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Uric acid, salts

Gout is an inflammatory condition that attacks joints, tendons, and other tissues. The most common site is at the joint of the big toe. Gout is caused by problems metabolizing uric acid and purine, which is produced by proteins. The inability to metabolize uric acid and purine results in a buildup of urates (uric acid salts) and uric acid called hyperuricemia. Uric acid is also not cleared by the kidneys. Urate crystals form urate calculi known as stones that appear as tophi (bumps) in the subcutaneous tissue of earlobes, elbows, hands, and the base of the large toe. [Pg.136]

The fraction B, highly absorbing in the U.V., represents 12-15/ of the whole, and is composed mainly of uric acid salts. Fraction A would seem a degradation product of the A. This fraction is inactive and has a low molecular weight (< 4,000) the is an urinary pigment as well as the B which is also an urinary pigment connected with uric acid. [Pg.549]

Works on the oxidation of uric acid has unequivocally established the triazine structure > ° (9) of oxonic acid. This is further confirmed by the straightforward synthesis described by Piskala and Gut. ° The reaction of biuret (11) with potassium ethyloxalate yielded a potassium salt (24), that with ethyl oxamate, the amide of oxonic acid (25). Both these compounds were converted to 5-azauracil. An analogous reaction with diethyloxalate which should produce an ester of oxonic acid resulted in a mixture of urethane and parabanic acid, however. [Pg.200]

Uric acid is the endproduct of purine metabolism in man. Uric acid has a lower solubility than its progenitor metabolites, hypoxanthine and xanthine. Impaired uric acid elimination and/or increased uric acid production result in hyperuricemia and increase the risk of gouty arthritis. At physiological pH, 99% of the uric acid molecules are actually in the form of the urate salt. A decrease in pH increases the fraction of uric acid molecules relative to urate molecules. Uric acid possesses lower solubility than urate. [Pg.1267]

Humans catabolize purines to uric acid (pA 5.8), present as the relatively insoluble acid at acidic pH or as its more soluble sodium urate salt at a pH near neutrality. Urate crystals are diagnostic of gout. Other disorders of purine catabolism include Lesch-Nyhan syndrome, von Gierke s disease, and hypo-uricemias. [Pg.301]

Uric acid CAS 69-93-2, (C5H4O3N4) is a white solid, insoluble in cold water, alcohol or ether, sparingly soluble in hot water. Uric acid is a weak dibasic acid thus forming two series of salts, most of which are very slightly soluble in water (lithium urate soluble),... [Pg.1382]

Pyrimidines and purines derivatives act as bases and can be acquired through the diet. In particular, organ meats such as liver are a rich source of DNA and RNA. Most dietary purines are oxidized by enzymes to uric acid in the intestinal mucosa that is their excretory product in humans. The desease known as gout is related to high levels of uric acid in serum and the result of deposition of urate salts in various tissues. [Pg.902]

Acetylcholineesterase and choline oxidase Carbon-fiber electrode having a recessed tip into which crystals of the conducting salts tetrathiafulva-lene—tetracyanoquinodimethane were galvanostatically deposited followed by AChE and ChO which were co-immobilized in the recess. No interference from uric acid. The electrode responded to 5 pM or 800 pM ACh within 4 s. Kinetic studies of the biosensor were reported. [22]... [Pg.29]

However laboratory experiments showed that it did not in fact dissolve uric acid crystals, and its use started to decline. Uric acid also dropped out of fashion. However old ideas and practices can take a long time to die out. Lithium continued to be prescribed for gout, arthritis, rheumatism and other complaints. It was listed as a recommended treatment for these conditions until the 1930s in major pharmacopoeias. Even when these publications admitted there was no rational foundations for the use of these (lithium) salts, they still listed indications for lithium use and instructions on how to administer it... [Pg.179]

Uric acid is one of the principal end products of purine metabolism. Gout is caused by elevated levels of uric acid in the body, causing crystals of urate salts to precipitate in the joints. [Pg.1141]

In aquatic animals, ammonia diffuses out of the body through the skin, but land animals excrete excess ammonia either as urea or uric acid. Ammonia is excreted by humans on high meat diets as a strategy to conserve Na+ and K +. Excess PO4- and SO4- produced from phosphoproteins and S-containing amino acids are excreted as ammonium salts Na+ and K+ are exchanged for NH in the kidney. The excretion of urea requires a plentiful supply of water, as it is normally excreted in solution, whereas uric acid is very insoluble and is excreted as a solid by birds and reptiles. Thus, in animals in which weight, or the conservation of water, is important (e.g., birds), excess ammonia is excreted as uric acid. [Pg.434]

SYNS MONOSODIUM URATE IH-PURINE-2,6,8(3H)-TRIONE, 7,9-DIHYDRO-, MONOSODIUM SALT (9CI) URIC ACID, MONOSODIUM SALT... [Pg.1272]


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