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Phosphate sodium-dependent

Vitamin A (845 RE/L) and vitamin D (913 RE/L) may be added to fortify evaporated milk. Other possible ingredients are sodium citrate, disodium phosphate, and salts of carrageenan. Phosphate ions maintain an appropriate salt balance to prevent coagulation of the protein (casein) during sterilization. The amount of phosphate added depends on the amount of calcium and magnesium present. [Pg.365]

Glassy phosphates (sodium polymetaphosphate [50813-16-6] sodium hexametaphosphate [10124-56-8J) vary in composition, depending upon the... [Pg.527]

Authorities names given in full in the text. EPRI values depend on pressure. Depends on pH and sodium to phosphate ratio. Depends on PO4 and ammonia. CEGB also specified a minimum NaOH. Depending on pressure. [Pg.853]

Feild, J. A., et al. Cloning and functional characterization of a sodium-dependent phosphate transporter expressed in human lung and small intestine. Biochem. Biophys. Res. Commun. 1999, 258, 578-582. [Pg.286]

FAD and riboflavin phosphate in foods are hydrolyzed in the intestinal lumen by nucleotide diphosphatase and a variety of nonspecific phosphatases to yield free riboflavin, which is absorbed in the upper small intestines by a sodium-dependent saturable mechanism the peak plasma concentration is related to the dose only up to about 15 to 20 mg (40 to 50 /xmol). Thereafter,... [Pg.175]

K s is independent of pH and temperature, but depends on the nature of the protein and of the salt. Even so, these variations are not enormous with ammonium sulfate the variation of Ks with different proteins does not appear to be more than twofold. With the same protein and different salts, Ks decreases in the following order potassium phosphate, sodium sulfate, ammonium sulfate, sodium citrate, magnesium sulfate (Table I), f or chlorides the value is very much lower. [Pg.200]

Glassy phosphates (sodium polymetaphosphate, sodium hexametaphosphate) vary in composition, depending on the manufacturing process. They exert a powerful sequestering and suspending effect combined with a low-solution pH, about 6 or 7, and tend to hydrolyze or revert in aqueous solution and heat to pyrophosphates and orthophosphates. [Pg.3125]

Foscarnet competitively inhibits Na -Pj cotransport in animal and human kidney proximal tubule brush border membrane vesicles, reversibly inhibiting sodium-dependent phosphate transport [48, 49]. Renal cortical Na-K-ATPase and alkaline phosphatase activity are not inhibited by foscarnet, nor is proline, glucose, succinate, or Na" transport [48,49]. Foscarnet induces isolated phosphaturia without hypophosphatemia in thyroparathyroidectomized rats maintained on a low phosphorus diet, without affecting glomerular filtration rate, urinary adenosine 3 5 -cyclic monophosphate (cAMP) activity, or urinary calcium, sodium or potassium excretion [48,50]. Sodium-Pj cotransport in brush border membrane vesicles from human renal cortex was reported to be even more sensitive to inhibition by foscarnet than in rat renal brush border membrane vesicles [49]. [Pg.386]

MDR multidrug resistance NPT sodium-dependent phosphate transporter... [Pg.948]

Pantothenic acid is taken in as dietary CoA compounds and dCphosphopantetheine and hydrolyzed by pyrophosphatase and phosphatase in the intestinal lumen to dephospho-CoA, phosphopantetheine, and pantetheine. This is further hydrolyzed to pantethenic acid. The vitamin is primarily absorbed as pantothenic acid by a saturable process at low concentrations and by simple diffusion at higher ones. The saturable process is facilitated by a sodium-dependent multivitamin transporter, for which biotin and lipoate compete. After absorption, pantothenic acid enters the circulation and is taken up by cells in a manner similar to its intestinal adsorption. The synthesis of CoA from pantothenate is regulated by pantothenate kinase, which itself is subject to negative feedback from the products CoA and acyi-CoA. The steps involved were outlined above. Pantothenic acid is excreted in the urine after hydrolysis of CoA compounds by enzymes that cleave phosphate and the cys-teamine moieties. Only a small fraction of pantothenate is secreted into milk and even less into colostrum. [Pg.1117]

Several disorders of tubular phosphate handhng have been described. The best known of these is X-linked dominant hypophosphatemic rickets (previously known as vitamin D-resistant rickets). This disorder arises because of a defect in the PHEX gene. A defect of the sodium-dependent/ phosphate co-transporter has also been described, giving rise to autosomal recessive hereditary hypophosphatemic rickets with hypercalciuria. The molecular biology of tliese and other renal phosphate transport disorders has been reviewed. ... [Pg.1710]

The type El sodium-dependent phosphate (Na/Pi) transporters involved in mineralization are members of the inorganic phosphate transporter (PiT) family, which is conserved in all biology. El osteoclasts, a proton (H+) gradient instead of a sodium (Na+) gradient transports Pi. These transporters are antiports the Na+ or H+ is transported out as the Pi is transported in (Sects. 2.2.3 and 10.1.4). All these transporters are composed of repeating alpha helices that weave in and out of a membrane with intra- and extracellular turns (Fig. 9.7). A similar kind of structure is proposed for the annexins that mediate calcium ion transport. [Pg.140]

Dietary riboflavin is present mostly as a phosphate, which is rapidly hydrolyzed before absorption in the duodenum.In humans, the rapid, saturable absorption of riboflavin following an oral dose suggests that it is transported by a carrier-mediated pathway located predominantly in duodenal enterocytes. The process may be sodium-dependent. Bile salts enhance absorption of riboflavin. Fecal riboflavin is derived from the intestinal mucosa and the intestinal flora. This is the predominant excretory route for the vitamin. [Pg.916]

Uchino et al. [84] cloned and characterized an apical PAH transporter isolated from human kidney, named NPTl. NPTl was first identified as a low affinity sodium-dependent phosphate transporter, later it was characterized as an organic anion transporter. In human embryonic kidney cells transfected with NPTl, PAH, urate, benzyl penicillin, faropenem, estradiol-P-glucuronide are transported, and PAH uptake can be inhibited by various organic anions. NPTl does not function as an organic anion exchanger, and thus is... [Pg.32]

Besides the role of 1,25-(OH)2D3 in the transfer of calcium across the intestinal membrane it is known that this substance also activates the transfer of inorganic phosphate across intestinal illeum and jejunum 307-3io) process has been shown to be independent of calcium transport and thus represents an entirely different function of the vitamin. Evidence has been presented that 1,25-(OH)2D3 rather than 25-OH-D3 functions in this process Little is known concerning the mechanism of phosphate transfer except that it is a sodium dependent and active process ° So far a specific phosphate binding protein has not yet been found. [Pg.30]

Cantley al. (50) found that vanadate binds to one high-affinity and one low affinity site per (Na, K)-ATPase enzyme molecule. The low-affinity site was apparently responsible for inhibition of (Na, K)-ATPase activity and was the high-affinity ATP site where sodium-dependent protein phosphorylation occurs. Cantley al. (56) proposed that the unusually high affinity of vanadate for (Na, K)-ATPase was due to its ability to form a trigonal blpyramldal structure analogous to the transition state for phosphate hydrolysis. [Pg.34]

Wu, X. Itoh, N. Taniguchi, T. Nakanishi, T. Tanaka, K. 2003a. Requirement of calcium and phosphate ions in expression of sodium-dependent vitamin C transporter 2 and osteo-pontin in MC3T3-E1 osteoblastic cells. Biochem. Biophys. Acta. 1641(1) 65-70. [Pg.277]

Active transport is the accumulation of a higher concentration of a compound on one side of a cell membrane than on the other, without chemical modification such as phosphorylation. The process is dependent on hydrolysis of ATP to ADP and phosphate, either directly, as in the case of ion pumps, or indirectly, as is the case when metabolites are transported by sodium-dependent transporters. [Pg.55]

Precipitation of /-element phosphates from molten salts was previously studied for NaCl-, KC1-, NaCl-KCl- and LiCl-KCl-based melts. The elements studied included uranium [1,2], plutonium [3,4], americium and curium [5] and lanthanides [1, 6-12]. A range of phosphates (sodium, potassium, lithium and ammonium) were employed as precipitants. Depending on the experimental conditions (melt composition, temperature, nature of the phosphate preeursor) the reactions resulted in the formation of single (LnP04) or double [M3Lu2(P04)3, M3Ln(P04)2l phosphates. [Pg.481]

The most common inhibitors of this category are the silicates and the phosphates. Sodium silicate, for example, is used in many domestic water softeners to prevent the occurrence of rust water. In aerated hot water systems, sodium silicate protects steel, copper, and brass. However, protection is not always rehable and depends heavily on pH and a saturation index that depends on water composition and temperature. Phosphates also require oxygen for effective inhibition. SUicates and phosphates do not afford the degree of protection provided by chromates and nitrites however, they are veiy useftd in situations where nontoxic additives are required. [Pg.838]

In food, thiamin occurs mainly as phosphate coenzymes and the predominant form is TDP (also called thiamin pyrophosphate and cocarboxylase). The phosphate coenzymes are broken down in the gut by phosphatases to give free thiamin for absorption. Thiamin is absorbed mainly from the upper intestine, and less thiamin is absorbed on an empty stomach than when taken with a meal. The latter could be due to the alkaline conditions in the duodenum, which are prevented by the presence of food. Absorption of up to 2 mg per meal occurs by an active saturable process involving a sodium-dependent adenosine triphosphatase and against a concentration gradient. During absorption, thiamin is phosphorylated to the monophosphate ester (TMP). Thiamin is absorbed via the portal venous system. Further phosphorylation to TDP occurs on entry into all tissues. TDP can cross the blood-brain barrier, where a portion is converted to TTP, although even in the brain, TDP is the predominant form of thiamin. A second passive absorption process operates when intakes of thiamin are >5 mg but the maximum that can be absorbed from an oral dose is 2-5 mg. [Pg.392]

According to this proposal, formation of an enzyme-phosphate-sodium complex is the first step in the reaction. Enzyme phosphorylation requires the presence of Na+ and Mg +, although the role of is not well defined [step (2)]. Phosphorylation of the enzyme [step (1)] is strictly dependent on Na". The release of Na" from the phosphoryl-... [Pg.410]

The sodium-dependent inorganic phosphate transporter SLC34A1 (NaPi-lIa) is not localized in the mouse brain a case of tissue-specific antigenic cross-reactivity. J Histochem Cytochem 59 807-812... [Pg.297]


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See also in sourсe #XX -- [ Pg.580 ]




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