48-Vanadic acid-2-phosphates

Neither inhibitors of glycolysis, nor uncouplers of cellular energy-releasing processes had any significant effect on the rate of vanadate influx. Phosphate, which is readily taken up by the cells inhibited vanadate influx. Sulfate is not accumulated by the cells, and neither sulfate nor chromate appreciably inhibited vanadate influx at concentrations up to 10.9 mM and 200, uM, respectively. Most significantly, inhibitors of anion exchange across the human red cell membrane such as DIDS (4,4 - diisothiocyanostilbene - 2,2 -disulfonic acid) were also found to block vanadate transport into vanadocytes. 

Vanadium is a hard, grey metal. It melts at 1900°C. Vanadium cannot be dissolved in hydrochloric, nitric, or sulphuric acids or in alkalis. It dissolves readily in aqua regia, or in a mixture of concentrated nitric acid and hydrogen fluoride. In its compounds vanadium may have the oxidation numbers +2, +3, +4, +5, and -1-7 among these -1-5 is the most common and -1-4 also occurs frequently. Vanadates contain pentavalent vanadium these are analogous to phosphates. Vanadic acid, like phosphoric acids, exists in the... 

The sample is first ashed and dissolved in hydrochloric acid the phosphate can then be determined titri-metrically or colorimetrically. The most widely accepted method is a colorimetric method using Mission s reagent, which is based on the reaction between the acidified sample solution and an acid reagent containing molybdic acid and vanadic acid, to produce the stable orange-yellow vanadomolybdo-phosphoric acid. 

Potassium phosphate see phosphoric acid, tripotassium salt Potassium vanadate see vanadic acid, dipotassium salt 2-Propanone (aqueous)... 

On 26 August 1867 Roscoe gave the true valency of vanadium and the correct formulae of its compounds. On 12 September he wrote Please ask Joseph [Heywood, the lecture assistant] to send me per book post Pogg. Atm.j vol. 98, in which is Rammelsberg s paper on the isomorphism of vanadates and phosphates. There is no doubt in my mind that vanadic acid is VtO(, and it will be exceedingly interesting to work out the vanadates which must all be ei lained as phosphates. The ordinary white NHs salt is NH4VO3 (like NaPO,) and is a meta-vanadate. The bi-vanadates can also be explained, but all need re-preparation and analysis. Did I tell you that we have now got VjOs, V 04, V 0 V 0 (I wish we had V also) VtO.Cl, V-O.Ch, VsO,Cl and V.O.CU, or VOCl VOCl VOCl. ... 

Certain vertebrates have an astonishing ability to accumulate vanadium in their blood. For example, the ascidian seaworm Phallusia mammilata has a blood concentration of V up to 1900 ppm, which represents more than a millionfold concentration with respect to the sea-water in which it lives. The related organism Ascidia nigra has an even more spectacular accumulation with concentrations up to 1.45% V (i.e. 14 500 ppm) in its blood cells, which also contain considerable concentrations of sulfuric acid (pH 0). One possibility that has been mooted is that the ascidia accumulates vanadate and polyvanadate ions in mistake for phosphate and polyphosphates (p. 528). 

Arsenites may also be determined by this procedure but must first be oxidised by treatment with nitric acid. Small amounts of antimony and tin do not interfere, but chromates, phosphates, molybdates, tungstates, and vanadates, which precipitate as the silver salts, should be absent. An excessive amount of ammonium salts has a solvent action on the silver arsenate. 

For in vitro studies there are a number of compounds available to block protein phosphatase activity. Phosphate buffers inactivate all of these enzymes. Several naturally occurring toxins are potent inhibitors of PPPs, e.g., okadaic acid or microcystin, and are frequently used tools. PPM and PTP family members are not affected by these toxins. Vanadate containing solutions are competitive inhibitors of PTPs, pervanadate is an irreversible inhibitor of PTPs. 

Test 2 Mandelin s Test Dissolve 0.5 g of ammonium vanadate in 1.5 mL of water and dilute to 100 mL with sulfuric acid. Filter the solution through glass wool. Add a drop of the reagent to the primaquine phosphate sample on a white tile. A orange — violet color is produced [2]. 

It is not clear whether V(V) or V(IV) (or both) is the active insulin-mimetic redox state of vanadium. In the body, endogenous reducing agents such as glutathione and ascorbic acid may inhibit the oxidation of V(IV). The mechanism of action of insulin mimetics is unclear. Insulin receptors are membrane-spanning tyrosine-specific protein kinases activated by insulin on the extracellular side to catalyze intracellular protein tyrosine phosphorylation. Vanadates can act as phosphate analogs, and there is evidence for potent inhibition of phosphotyrosine phosphatases (526). Peroxovanadate complexes, for example, can induce autophosphorylation at tyrosine residues and inhibit the insulin-receptor-associated phosphotyrosine phosphatase, and these in turn activate insulin-receptor kinase. 

It is also of interest to point out that the amino acid sequence and structure of the active site of vanadium haloperoxidases is conserved within several families of phosphatases, with conservation of the amino acids involved in vanadate binding in one and phosphate binding in the other. 

The limit test for phosphate is based upon the formation of ayellow colour reaction with molybdovanadic reagent (combination of ammonium vanadate and ammonium molybdate) in an acidic medium. However, the exact composition of the molybdovanadophosphoric acid complex is yet to be established. 

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