Cells calcium pools

Fig. 2. Effect of calcium antagonists (CA) on a cardiac cell. Top typical cardiac action potential. The calcium (slow) inward current flows during the characteristic plateau phase (phase 2) of the action potential. This calcium influx is selectively inhibited by CA. Activation of the sarcoplasmic reticulum (SR) and other cellular calcium pools occurs via Ca + and Na+ ions which flow into the cell. The SR and other pools donate activator Ca + ions which stimulate the contractile proteins. The presence of tubular systems (invaginations), which are characteristic of cardiac tissues, results in considerable enlargement of the cellular surface, thus enabling an effective influx of Na+ and Ca + ions. Inhibition of the calcium inward flux by a CA causes diminished activation of the contractile proteins.

Studies of the efflux of Ca by stimulated rabbit atria have characterized three calcium pools. Phase I may represent extracellular washout of the Ca that binds to the surface of muscle membrane and is characterized by a high rate constant. Phase II may represent loosely bound calcium present in cell membrane and calcium released at the sarcoplasmic reticulum. Calcium in this pool is directly related to contractility.65,84,93 phase III may represent the tightly bound calcium that exchanges very slotrly and does not play a role in maintaining calcium concentrations. Recent study has shown that the storage or release of calcium at the sarcoplasmic reticulum and other loosely bound calcium sites (cell membrane) that are involved in muscle contractility can be directly affected by 2-PAM.21 These results Indicate that 2-PAM increases the rate of release of Phase II calcium. 

Superimposed on these records are markings of environmental perturbations which sometimes inhibit, and sometimes accelerate carbonate deposition. In the final analysis, however, there has to be an answer, why organisms respond in such a systematic fashion. In all probability these phenomena are connected to the high demand for calcium at all levels of the cell regulatory system. Only at times of lower activities or when the calcium pool runs over will the excretory system package and export the surplus calcium to the periphery of the cell where it may be utilized in carbonate deposition. 

It has become increasingly clear that there is a non-mitochondrial, intracellular calcium pool which plays an important role in cell activation in a large number of nonmuscle cells as well as in smooth and skeletal muscle. This pool is relatively enormous in skeletal muscle, provides the bulk of the Ca2+ needed to regulate skeletal muscle contraction, and is located in a distinct organelle, the sarcoplasmic reticulum. The pool is smaller in non-muscle and in smooth muscle cells, and its location less obvious [10,11]. To fill the pool requires ATP, i.e., uptake of Ca2+ into the pool is driven by a distinct Ca2+-ATPase, an enzyme which purifies with the mi-... 

The mitochondrial Ca2+ pool plays a second role in cellular Ca2+ homeostasis by serving as a sink for Ca2+ during times of excessive Ca2+ uptake by the cell. Under this circumstance, the non-ionic calcium pool in the matrix space can increase 10-fold or more, thereby protecting the cell from Ca2+ intoxication. This mechanism provides a temporary device by which the cell can protect itself, but in the long term only by regulating Ca2+ fluxes across the plasma membrane can the cell maintain Ca2+ homeostasis [14]. 

Fig. 3. The interrelated changes in the metabolism of phosphatidylinositol 4,5-bisphosphate (PIP2) and Ca2+ during activation of the cell by a typical Ca2+-dependent hormone. R, receptor G, guanine regulatory protein PLC, phospholipase C DG, diacylglycerol CK, protein kinase C [Ca2+]sm, the Ca2+ concentration in a cellular domain just beneath the plasma membrane (striped area) Insl,4,SP3, inositol 1,4,5-trisphosphate Insl,3,4,5P4, inositol 1,3,4,5-tetrakisphosphate [Ca2+]c, cytosolic Ca2+ concentration CaM, calmodulin arrows (=>), fluxes of Ca2+ across membranes s=>, energy-dependent fluxes CaY, a calcium pool in specialized compartment of the endoplasmic reticulum. See text for discussion.

The mobilization of calcium results not only in the observed transient rise in intracellular free calcium and enhanced cellular efflux, but also in a net loss of calcium from the cell (Fig. 1). Thus, total cell calcium declines with All stimulation of adrenal and vascular smooth muscle cells [44]. Furthermore, total cell calcium remains low throughout the duration of exposure to All, suggesting that the continued formation of small amounts of 1,4,5-IP3 prevents refilling of the ER pool. Upon the removal of All and the immediate reduction in IP3 concentration, total cell calcium rapidly recovers to prestimulation levels without a detectable change in cytosolic free calcium, as measured by calcium-sensitive dyes. This observation has been taken as evidence that the IP3-releasable ER pool is in direct communication with the plasma membrane and that extracellular calcium refills the pool without entering the bulk cytosol (see Ref. 45). The location of this pool within the cell (cytosolic vs. adjacent to the plasma membrane) remains a matter of controversy (see Rasmussen arid Barrett, Chapter 4). 

Luo X, He Q, Huang Y, Sheikh MS (2005) Transcriptional upregulation of PUMA modulates endoplasmic reticulum calcium pool depletion-induced apoptosis via Bax activation. Cell Death Differ 12 1310-1318... 

C signal transduction pathway. Secretion of calcitonin is stimulated by hypercalcemia but the effect of the hormone on calcium transport appears to be secondary to increased phosphate uptake by target cells. The number and activity of osteoclasts are decreased, and urinary excretion of hy-droxyproline is decreased, Calcitonin may also inhibit release of calcium from the extracellular fluid calcium pool, but it increases calcium and phosphate excretion by renal tubules. Some tubular cells respond to calcitonin, PTH, and vasopressin, while others respond only to one or two of these hormones. In general, the actions of calcitonin in kidney and in bone are antagonistic to those of PTH. Calcitonin decreases secretion of gastrin and of gastric acid, and inhibits bile flow. 

Dolor, R., L. Hurwitz, Z. Mirza, H. Strauss R. Whorton. 1992. Regulation of extracellular Ca entry in endothelial cells role of intracellular calcium pool. J. Am. Physiol 262 C171-C181. 

Dupont, G. A. Goldbeter. 1993. One-pool model for Ca " oscillations involving Ca and inositol 1,4,5-trisphosphate as co-agonists for Ca release. Cell Calcium 14 311-22. 

It is well documented that N-formyl peptides induce a rapid, transient rise in intracellular calcium in neutrophils. It is also well established that inositol 1,4,5-trisphosphate released by the action of PLC triggers the release of Ca from intracellular stores. With the exception of the specific condition of neutrophils migrating on fibronectin and vitronectin [91], migration appears to occur in the absence of the intracellular calcium transient [196, 299, 456]. However, the studies that demonstrated this conclusion utilized indicators and buffers of cytosolic calcium that may not probe the entire calcium pool. Evidence suggests two additional mechanisms for regulating calcium that may have an impact on cell migration. 

Korchak, J.M., Vienne, K., Wilkenfeld, C., Roberts, C.S., Rutherford, L.E., Haines, K.A. and Weissmann, G. (1983). The role of calcium in neutrophil activation—mobilization of multiple calcium pools. J. Cell Biol. 97, 160a. 

Severson. D. L., Denton, R. M., Bridges, B. J., and Randle, P. J., 1976, Exchangeable and total calcium pools in mitochondria of rat epidid3nnal fat pads and isolated fat cells. Role in the regulation of pyruvate dehydrogenase activity. Biochem. ]. 154 209. 

Hydroxy vitamin D pools ia the blood and is transported on DBF to the kidney, where further hydroxylation takes place at C-1 or C-24 ia response to calcium levels. l-Hydroxylation occurs primarily ia the kidney mitochondria and is cataly2ed by a mixed-function monooxygenase with a specific cytochrome P-450 (52,179,180). 1 a- and 24-Hydroxylation of 25-hydroxycholecalciferol has also been shown to take place ia the placenta of pregnant mammals and ia bone cells, as well as ia the epidermis. Low phosphate levels also stimulate 1,25-dihydtoxycholecalciferol production, which ia turn stimulates intestinal calcium as well as phosphoms absorption. It also mobilizes these minerals from bone and decreases their kidney excretion. Together with PTH, calcitriol also stimulates renal reabsorption of the calcium and phosphoms by the proximal tubules (51,141,181—183). 

The moist cells were suspended in 750 parts of volume of ethanol and extracted by warming at 60°C for 1 hour. A total of 3 extractions were carried out in a similar manner and the extracts were pooled, diluted with water and further extracted three times with 1,000 parts of volume portions of n-hexane. The n-hexane layer was concentrated to dryness under reduced pressure to recover 4.12 parts of a yellow oil. This oily residue was dissolved in 6 parts by volume of benzene and passed through a column (500 parts by volume capacity) packed with Floridil (100 to 200 meshes). Elution was carried out using benzene and the eluate was collected in 10 parts by volume fractions. Each fraction was analyzed by thin-layer chromatography and color reaction and the fractions rich in ubiquinone-10 were pooled and concentrated under reduced pressure. By this procedure was obtained 0.562 part of a yellow oil. This product was dissolved in 5 parts by volume of chloroform, coated onto a thin layer plate of silica gel GF254 (silica gel with calcium sulfate) and developed with benzene. The fractions corresponding to ubiquinone-10 were extracted, whereby 0.054 part of a yellow oil was obtained. This oil was dissolved in 10 parts by volume of ethanol and allowed to cool, whereupon 0.029 part of yellow crystals of ubiquinone-10 were obtained, its melting point 4B°to 50°C. 

Oxidizing bleaches kill microbes by reacting with cell membranes and cell proteins. The most widely used is sodium hypochlorite for household and hospital uses, and calcium hypochlorite for drinking water and swimming pool disinfecting. 

The electrolyte salt must be processed to recover the ionic plutonium orginally added to the cell. This can be done by aqueous chemistry, typically by dissolution in a dilute sodium hydroxide solution with recovery of the contained plutonium as Pu(OH)3, or by pyrochemical techniques. The usual pyrochemical method is to contact the molten electrolyte salt with molten calcium, thereby reducing any PUCI3 to plutonium metal which is immiscible in the salt phase. The extraction crucible is maintained above the melting point of the contained salts to permit any fine droplets of plutonium in the salt to coalesce with the pool of metal formed beneath the salt phase. If the original ER electrolyte salt was eutectic NaCl-KCl a third "black salt" phase will be formed between the stripped electrolyte salt and the solidified metal button. This dark-blue phase can contain 10 wt. % of the plutonium originally present in the electrolyte salt plutonium in this phase can be recovered by an additional calcium extraction stepO ). 

There is evidence for immunosuppressive effects of PAHs in rodents (Davila et al. 1997). For example, strong immunosuppressive effects were reported in mice that had been dosed with benzo[fl]pyrene and 3-methyl cholanthrene, effects that persisted for up to 18 months (Environmental Health Criteria 202). Multiple immu-notoxic effects have been reported in rodents, and there is evidence that these result from disturbance of calcium homeostasis (Davila et al. 1997). PAHs can activate protein tyrosine kinases in T cells that initiate the activation of a form of phospholipase C. Consequently, release of inositol triphosphate—a molecule that immobilizes Ca + from storage pools in the endoplasmic reticulum—is enhanced. 

The hypochlorous acid oxidizes the cell walls and kills bacteria. Solid calcium hypochlorite, Ca(OCl)2, and liquid solutions of sodium hypochlorite, NaOCl, can be used to generate hypochlorous acid in place of chlorine gas, for example, in chlorinating swimming pools. The hypochlorite ion generated from Ca(OCl)2 and NaOCl forms an equilibrium with water represented by the equation ... 

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