Calcium binding compounds

Table IV. Calcium-Binding Compounds of Cell Walls...

Effective atomic number Rule, 24 226 and cluster compounds, 24 230-231 exceptions, 24 226-227, 235 and mononuclear species, 24 234-235 Effective g values, calculation, 38 195-197 EF hand domains, calcium-binding proteins, 46 442, 443 45... 

Mechanism of Action A nonabsorbable compound that alters urinary composition of calcium, magnesium, phosphate, and oxalate. Calcium binds to cellulose sodium phosphate, thus preventing intestinal absorption of it. Therapeutic Effect Prevents the formation of kidney stones. 

Compounds with vitamin K activity (Table 6.2) are required in our diets for y-carboxyglutamate biosynthesis (Table 4.1). This amino acid is produced from certain protein glutamyl residues by carboxylation. Proteins that contain y-carboxyglutamate are blood prothrombin and coagulation factors VII, IX, and X (see Chapter 7). Other proteins of this type are osteocalcin from bone and several kidney and muscle calcium-binding proteins. 

In sequestration (chelation) the hardness ions are bound to the builder in the form of soluble complexes. Phosphates, citrates, and nitrilotriacetic acid (NTA) are examples of this class of builder compound. Table 8.3 lists the calcium binding capacities of various builders. Other strongly chelating compounds exist, such as phosphonates and EDTA, but they are generally not extensively used in HDLDs. The most efficient builder is sodium tripolyphosphate (STPP). Unfortunately, tripolyphosphate has been identified as a possible cause of eutrophication in lakes and rivers. It is severely controlled and even banned in several countries. As a result, most countries in North America and Europe have converted to nonphosphate formulations. Other regions are also gradually imposing restrictions on the use of phosphates. 

If vitamin D has no effect on calcium absorption, it does affect calcium mobilization and thereby restores plasma concentrations of calcium. This finding explains why vitamin D deficiency was associated with hypocalcemia. The effect on the bone seems to require a synergetic action of vitamin D and parathormone. The 1,25-hydroxylated derivative seems to be the major active compound causing calcium release from the bone. The 25-hydroxyl derivative has, however, been shown to be active as well. Finally, vitamin D increases renal proximal tubular reabsorption of phosphate in normal and vitamin D deficient animals. Consequently phosphate excretion is decreased. Inasmuch as this effect occurs in parathyroidectomized animals, the effect of vitamin D or its metabolites must be direct. Again, the active metabolites are the 25 and 1,25-hydroxy derivatives. A calcium binding protein has been isolated from the kidney cortex, but its role in renal reabsorption is not known. 

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