Calcium competition with

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The process was complicated by the formation of calcium manganite, CaMn206, known as Weldon mud. Invented by W. Weldon in 1866 and developed at St. Helens from 1868 to 1870. Operated in competition with the Deacon process until both were overtaken by the electrolytic process for making chlorine from brine. Weldon mud has been used as a catalyst for oxidizing the hydrogen sulfide in coal gas to elemental sulfur. 

Magnesium sulfate, applied intravenously is often used as tocolytic. The mechanism of action is not completely clear but might involve a competition with calcium on the cellular level. Precautions in the sense of magnesium plasma level monitoring must be taken in patients with renal insufficiency since this divalent kation is eliminated by the kidneys. Relatively high plasma concentrations are necessary to achieve a sufficient tocolysis. The relatively frequent side effects are respiratory depression, depressed reflexes, headaches, palpitation and skin flushing in the mother and muscle relaxation and, rarely, CNS depression in the fetus. 

Prostatic acid phosphatase is partially and reversibly inactivated by calcium ion (45). Anions such as chloride, bromide, and thiocyanate inhibit prostatic acid phosphatase competitively with regard to substrate as well as noncompetitively. A kinetic analysis by London et al. (46) indicates that the noncompetitive inhibition was related to changes in charge on the protein molecule. A variety of nonspecific anions accelerate thermal denaturation of the enzyme. The enzyme is quite sensitive to a number of electrolyte changes, but it is not clear whether these factors are involved in biological control. 

Troponin C from rabbit skeletal and bovine cardiac muscle has a molecular weight of about 18 000. Skeletal TN-C has four sites for Ca2+. Two of these (III and IV) are high affinity sites (K < 107 dm3 mol-1) which also bind Mg2+ competitively, with K = 103 dm3 mol-1. The remaining two (I and II) appear to be specific for Ca2+, although of lower affinity (K 105 dm3 mol-1).234 These two sites are the only sites in calcium-binding proteins that do not bind Mg2+ with constants in the range 102-103 dm3 mol-1. Cardiac TN-C contains two Ca2+-Mg2+ sites, one Ca2+-specific site and one low affinity site for Ca2+, in which the two aspartate residues in the skeletal TN-C protein are replaced by leucine and alanine residues.235... 

The calcium sites in troponin C have been studied by X-ray absorption near edge structure (XANES).244 In all four cases, Ca2+ appears to be coordinated to carboxylate and carbonyl groups, and no structural differences could be found between the two classes of sites. Binding of Mg2+ causes a distortion of the geometry of the calcium site. Thus, the reduced affinity for Ca2+ of the Ca2+-Mg2+ sites in the presence of Mg2+ may not simply be due to competition with Mg2+, but due to some conformational change induced at these sites by Mg2+. The similarity of all four Ca2+ sites means that local bonding effects do not explain the inability of Mg2+ to bind to the calcium-specific sites I and II. The XANES of parvalbumin differs from that of troponin C. 

At higher seed concentrations (about 230 mg HAP 1 ) a more basic calcium phosphate with Ca P = 1.52 + 0.04 crystallizes on the growth sites of the HAP seed material and no evidence is found for the presence of DCPD. The dependence of the growth phase on solid/solution ratio is of particular importance not only for the interpretation of the results of biological precipitation studies but also for the formation of calciiam phosphate in environmental systems. It may be e2q>lained by the competition between heterogeneous nucleation of DCPD and the growth of the active sites already present on the seed si >strate surface. The latter process occurs more extensively in the initial stages of reaction when the seed concentration is... 

The precise mechanism and sight of action of most compounds categorized as calcium inhibitory compounds, therefore, remains obscure. Future refinements in experimental models and techniques will undoubtedly will lead to the classification of calcium inhibitory compounds based upon their primary mechanism of action and specific site(s) of action (extracellular vs. intracellar). Because of the uncertainty surrounding the precise mechanisms of action of calcium inhibitory compounds, I will describe their cardiac electrical and mechanical effects illuding when possible to those compounds that are believed to act l) competitively with Ca + for specific calcium channels (e.g., Co +, Mn +, La2+, etc.) 2) at the cardiac cell membrane and possibly by one of several intracellular mechanisms (e.g., verapamil, diltiazem, nifedipine) and 3) intracellularly (e.g., 2-n-propyl and 2-n-butyl MDI). 

In trade sale coatings, plastic pigments and microvoids will be directly competitive with ultrafine particle size natural calcium carbonates and "thermooptic" calcined clays. It is probable, however, that the future will see greater rather than less emphasis placed upon the fire retardancy of architectural coatings, and the flammability of the plastic products may prove to be a deterrent to their widespread use, as has been true of plastic wall panels. 

Dupuis Y, Porembska Z, Tardivel S, et al. 1992. Intestinal transfer of manganese Resemblance to and competition with calcium. Reprod Nutr Dev 32 453-460. 

Caffeine is apparently influential on other ion transport process that are not under the control of adenosine receptors or affected by ryanodine. It increases the concentration of free calcium ion in pancreatic beta cells and also inhibits potassium channels [494]. Sparteine has a similar effect on the same cells [495]. In another example caffeine stimulates release of calcium from intracellular stores in liver cells and is not competitive with ryanodine [496]. Senecionine acts similarly [497]. Conversely, caffeine inhibits a calcium channel in rat cerebellar microsomes [212]. 

Calcium carbide (CaC2), which can be produced by thermal reaction of calcium oxide with coke, is not only the basis for acetylene and acetylene-based chemicals (however with decreasing importance due to the strong competition from crude oil and oil products), but also the basis for calcium cyanamide (CaNC = N) (Langhammer 2002). 

Calcium (>50yM) inhibits basal, hormone-stimulated. GppNHp stimulated, and forskolin stimulated adenylate cyclase. 3 This inhibition is not competitive with forskolin and has been suggested to be due to the interaction of the metal ion at a cation binding site on the catalytic subunit. 

Ca is an essential cofector in oxj en evolution. Depleting this cofactor suppresses OEC activity, which can be restored (up to 90%) by replenishing with Ca. Various cations compete vdth calcium for its binding site(s) in PSII. Sodium, potassium and cesium are weakly competitive with calcium, but they do not suppon oxygen evolution activity. Partial reactivation (up to 40%) results from addition of strontium to Ca-depleted PS II membranes and no other metal ions (excqjt VO, vanadyl ion) can restore activity. ... 

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