Calcium cytosolic free concentrations

Figure 2. Reporting of cytosolic free calcium levels by indo-1. Increases in cytosolic calcium, due either to entry of extracellular calcium via calcium channels or to release of intracellular calcium sequestered in organelles such as smooth endoplasmic reticulum, results in formation of the indo-l-calcium complex. Fluorescence intensity at 400 nm (excitation at 340 nm) is proportional to the concentration of this complex the dissociation constant for this complex is about 250 nff (24), making this probe useful for detecting calcium activities in the range of 25 to 2500 nJ. ...

How pectic signals were transduced was unknown, but information suggested that cytosolic free Ca might be involved [22]. Fluorescence ratio imaging has then been used to follow the evolution of free calcium concentrations ([Ca " ] ) after stimulation of carrot protoplasts by oligogalacturonides [23]. 

ATP-dependent Ca2+ pumps and Na+,Ca2+ antiporters act in concert to maintain a low concentration of free cytosolic Ca2+. The concentration of cytosolic free calcium ion, [Ca2+] , in unstimulated cells is between 10 8 and 1 O 7 mol/1, which is more than 10,000-fold lower than extracellular free Ca2+. Most intracellular Ca2+ is stored in... 

The cytosolic concentration of free Ca2+ is generally at or below 100 mi, far lower than that in the surrounding medium, whether pond water or blood plasma. The ubiquitous occurrence of inorganic phosphates (Pj and I l ,) at millimolar concentrations in the cytosol necessitates a low cytosolic Ca2+ concentration, because inorganic phosphate combines with calcium to form relatively insoluble calcium phosphates. Calcium ions are pumped out of the cytosol by a P-type ATPase, the plasma membrane Ca2+ pump. Another P-type Ca2+ pump in the endoplasmic reticulum moves Ca2+ into the ER lumen, a compartment separate from the cytosol. In myocytes, Ca2+ is normally sequestered in a specialized form of endoplasmic reticulum called the sarcoplasmic reticulum. The sarcoplasmic and endoplasmic reticulum calcium (SERCA) pumps are closely related in structure and mechanism, and both are inhibited by the tumor-promoting agent thapsigargin, which does not affect the plasma membrane Ca2+ pump. 

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). 

Calcium ions (Ca ) are important for the mediation of hepatic injury. Cytosolic free calcium is maintained at relatively low concentrations compared to the extracellular levels. The majority of intracellular calcium is sequestered within the mitochondria and endoplasmic reticulum. Membrane associated calcium and magnesium ATPases are responsible for maintaining the calcium gradient (Farrell et ah, 1990). Significant and persistent increases in the intracellular calcium result from nonspecific increases in permeability of the plasma membrane, mitochondrial membranes, and membranes of the smooth endoplasmic reticulum. Calcium pumps in the mitochondrial membrane require NADPH, thus depletion of available NADPH can cause calcium release from mitochondria (Cullen, 2005). 

Ginsenoside Rgi had no effect on arachidonate metabolism, but it did reduce the elevation of cytosolic free calcium concentration [Ca2+]i shown in the second phase (Ca2+ influx) induced by adrenaline and thrombin "Fig. (37)". The results suggest that ginsenoside Rgl in red ginseng roots may be effective as a drug for the treatment of arteriosclerosis and thrombosis. 

Aluminum ions (Al3+) have toxic effect on plants, and number of studies documented the toxic impact of Al3+ on roots,1 hypocotyls,2 and germinating pollen.3,4 It has been proposed that early effects of Al3+ toxicity at the root apex, such as those on cell division, cell extension or nutrient transport, involve the direct intervention of A1 on cell function.5 Model mechanisms of Al3+ toxicity has been proposed that A1 stimulates the NADPH oxidase and induces the generation of superoxide (02j that triggers the influx of calcium ion (Ca2+). The resultant reactive oxygen species (ROS) and cytosolic free Ca2+ concentration elevation may lead to development of phytotoxicity.6... 

Noel, J., K. Fukami, A.M. Hill T. Capiod. 1992. Oscillations of cytosolic free calcium concentration in the presence of intracellular antibodies to phosphatidylinositol 4,5-bisphosphate in voltage-clamped guinea-pig hepatocytes. Biochem. J. 288 357-60. 

As mentioned above, palytoxin produces multiple pharmacological actions at the cellular, tissue, and organism level. Alterations in the Na" and gradients by the toxin will initiate a complex chain of cellular events it could alter the active transport of various ions as well as the transport processes across intracellular membranes. One important parameter that can be altered by palytoxin is the cytosolic free calcium concentration, which will produce alterations in numerous cellular processes. 

Schlatterer, C., GoUnick, F., Schmidt, E., Meyer, R., and Knoll, G. (1994) Challenge with high concentrations of cyclic AMP induces transient changes in the cytosolic free calcium concentration in Dictyostelium discoideum. J. CellSci. 107,2107-2115. 

The tributyltin benzoates were toxic to the K562 cellsJ Tributyltin benzoate (TBSB)-treated R562 cells showed a greater initial extracellular calcimn ion influx compared with the tributyltin halobenzoates. This is consistent with an early activation of endonucleases and DNA fragmentation in the TBSB-treated cells. This is also consistent with an earlier report by Chow et al. where the cytosolic-free calcimn ion concentration increases because of an extracellular calcium ion influx, an inhibition of the calcimn ion extrusion system, and the release of calcium from the intracellular reserves. These, and other studies, suggest involvement of nonspecific cation channels in the extracellular calcium ion influx that leads to an increase in observed cell viability. When the calcium channels were blocked with either verapamil or nefidipine, the extracellular calcium ion influx was partly inhibited and apotosis observed. 

Chen J, Armstrong LC, Liu SJ, Gerriets JE, Last JA. Silica increases cytosolic free calcium ion concentration of alveolar macrophages in vitro. Toxicol Appl Pharmacol 1991 111 211-220. 

The inhibitory effect of a2 agonists on noradrenaline release involves a hyperpolarization of the presynaptic membranes by opening potassium ion channels. The reduction in the release of noradrenaline following the administration of an a2 agonist is ultimately due to a reduction in the concentration of free cytosolic calcium, which is an essential component of the mechanism whereby the synaptic vesicles containing noradrenaline fuse to the s)maptic membrane before their release. 

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