be proteolyzed by calpain I while no actin or NR1a cleavage was observed. Based on immunoblot analysis, calpain cleavage of NR2A, NR2B and NR2C subunits was limited to their C-terminal region. In vitro calpain digestion of fusion protein constructs containing the C-terminal region of NR2A yielded two cleavage sites at amino acids 1279 and 1330. Although it has been suggested that calpain cleavage of the NMDA receptor may act as a negative feedback mechanism, the current findings demonstrated that calpain cleavage did not alter [(125)I]MK801 binding and that receptors truncated to the identified cleavage sites had peak intracellular calcium levels, (45)Ca uptake rates and basal electrophysiological properties similar to wild type.

Phospholamban Decreases the Energetic Efficiency of the Sarcoplasmic Reticulum Ca Pump

We tested the hypothesis that increased Sarcoplasmic reticulum (SR) Ca content ([Ca](SRT)) in phospholamban knockout mice (PLB-KO) is because of increased SR Ca pump efficiency defined by the steady-state SR [Ca] gradient. The time course of thapsigargin-sensitive ATP-dependent (45)Ca influx into and efflux out of cardiac SR vesicles from PLB-KO and wild-type (WT) mice was measured at 100 nm free [Ca]. We found that PLB decreased the initial SR Ca uptake rate (0.13 versus 0.31 nmol/mg/s) and decreased steady-state (45)Ca content (0.9 versus 4.1 nmol/mg protein). Furthermore, at similar total SR [Ca], the pump-mediated Ca efflux rate was higher in WT (0.065 versus 0.037 nmol/mg/s). The pump-independent leak rate constant (k(leak)) was also measured at 100 nm free [Ca]. The results indicate that k(leak) was < 1% of pump-mediated backflux and was not different among nonpentameric mutant PLB (PLB-C41F), WT pentameric PLB (same expression level), and PLB-KO. Therefore differences in passive SR Ca leak cannot be the cause of the higher thapsigargin-sensitive Ca efflux from the WT membranes. We conclude that the decreased total SR [Ca] in WT mice is caused by decreased SR Ca influx rate, an increased Ca-pump backflux, and unaltered leak. Based upon both thermodynamic and kinetic analysis, we conclude that PLB decreases the energetic efficiency of the SR Ca pump.

Kinetic Analysis of a Model of the Sarcoplasmic Reticulum Ca-ATPase, with Variable Stoichiometry, which Enhances the Amount and the Rate of Ca Transport

The sarcoplasmic reticulum (SR) Ca-dependent adenosinetriphosphatase (Ca-ATPase) actively transports Ca2+from the myoplasm to the SR lumen. Under optimal conditions a 2:1 stoichiometry of Ca transport/ATP hydrolysis has been observed, but lower stoichiometries have been reported under several circumstances. A lower stoichiometry under conditions of high Ca2+load, although thermodynamically less efficient, could in theory increase the rate and the maximal amount of Ca uptake. We analysed, by computing simulation, the transient kinetics of a model of the SR Ca-ATPase with variable stoichiometry. The model is based on current experimental reports and includes the most relevant properties of the system. The results show an acceleration in the rate of Ca uptake, an increase in the net Ca transport, and an increase in the rate of [Ca2+] reduction in the medium, which might be physiologically useful to increase the rate of Ca pumping at high Ca load of the sarcoplasmic reticulum.

Sarcoplasmic reticulum function and carnitine palmitoyltransferase-1 inhibition during progression of heart failure.

Failing cardiac hypertrophy is associated with an inadequate sarcoplasmic reticulum (SR) function. The hypothesis was examined that pressure overloaded hearts fail to increase SR Ca(2+) uptake rate proportionally to the hypertrophy and that carnitine palmitoyltransferase-1 inhibition by etomoxir ((+/-)-ethyl 2[6(4-chlorophenoxy)hexyl] oxirane-2-carboxylate) can counteract this process. Severe left ventricular pressure overload was induced in rats by constricting the ascending aorta for 8, 10, 14 and 28 weeks leading to cardiac hypertrophy (+62 - +103% of sham-operated rats) and pulmonary congestion. Homogenate oxalate-facilitated SR Ca(2+) uptake rate g wet wt(-1) was reduced (P<0.05) by 29.9+/-1.8% irrespective of phospholamban phosphorylation (in the presence of catalytic subunit of protein kinase A) and inhibition of SR Ca(2+) release channel by ruthenium red. SERCA2 protein level was reduced (P<0.05) by 30.4+/-0.8%. SR Ca(2+) uptake rate was inversely correlated (P<0.05) with left ventricular weight but was not affected by the occurrence of pulmonary congestion. Because SR Ca(2+) uptake rate of whole ventricles was not reduced, a hypertrophy proportional dilution of SR Ca(2+) uptake has to be inferred which precedes pulmonary congestion. Treatment with etomoxir (15 mg kg body wt(-1) day(-1) for 10 weeks) did not affect left ventricular weight but decreased (P:<0.05) the right ventricular hypertrophy related to pulmonary congestion. In parallel, SR Ca(2+) uptake rate of left ventricle and myosin isozyme V(1) were increased (P<0.05). Etomoxir represents a candidate approach for prevention of heart failure by inducing a hypertrophy proportional increase in SR Ca(2+) uptake rate.

Calcium Depletion in a Southeastern United States Forest Ecosystem

Forest soil Ca depletion through leaching and vegetation uptake may threaten long‐term sustainability of forest productivity in the southeastern USA. This study was conducted to assess Ca pools and fluxes in a representative southern Piedmont forest to determine the soil Ca depletion rate. Soil Ca storage, Ca inputs in atmospheric deposition, and outputs in soil leaching and vegetation uptake were investigated at the Panola Mountain Research Watershed (PMRW) near Atlanta, GA. Average annual outputs of 12.3 kg ha−1 yr−1 in uptake into merchantable wood and 2.71 kg ha−1 yr−1 soil leaching exceeded inputs in atmospheric deposition of 2.24 kg ha−1 yr−1 The annual rate of Ca uptake into merchantable wood exceeds soil leaching losses by a factor of more than five. The potential for primary mineral weathering to provide a substantial amount of Ca inputs is low. Estimates of Ca replenishment through mineral weathering in the surface 1 m of soil and saprolite was estimated to be 0.12 kg ha−1 yr−1 The weathering rate in saprolite and partially weathered bedrock below the surface 1 m is similarly quite low because mineral Ca is largely depleted. The soil Ca depletion rate at PMRW is estimated to be 12.7 kg ha−1 yr−1 At PMRW and similar hardwood‐dominated forests in the Piedmont physiographic province, Ca depletion will probably reduce soil reserves to less than the requirement for a merchantable forest stand in ≈80 yr. This assessment and comparable analyses at other southeastern USA forest sites suggests that there is a strong potential for a regional problem in forest nutrition in the long term.

Characterization of Isolated Acidocalcisomes of Trypanosoma cruzi

The acidocalcisome is an acidic calcium store in trypanosomatids with a vacuolar-type proton-pumping pyrophosphatase (V-H(+)-PPase) located in its membrane. In this paper, we describe a new method using iodixanol density gradients for purification of the acidocalcisome from Trypanosoma cruzi epimastigotes. Pyrophosphatase assays indicated that the isolated organelle was at least 60-fold purified compared with the large organelle (10,000 x g) fraction. Assays for other organelles generally indicated no enrichment in the acidocalcisome fraction; glycosomes were concentrated 5-fold. Vanadate-sensitive ATP-driven Ca(2+) uptake (Ca(2+)-ATPase) activity was detectable in the isolated acidocalcisome, but ionophore experiments indicated that it was not acidic. However, when pyrophosphate was added, the organelle acidified, and the rate of Ca(2+) uptake increased. Use of the indicator Oxonol VI showed that V-H(+)-PPase activity generated a membrane potential. Use of sulfate or nitrate in place of chloride in the assay buffer did not affect V-H(+)-PPase activity, but there was less activity with gluconate. Organelle acidification was countered by the chloride/proton symport cycloprogidiosin. No vacuolar H(+)-ATPase activity was detectable in isolated acidocalcisomes. However, immunoblots showed the presence of at least a membrane-bound V-H(+)-ATPase subunit, while experiments employing permeabilized epimastigotes suggested that vacuolar H(+)-ATPase and V-H(+)-PPase activities are present in the same Ca(2+)-containing compartment.

Loss of the Major Isoform of Phosphoglucomutase Results in Altered Calcium Homeostasis in Saccharomyces cerevisiae

Phosphoglucomutase (PGM) is a key enzyme in glucose metabolism, where it catalyzes the interconversion of glucose 1-phosphate (Glc-1-P) and glucose 6-phosphate (Glc-6-P). In this study, we make the novel observation that PGM is also involved in the regulation of cellular Ca(2+) homeostasis in Saccharomyces cerevisiae. When a strain lacking the major isoform of PGM (pgm2Delta) was grown on media containing galactose as sole carbon source, its rate of Ca(2+) uptake was 5-fold higher than an isogenic wild-type strain. This increased rate of Ca(2+) uptake resulted in a 9-fold increase in the steady-state total cellular Ca(2+) level. The fraction of cellular Ca(2+) located in the exchangeable pool in the pgm2Delta strain was found to be as large as the exchangeable fraction observed in wild-type cells, suggesting that the depletion of Golgi Ca(2+) stores is not responsible for the increased rate of Ca(2+) uptake. We also found that growth of the pgm2Delta strain on galactose media is inhibited by 10 microM cyclosporin A, suggesting that activation of the calmodulin/calcineurin signaling pathway is required to activate the Ca(2+) transporters that sequester the increased cytosolic Ca(2+) load caused by this high rate of Ca(2+) uptake. We propose that these Ca(2+)-related alterations are attributable to a reduced metabolic flux between Glc-1-P and Glc-6-P due to a limitation of PGM enzymatic activity in the pgm2Delta strain. Consistent with this hypothesis, we found that this "metabolic bottleneck" resulted in an 8-fold increase in the Glc-1-P level compared with the wild-type strain, while the Glc-6-P and ATP levels were normal. These results suggest that Glc-1-P (or a related metabolite) may participate in the control of Ca(2+) uptake from the environment.

Aluminum toxicity perturbs long bone calcification in the embryonic chick.

Long bone calcification in chick embryos acutely- or chronically-treated with aluminum (Al) citrate was investigated. Acutely treated embryos received 100 microl of 60 mM Al citrate, 60 mM sodium (Na) citrate, or 0.7% sodium chloride on day 8 of incubation. Chronically treated embryos received a daily 25 microl dose of the above solutions beginning on day 8. Following 2-8 days of additional incubation, blood was collected, embryos killed, hind limbs radiographed, and tibias collected. Radiography indicated that Al administration resulted in a persistent angulation in the mid-diaphysis of tibias and femurs and a transient mineralization defect during the 10- to 12-day period of incubation. Tibias from 10- to 12-day embryos which were administered Al contained significantly less (P < 0.005) bone calcium (Ca) compared with tibias from NaCl-treated embryos. By day 14 there were no significant differences among the Ca content of tibias from embryos acutely treated with Al citrate, Na citrate or NaCl. Similarly, the rate of (45)Ca uptake by tibias of embryos treated with Al was significantly lower on days 10 (acute) and 12 (chronic) with no significant differences in Ca uptake rate among the three treatment groups by day 16. In each treatment group bone alkaline phosphatase (ALPase) activity increased approximately tenfold between days 10 and 16. At all stages, bone ALPase activity was consistently higher and significantly different (chronic) compared with levels in NaCl-treated embryos. In contrast, Al had no significant effect on the rate of tibia collagen and noncollagenous protein synthesis or serum levels of procollagen carboxy-terminal propeptide (PICP), osteocalcin, and parathyroid hormone (PTH).

Ca(2+) uptake in the sarcoplasmic reticulum from the systemic heart of octopod cephalopods.

We have measured Ca(2+) uptake in crude homogenates of heart tissue, as well as cell shortening and ionic currents in isolated myocytes exposed to caffeine, to characterize Ca(2+) uptake in the sarcoplasmic reticulum (SR) of the systemic heart of octopus. The maximal rate of SR Ca(2+) uptake in crude homogenates of octopus heart was 43+/-4 (mean +/- s.e.m., N=7), compared with 28+/-2 nmol min(-)(1 )mg(-)(1) protein (N=4) in homogenates of rat heart. The Ca(2+)-dependency of SR Ca(2+) uptake was similar for the two species, with a Ca(2+) activity at half-maximal uptake rate (pCa(50)) of 6.04+/-0.02 for octopus and 6.02+/-0.05 for rat. Exposure of isolated myocytes to 10 mmol l(-)(1) caffeine resulted in cell shortening to 53+/-2 % of the resting cell length and an inward trans-sarcolemmal ionic current. The charge carried by this current was 3.28+/-0.70 pC pF(-)(1) (mean +/- s.e.m., N=5) corresponding to extrusion of 34.0+/-0.7 amol Ca(2+ )pF(-)(1) from the cell by Na(+)/Ca(2+) exchange. This is approximately 50 times more than the Ca(2+) carried by the Ca(2+) current elicited by a 200 ms depolarization from -80 to 0 mV and corresponds to an increase in the total intracellular [Ca(2+)] of 404+/-86 (&mgr;)mol l(-)(1) non-mitochondrial volume due to Ca(2+) release from the SR. Thus, we find that at 20 degrees C in the SR both Ca(2+) content and Ca(2+) uptake rate in the systemic heart of octopus are comparable with or larger than the corresponding values obtained in the rat heart. These results support the argument that the SR may play an important role in the regulation of contraction in the systemic heart of cephalopods.

Na-dependent changes in intracellular Ca in spontaneously hypertensive rat hearts

To determine whether Na/Ca exchange is altered in primary hypertension, Na-dependent changes in intracellular Ca, ([Ca] i), were measured in isolated perfused hearts from Wistar–Kyoto (WKY) and spontaneously hypertensive (SHR) rats. Intracellular Na, (Na i, mEq/kg dry wt), and [Ca] i were measured by NMR spectroscopy. Control [Ca] i was less in WKY than SHR (176±18 vs 253±21 nmol/l; mean±S.E., P<0.05), whereas Na i was not significantly different. One explanation for this is that net Na/Ca exchange flux is decreased in SHR. If this hypothesis is correct, the rate of Ca uptake in SHR should be less than WKY when Na/Ca exchange is reversed by decreasing the transmembrane Na gradient. The Na gradient was reduced by decreasing extracellular Na, ([Na] o) and/or by increasing [Na] i. To increase [Na] i, Na uptake was stimulated by acidification while Na extrusion by Na/K ATPase was inhibited by K-free perfusion. Seventeen minutes after acidification, Na i had increased but was not significantly different in SHR and WKY (18.0±2.3 to 57.4±7.6 vs 20.3±0.6 to 66.5±4.8 mEq/kg dry wt, respectively). Yet [Ca] i was greater in WKY than SHR (1768±142 vs 1201±90 nmol/l; P<0.05). [Ca] i was also measured after decreasing [Na] o from 141 to 30 mmol/l. Fifteen minutes after reducing [Na] o, [Ca] i was greater in WKY than SHR (833±119 vs 425±94 nmol/l; P<0.05). Thus for both protocols, decreasing the transmembrane Na gradient led to increased [Ca] i in both SHR and WKY, but less increase in SHR. The results are consistent with the hypothesis that Na/Ca exchange activity is less in SHR than WKY myocardium.

Tansley Review No. 104

SummaryCalcium occupies a unique position among plant nutrients both chemically and functionally. Its chemical properties allow it to exist in a wide range of binding states and to serve in both structural and messenger roles. Despite its importance in many plant processes, Ca mobility is low, making Ca uptake and distribution rate a limiting process for many key plant functions. Ca plays an essential role in regulating many physiological processes that influence both growth and responses to environmental stresses. Included among these are: water and solute movement, influenced through effects on membrane structure and stomatal function; cell division and cell wall synthesis; direct or signaling roles in systems involved in plant defense and repair of damage from biotic and abiotic stress; rates of respiratory metabolism and translocation; and structural chemistry and function of woody support tissues. Forest trees, because of their size and age capacity, have been examined for evidence of limitations imposed by the timing and level of Ca supply. Examination of Ca physiology and biogeochemical cycling for forested systems reveals many indications that Ca supply places important limitations on forest structure and function. These limitations are likely to be most significant with older trees, later successional stages, high levels of soil acidity and/or high canopy Ca leaching losses, or under conditions where plant competition is high or transpiration is limited by high humidity or low soil moisture. Evidence of structural and physiological adaptations of forests to limited Ca supply; indicators of system dysfunction at many levels under reduced Ca supply; and the positive responses of diverse indicators of forest vitality in liming experiments indicate that Ca is more important to forest function and structure than has generally been recognized. Lack of recognition of Ca limitations is due in part to that fact some important plant functions are controlled by changes in very small physiologically active pools within the cytoplasm, and whole‐leaf Ca levels may not reflect these limitations. An additional aspect is the fact that Ca availability has declined significantly for many forests in just the past few decades. Additional research on the role of Ca supply in resistance of forests to disease, changes in structural integrity of woody tissues, restrictions on rooting patterns and function, and uptake of other nutrients, notably N, is needed. Increased understanding of the physiological ecology of Ca supply can be anticipated to provide important insights that will aid in future protection and management of both natural and commercial forest systems. contents Summary I. introduction – a hypothesis 374 II. effects of calcium on physiological processes 376 III. calcium uptake and distribution at the whole‐plant level 382 IV. ecosystem processes and calcium supply 387 V. plant and ecosystem responses to human alterations in calcium supply 391 VI. conclusion 407 VII. evaluation of the hypothesis 410 Acknowledgements 411

Excitation-induced Ca2+ uptake in rat skeletal muscle.

In isolated rat extensor digitorum longus (EDL) muscle mounted for isometric contractions, chronic low-frequency electrical stimulation was found to lead to an increased uptake of 45Ca (154% above control after 240 min) and a progressive accumulation of Ca2+ (85% above control after 240 min). In soleus, however, this treatment led to a small, but significant, increase in 45Ca uptake (30% above control after 180 min) but no significant accumulation of Ca2+. In muscles mounted for isotonic contractions without any external load, electrical stimulation gave rise to a larger 45Ca uptake and accumulation of Ca2+ in both EDL and soleus. These uptakes of Ca2+ coincided with an accumulation of Na+. During isometric or isotonic contractions, stimulation at 40 Hz increased the initial (60 s) rate of 45Ca uptake in soleus muscle 15- and 30-fold, respectively. The stimulation-induced increase in 45Ca uptake was only reduced by 17% by the Ca2+-channel blockers nifedipine and verapamil but was blocked by tetrodotoxin. The initial rate of stimulation-induced 22Na and 45Ca uptake was correlated (r = 0.80; P < 0.003). Stimulation of Na+ channels with veratridine increased 45Ca uptake by 93 and 139% in soleus and EDL, respectively (P < 0.001), effects that were abolished by tetrodotoxin. The results indicate that in skeletal muscle, excitation induces a considerable influx of Ca2+, mediated by Na+ channels.

Ca uptake by heart cells: II. Most entering Ca appears to leave without mixing with the sarcoplasmic reticulum Ca pool

The rate of verapamil-sensitive uptake of 45Ca by rat heart cells stimulated to beat in suspension with 0.2 mM Ca and isoproterenol was increased > 2-fold by cell loading with the chelator Quin-2. No effect of Quin-2 loading was observed on the rate of uptake of trace levels of 54Mn, present in addition to Ca, which was used as an index of Ca channel activity. Quin-2 loading also had little effect on the rate of 45Ca uptake by cells diluted into a high K/low Na medium, where Ca uptake was primarily by Na/Ca exchange. The fast chelator 1,2- bis(o-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid (BAPTA) was 3-fold more effective than the slow chelator EGTA at preventing Ca efflux. BAPTA loading also caused an increase in sarcoplasmic reticulum (SR) Ca content. These results suggest that chelator loading had little effect on the rate of Ca influx by Ca channels or by Na/Ca exchange, and that the increased rate of 45Ca uptake seen with Quin-2 loading was caused by an inhibition of Ca efflux, either directly by chelation or by increased Ca uptake by the SR or by other intracellular organelles. This further suggests that most of the Ca entering the cell without chelator leaves again within the same beat, and that this may result from Ca efflux from a kinetically limited Ca pool in or around the diad cleft.

Interaction of light metals and protons with seaweed biosorbent

Based on their displacement by protons, the following ascending order of light metals affinity toward Sargassum fluitans biomass was observed: Na + ⩽ K + < Mg 2+ < Ca 2+ < Al 3+. Higher biomass-metal affinities resulted in lowering the leaching tendency of (polysaccharidic) biomass components during the sorption process. More than 12% weight loss of protonated biomass occurred during 2 min of sorption, which should be considered in all stoichiometric and sorption calculations. The rate of proton uptake for Na-loaded and Ca-loaded S. fluitans biomass at pH 4.5 was lower than the rate of desorption at pH 1.1. In the case of Na-loaded S. fluitans, the predominant proton uptake rate was of a zero order. Na uptake by protonated S. fluitans biomass did not take place at all in the presence of Ca and Al ions. However, it increased in the absence of other light metals. Since the affinity of Ca 2+ for the biomass was much greater than that of Na +, the three-component system of Na +, H + and Ca 2+ could be simplified into proton-calcium ion exchange. The initial rate of Ca uptake with protonated S. fluitans biomass at pH 4.5 was lower than that of proton release from biomass. Approximately 20% of Ca 2+ sorbed was bound to the binding site as a mono-valent ion. Titration and stoichiometric indications pointed to the fact that Al was being sorbed as a hydroxyl complex.

Flow Rate as an Important Physiological Factor Associated to Calcium Concentration in Pods of Snap Bean (Phaseolus vulgaris L.) Plants Grown Aeroponically

To understand physiological factors associated with genetic differences for pod Ca concentration between snap bean genotypes, flow rate and Ca uptake of sieve sap were measured, as well as pod Ca concentration. Measurements for flow rate and Ca uptake were done at three developmental stages (fl owering and 1 and 3 weeks after) in two commercial snap bean cultivars (Hystyle and Labrador) grown aeroponically. Pods were collected 2 weeks after flowering only. Flow rate and Ca uptake sampling began 4 weeks after transplanting and consisted of: 1) decapitation of the plant at the first node; 2) covering the stem with pre-weighed dry cotton; and 3) removing the cotton, reweighing it, and saving it for Ca determination. Flow rate was defined as the difference in cotton weight (expressed as ml) per 17 hr divided by foliage mass. Ca uptake was defined as mg of Ca per total volume of sieve sap after 17 hr divided by foliage mass. Ca determinations were made using an atomic absorption spectrophotometer. A positive correlation between flow rate and total Ca uptake of sieve sap (R2 = 0.90), flow rate and pod Ca concentration (R2 = 0.47), and Ca uptake and pod Ca concentration (R2 = 0.42) were found. Hystyle reflected 1.5 times more flow rate and pod Ca concentration than Labrador. Significant differences between genotypes for pod Ca concentration, Ca uptake, and flow rate were observed. Results were consistent across developmental stages.

Developmental changes in the45Ca2+ uptake byTrichoderma viride mycelium

The rate of the(45)Ca(2+) uptake by the submergedTrichoderma viride mycelium increased with the age of the culture from 6 h until a maximum which was reached at about 30 h, and then decreased until the uptake was virtually zero. The decrease in the rate of the(45)Ca(2+) uptake was accompanied by an increase of mycelial mass. The uptake rate could not be reactivated upon substituting the medium for a fresh one, without or with dilution of the mycelium. The results suggest that the rate of(45)Ca(2+) uptake reflects the biological age of the submerged culture. The surface-cultivated mycelium took up(45)Ca(2+) proportionally with time. The autoradiography of colonies showed that(45)Ca(2+) was distributed homogeneously throughout the mycelium during vegetative growth while conidiation was accompanied by a massive accumulation of(45)Ca(2+) in conidia.