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Uric acid is a heterocyclic compound of carbon, nitrogen, oxygen, and hydrogen with the formula C 5 H 4 N 4 O 3. It forms ions and salts known as urates and acid urates, such as ammonium acid urate. Uric acid is a product of the metabolic breakdown of purine nucleotides, and it is a normal component of urine. [1]
5-Hydroxyisourate is an organic compound that is produced by the oxidation of uric acid. The conversion is a major pathway in the antioxidant properties of urate. The conversion is catalysed by urate oxidase. [1] [2] sequence of oxidation of ureate. 5-Hydroxyisourate rearranges to allantoin.
Urate oxidase is the first enzyme in a pathway of three enzymes to convert uric acid to S-(+)-allantoin. After uric acid is converted to 5-hydroxyisourate by urate oxidase, 5-hydroxyisourate (HIU) is converted to 2-oxo-4-hydroxy-4-carboxy-5-ureidoimidazoline (OHCU) by HIU hydrolase, and then to S-(+)-allantoin by 2-oxo-4-hydroxy-4-carboxy-5-ureidoimidazoline decarboxylase (OHCU decarboxylase).
Methotrexate also indirectly inhibits purine synthesis by blocking the metabolism of folic acid (it is an inhibitor of the dihydrofolate reductase). Allopurinol is a drug that inhibits the enzyme xanthine oxidoreductase and, thus, lowers the level of uric acid in the body. This may be useful in the treatment of gout, which is a disease caused ...
Mutations that lead to super-activity (increased enzyme activity or de-regulation of the enzyme) result in purine and uric acid overproduction. Super-activity symptoms include gout, sensorineural hearing loss, [10] weak muscle tone (hypotonia), impaired muscle coordination (ataxia), hereditary peripheral neuropathy, [11] and neurodevelopmental ...
The starting material for the reaction sequence was uric acid (8), which had been isolated from kidney stones by Carl Wilhelm Scheele in 1776. [12] Uric acid was reacted with PCl 5 to give 2,6,8-trichloropurine, which was converted with HI and PH 4 I to give 2,6-diiodopurine. The product was reduced to purine using zinc dust.
But it is not clear whether this could be a direct or casual association or link between serum uric acid concentration (and by proxy, xanthine oxidase activity) and cardiovascular health. [19] States of high cell turnover and alcohol ingestion are some of the most prominent cases of high serum uric acid concentrations. [18]
By decreasing plasma uric acid levels, help dissolve these crystals, while limiting the formation of new ones. However, the increased uric acid levels in urine can contribute to kidney stones. Thus, use of these drugs is contraindicated in persons already with a high urine concentration of uric acid (hyperuricosuria). In borderline cases ...
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