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Calcium-magnesium-ATPase pump

Vanadate, dioxybis(oxamato)-bond-length ratios, 1,57 Vanadate, heptacyano-potassium salt structure, I, 72 Vanadate, hexafluoro-dipotassium salt history, I, 21 potassium salt history, 1,21 tripotassium salt history, 1,21 Vanadate, pentachloro-stereochemistry, 1,40 Vanadate, pentafluorooxy-stereochemistry, I, 50 Vanadates biochemistry, 3,456 calcium/magnesium ATPase inhibition, 6, 567 competition with phosphates physiology, 6,665 protonation, 3,1026 sodium pump, 6, 557 in uranium purification from ore, 6, 899 Vanadates, hexafluoro-, 3. 482,531 Vanadates, oxoperoxo-, 3,501 Vanadates, pentacarbonyl-, 3, 457 Vanadium biology, 6,665 determination, 1. 548 extraction... [Pg.243]

In binding experiments, the affinity of magnesium ADP to native membranes and to the isolated calcium dependent ATPase was found to be considerably lower than that of magnesium ATP173. On the other hand, from the inhibition of the calcium-dependent ATPase or the activation of calcium release and ATP synthesis apparent affinities for ADP are obtained that are very similar to those of ATP (Fig. 12). The affinity of ADP for the enzyme apparently depends on its functional state. The affinity of ADP for the membranes under conditions of calcium release depends markedly on the pH of the medium. When the medium pH is reduced from 7.0 to 6.0, the affinity drops by a factor of 10. At pH 7.0 the affinity of the membrane for ADP corresponds to the affinity for ATP to the high affinity binding sites in the forward running mode of the pump. In contrast to the complex dependence of the forward reaction on the concentration of ATP, the dependence of the reverse reaction on ADP seems to follow simple Michaelis-Menten kinetics. [Pg.38]

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). [Pg.555]

B. Magnesium has a direct effect on the Na, K -ATPase pump in both cardiac and nerve tissues. Further, magnesium has some calcium-blocking activity and may indirectly antagonize digoxin at the myocardial Na, K -ATPase pump. [Pg.463]

Calcium plays a vitally important part in possibly as many as three sequences of the contraction—relaxation cycle of vertebrate muscle (Taylor, Lymn and Moll, 1970). In the sarcoplasmic reticulum, calcium is stored in calsequestrin, a protein which holds, with high affinity, 43 atoms of calcium per molecule. The calcium is released in response to nervous impulses and triggers a sequence of reactions that lead to contraction of the muscle. After the contraction, the calcium is pumped back into this reticulum by the calcium/magnesium-dependent ATPase. [Pg.440]

Magnesium is distinguished by the fact that it is required by most ATP-using enzymes. Here, Mg occurs as a complex with ATP, as shown in Figure 10,49. In other words, the true substrate for most ATF-requiring enzymes is not ATP, but the Mg-ATP complex. A deficiency in magnesium is uncommon. When it does occur, the physiological funchon that is most sensitive is neuromuscular activity. In molecular terms, the enzymes involved in neuromuscular activity that appear to be sensitive to Mg deficiency are those involved in the transport of sodium, potassium, and calcium, these enzymes are Na.K-ATPase and the calcium pump (Ca-ATPase). [Pg.795]

The question for the nutritionist and clinician is Which Mg-dependent function is most sensitive to depletion of the body s magnesium and to hypomagnesemia The answer is probably ion transport systems, such as the calcium pump and Np,K-ATPase. The impaired activity of these ion pumps is likely to be responsible for the neuromuscular problems that present with an Mg deficiency. The defects would involve a difficulty in maintaining the normal movements of calcium, sodium, and potassium ions required for nerve conduction and muscle contraction,... [Pg.798]


See other pages where Calcium-magnesium-ATPase pump is mentioned: [Pg.97]    [Pg.7184]    [Pg.7215]    [Pg.7222]    [Pg.161]    [Pg.1062]    [Pg.196]    [Pg.359]    [Pg.44]    [Pg.327]    [Pg.168]    [Pg.789]    [Pg.798]    [Pg.789]    [Pg.795]    [Pg.798]    [Pg.204]    [Pg.591]   
See also in sourсe #XX -- [ Pg.162 ]




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