Uric acids

Uric acid is a product of the metabolism of tire animal organism. It is usually prepared from guano, which is ticatcd first with dilute hydrochloric acid to remove phosphate of calcium. The uric acid is then dissoh ed out with hot caustic soda and the clear alkaline solution piecipitated with acid. 

Isolation of Uric Acid from Urine (Section 410).—Add 

of concentrated hydrochloric acid to 500 cc. of urine and set aside in a cool place for 24 hours. Pour off the liquid from the crystals of uric acid which adhere to the side of the vessel. Collect the crystals, dissolve them in the smallest possible amount of boiling water, boil with a little bone-black, and filter the solution hot. On cooling, colorless crystals of uric acid are obtained. Examine them under the microscope and sketch the crystals. 

Properties of Uric Acid (SECTION 410).—(a) Solubility of uric acid and its salts.—Shake up about 0.01 gram of uric acid with about 5 cc. of water. Does the acid dissolve Add a dilute solution of sodium hydroxide, drop by drop, and shake. When all the acid has dissolved add a slight excess of dilute hydrochloric acid, heat to boiling, filter and set aside. 

Repeat the test using bromine-water instead of nitric acid. 

Initial investigations using N-labelled uric acid provided information with 

The early labelled peak of incorporation [360] indicative of excessive uric acid production in gouty subjects was abolished by adenine or AIC administration. 

2 H2O2 + aminoantipyrine + TOOS reddish-purple chromogen 

TOOS = iV-ethyl-N-(2-hydroxy-3-sulfopropyl)-w-toIuidine sodium salt 

Storage The strips should be stored between 2-25°C. After opening the aluminium foil the strip should be used immediately. 

Sample material Serum, heparin, plasma, EDTA plasma or fluoride plasma. 

Samples with concentrations above this range should be diluted with distilled water (1 + 1). The result must be multiplied by 2. 

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A large variety of organic compounds char without melting, e.g., starch, oxamide, sulphonic acids, uric acid, etc. 

Uric acid C5H4N4O3 Purines Dissolves on gentle warming and is reprecipitated unchanged on dilution. The solution in cone. H2SO4 darkens on heating. 

Action of heat. Heat about 0 2 g. of uric acid in a hard-glass test-tube. Note the charring and also the formation of a white sublimate on the cooler parts of the tube. 

Murexide test. Place about o-i g. of uric acid in a small evaporating-basin and moisten with 2 3 drops of cone. HNO3. Heat very gently to dryness, and then add i drop of aqueous NHj from a glass rod a purple coloration is produced due to the formation of ammonium purpurate or murexide. Now add a drop of NaOH solution the coloration changes to blue. 

Schiff s test. Dissolve about o i g. of uric acid in NsjCOj solution and pour some of this solution on to a filter-paper which has been moistened with AgNO solution a black stain of metallic silver results. 

Reduction of Fehling s solution. Dissolve o i g. of uric acid in NajCOs solution, and to the clear solution add Fehling s solution drop by drop. Note the formation of a white precipitate of copper... 

Reduction of potassium permanganate. To a solution of uric acid in aqueous NajCO add KMnO solution drop by drop a brown precipitate of MnOj is produced immediately in the cold. 

Add dil. H2SO4 until the solution is acid to litmus. Cool, and scratch the sides of the vessel with a glass rod a white precipitate indicates an aromatic carboxylic acid or uric acid, or a solid phenol insoluble in water (e.g., i- or 2-naphthol). If a precipitate is obtained, filter off through a Buchner funnel, wash with water, recrystallise if necessary and identify. 

Almost insoluble in cold water. Higher alcohols (including benzyl alcohol), higher phenols (e.g., naphthols), metaformaldehyde, paraldehyde, aromatic aldehydes, higher ketones (including acetophenone), aromatic acids, most esters, ethers, oxamide and domatic amides, sulphonamides, aromatic imides, aromatic nitriles, aromatic acid anhydrides, aromatic acid chlorides, sulphonyl chlorides, starch, aromatic amines, anilides, tyrosine, cystine, nitrocompounds, uric acid, halogeno-hydrocarbons, hydrocarbons. 

Uric acid first gives white precipitate of copper urate and then reduces. 

Formation of silver mirror or precipitate of silver indicates reducing agent. (This is often a more sensitive test than I (a) above, and some compounds reduce ammoniacal silver nitrate but are without effect on Fehling s solution.) Given by aldehydes and chloral hydrate formates, lactates and tartrates reducing sugars benzoquinone many amines uric acid. 

This enzyme, sometimes also called the Schardinger enzyme, occurs in milk. It is capable of " oxidising" acetaldehyde to acetic acid, and also the purine bases xanthine and hypoxanthine to uric acid. The former reaction is not a simple direct oxidation and is assumed to take place as follows. The enzyme activates the hydrated form of the aldehyde so that it readily parts w ith two hydrogen atoms in the presence of a suitable hydrogen acceptor such as methylene-blue the latter being reduced to the colourless leuco-compound. The oxidation of certain substrates will not take place in the absence of such a hydrogen acceptor. 

XXVI, 2nd 1965 3794-4187 Four cyclic nitrogens, 321 Xanthine, 447. Caffeine, 461. Uric acid, 613. 

Birds excrete nitrogen as uric acid Uric acid is a purine having the molecular formula C5H4N4O3 it has no C—H bonds Write a structural formula for uric acid... 

Foiin s mixture (for uric acid) dissolve 500 g of ammonium sulfate, 5 g of uranium acetate, and 6 mL of glacial acetic acid, in 650 mL of water. The volume is about a liter. 

Although it might seem that adrninistration of enantiomericaHy pure substances would always be preferred, the diuretic indacrinone (3), is an example of a dmg for which one enantiomer mediates the harmful effects of the other enantiomer (4). (+)-Indacrinone, the diureticaHy active enantiomer or eutomer causes uric acid retention. Fortunately, the other enantiomer distomer) causes uric acid elimination. Thus, adrninistration of a mixture of the two enantiomers, although not necessarily racemic, may have therapeutic value. 

Of the water-soluble vitamins, intakes of nicotinic acid [59-67-6] on the order of 10 to 30 times the recommended daily allowance (RE)A) have been shown to cause flushing, headache, nausea, and moderate lowering of semm cholesterol with concurrent increases in semm glucose. Toxic levels of foHc acid [59-30-3] are ca 20 mg/d in infants, and probably approach 400 mg/d in adults. The body seems able to tolerate very large intakes of ascorbic acid [50-81-7] (vitamin C) without iH effect, but levels in excess of 9 g/d have been reported to cause increases in urinary oxaHc acid excretion. Urinary and blood uric acid also rise as a result of high intakes of ascorbic acid, and these factors may increase the tendency for formation of kidney or bladder stones. AH other water-soluble vitamins possess an even wider margin of safety and present no practical problem (82). 

In the enzymatic assays of cholesterol, glucose, and urea, oxygen is used and H2O2 is formed. The reaction for uric acid [69-93-2] is... 

Xanthine oxidase, mol wt ca 275,000, present in milk, Hver, and intestinal mucosa (131), is required in the cataboHsm of nucleotides. The free bases guanine and hypoxanthine from the nucleotides are converted to uric acid and xanthine in the intermediate. Xanthine oxidase cataly2es oxidation of hypoxanthine to xanthine and xanthine to uric acid. In these processes and in the oxidations cataly2ed by aldehyde oxidase, molecular oxygen is reduced to H2O2 (133). Xanthine oxidase is also involved in iron metaboHsm. Release of iron from ferritin requires reduction of Fe " to Fe " and reduced xanthine oxidase participates in this conversion (133). 

Deficiency or Toxicity in Humans. Molybdenum deficiency in humans results in deranged metaboHsm of sulfur and purines and symptoms of mental disturbances (130). Toxic levels produce elevated uric acid in blood, gout, anemia, and growth depression. Faulty utiH2ation results in sulfite oxidase deficiency, a lethal inborn error. 

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