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Home  ›  Ammonia Urea And Uric Acid

Ammonia Urea And Uric Acid

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End production of nucleic acid degradation

Uric acid

Harnsäure Ketoform.svg

Uric acid3D.png

Fluorescent uric acid.JPG

Crystals of urate in polarized calorie-free
Names
Preferred IUPAC name

vii,nine-Dihydro-1H-purine-2,6,8(threeH)-trione
Other names

2,6,8-Trioxypurine; 2,vi,8-Trihydroxypurine; 2,half dozen,8-Trioxopurine; 1H-Purine-2,6,8-trione
Identifiers

CAS Number
  • 69-93-2 check Y

3D model (JSmol)
  • lactam form: Interactive paradigm
  • intermediate form: Interactive epitome
  • lactim form: Interactive image
  • urate monoanion: Interactive prototype
3DMet
  • B00094

Beilstein Reference

 156158
ChEBI
  • CHEBI:27226 ☒ N
ChEMBL
  • ChEMBL792 check Y
ChemSpider
  • 1142 check Y
DrugBank
  • DB01696 check Y
ECHA InfoCard 100.000.655 Edit this at Wikidata
EC Number
  • 200-720-vii

IUPHAR/BPS
  • 4731
KEGG
  • C00366 ☒ N
MeSH Uric+Acid

PubChem CID

  • 1175 CID 1175
UNII
  • 268B43MJ25 check Y

CompTox Dashboard (EPA)

  • DTXSID3042508 Edit this at Wikidata

InChI

  • InChI=1S/C5H4N4O3/c10-3-1-2(7-four(11)vi-1)8-5(12)9-3/h5,12H,(H,ix,10)(H,vii,8,eleven)☒ Northward

    Key: DZGSAURIFGGOJK-UHFFFAOYSA-N☒ N

SMILES

  • lactam form: O=C1Nc2nc(=O)nc2C(=O)N1

  • intermediate form: Oc0nc(O)nc1c0NC(=O)N1

  • lactim form: Oc0nc(O)nc1c0N=C(O)N1

  • urate monoanion: Oc0nc(O)nc1c0N=C([O-])N1
Properties

Chemic formula

 C 5 H 4 N 4 O three
Molar mass 168.112 g·mol−1
Appearance White crystals
Melting signal 300 °C (572 °F; 573 Chiliad)

Solubility in water

 6 mg/100 mL (at 20 °C)
log P −1.107
Acidity (pK a) 5.6
Basicity (pK b) viii.4

Magnetic susceptibility (χ)

 −half-dozen.62×10−v cmiii mol−1
Thermochemistry

Heat capacity (C)

166.fifteen J Chiliad−1 mol−1 (at 24.0 °C)

Std tooth
entropy (S ⦵ 298)

173.2 J Yard−1 mol−1

Std enthalpy of
germination (Δf H ⦵ 298)

−619.69 to −617.93 kJ mol−ane

Std enthalpy of
combustion (Δc H ⦵ 298)

−1921.2 to −1919.56 kJ mol−1

Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).

☒ Nverify (what is check Y ☒ N  ?)

Infobox references

Chemical compound

Uric acid is a heterocyclic compound of carbon, nitrogen, oxygen, and hydrogen with the formula C5H4N4O3. It forms ions and salts known every bit urates and acid urates, such every bit ammonium acid urate. Uric acrid is a product of the metabolic breakdown of purine nucleotides, and it is a normal component of urine. High blood concentrations of uric acrid can atomic number 82 to gout and are associated with other medical atmospheric condition, including diabetes and the formation of ammonium acid urate kidney stones.

Chemical science [edit]

Uric acid was first isolated from kidney stones in 1776 by Swedish chemist Carl Wilhelm Scheele.[one] In 1882, the Ukrainian chemist Ivan Horbaczewski kickoff synthesized uric acid by melting urea with glycine.[2]

Uric acid displays lactam–lactim tautomerism (likewise often described equally keto–enol tautomerism[three]). Although the lactim grade is expected to possess some degree of aromaticity, uric acid crystallizes in the lactam form,[4] with computational chemistry as well indicating that tautomer to be the about stable.[5] Uric acid is a diprotic acrid with pYard a1 = 5.four and pOne thousand a2 = ten.3,[half dozen] thus at physiological pH, information technology predominately exists every bit the monoionic urate ion.

Tautomers of uric acrid and urate
Harnsäure Ketoform.svg
Equilibrium2.svg 		Harnsäure Enolform.svg pK a1
Equilibrium2.svg 		Urat.svg
Lactam class Lactim form Urate ion

Water solubility [edit]

In full general, the water solubility of uric acid and its brine metal and alkaline earth salts is rather low. All these salts exhibit greater solubility in hot water than cold, allowing for like shooting fish in a barrel recrystallization. This low solubility is significant for the etiology of gout. The solubility of the acid and its salts in ethanol is very low or negligible. In ethanol/water mixtures, the solubilities are somewhere between the end values for pure ethanol and pure h2o.

Solubility of urate salts (grams of h2o per gram of compound)
Compound Cold h2o Boiling h2o
Uric acid 15,000 2,000
Ammonium hydrogen urate — 1,600
Lithium hydrogen urate 370 39
Sodium hydrogen urate ane,175 124
Potassium hydrogen urate 790 75
Magnesium dihydrogen diurate 3,750 160
Calcium dihydrogen diurate 603 276
Disodium urate 77 —
Dipotassium urate 44 35
Calcium urate ane,500 1,440
Strontium urate 4,300 i,790
Barium urate 7,900 2,700

The figures given indicate what mass of water is required to dissolve a unit mass of compound indicated. The lower the number, the more soluble the substance in the said solvent.[seven] [eight] [9]

Biochemistry [edit]

Xanthine oxidase (found in mammals primarily equally xanthine dehydrogenase and rarely as an oxidase[10]) is an enzyme which catalyzes the germination of uric acrid from xanthine and hypoxanthine, which in turn are produced from other purines. Xanthine oxidase is a large enzyme whose active site consists of the metal molybdenum bound to sulfur and oxygen.[11] Inside cells, xanthine oxidase tin can be as xanthine dehydrogenase and xanthine oxireductase, which has also been purified from bovine milk and spleen extracts.[12] Uric acrid is released in hypoxic conditions (depression oxygen saturation).[13]

Genetic and physiological variety [edit]

Primates [edit]

In humans and other great apes, uric acid (actually hydrogen urate ion) is the concluding oxidation (breakdown) product of purine metabolism and is excreted in urine, whereas in most other mammals, the enzyme uricase further oxidizes uric acid to allantoin.[14] The loss of uricase in higher primates parallels the similar loss of the ability to synthesize ascorbic acid, leading to the suggestion that urate may partially substitute for ascorbate in such species.[fifteen] Both uric acid and ascorbic acid are strong reducing agents (electron donors) and potent antioxidants. In humans, over half the antioxidant capacity of blood plasma comes from hydrogen urate ion.[16]

Humans [edit]

The normal concentration range of uric acid (or hydrogen urate ion) in human blood is 25 to 80 mg/L for men and 15 to sixty mg/L for women[17] (simply see beneath for slightly different values). An individual tin can take serum values as high as 96 mg/L and not have gout.[18] In humans, about 70% of daily uric acid disposal occurs via the kidneys, and in 5–25% of humans, dumb renal (kidney) excretion leads to hyperuricemia.[xix] Normal excretion of uric acid in the urine is 270 to 360 mg per day (concentration of 270 to 360 mg/Fifty if one litre of urine is produced per day – higher than the solubility of uric acrid because it is in the grade of dissolved acrid urates), roughly one% every bit much every bit the daily excretion of urea.[twenty]

Dogs [edit]

The Dalmatian has a genetic defect in uric acrid uptake by the liver and kidneys, resulting in decreased conversion to allantoin, so this breed excretes uric acrid, and not allantoin, in the urine.[21]

Birds and reptiles [edit]

In birds and reptiles, and in some desert-dwelling mammals (such as the kangaroo rat), uric acid also is the finish product of purine metabolism, but it is excreted in feces as a dry mass. This involves a circuitous metabolic pathway that is energetically costly in comparison to processing of other nitrogenous wastes such equally urea (from the urea cycle) or ammonia, simply has the advantages of reducing h2o loss and preventing aridity.[22]

Invertebrates [edit]

Platynereis dumerilii, a marine polychaete worm, uses uric acid as a sexual pheromone. The female of the species releases uric acrid into the h2o during mating, to induce males to release sperm.[23]

Genetics [edit]

Although foods such as meat and seafood tin elevate serum urate levels, genetic variation is a much greater correspondent to high serum urate.[24] [25] A proportion of people have mutations in the urate transport proteins responsible for the excretion of uric acrid by the kidneys. Variants of a number of genes, linked to serum urate, have so far been identified: SLC2A9; ABCG2; SLC17A1; SLC22A11; SLC22A12; SLC16A9; GCKR; LRRC16A; and PDZK1.[26] [27] [28] GLUT9, encoded by the SLC2A9 gene, is known to send both uric acid and fructose.[19] [29] [xxx]

Clinical significance and research [edit]

In homo blood plasma, the reference range of uric acid is typically 3.4–7.2 mg per 100 mL(200–430 Î¼mol/L) for men, and 2.iv–6.1 mg per 100 mL for women (140–360 Î¼mol/L).[31] Uric acid concentrations in blood plasma above and below the normal range are known as, respectively, hyperuricemia and hypouricemia. Likewise, uric acid concentrations in urine above and below normal are known every bit hyperuricosuria and hypouricosuria. Uric acid levels in saliva may be associated with blood uric acrid levels.[32]

High uric acrid [edit]

Hyperuricemia (loftier levels of uric acid), which induces gout, has various potential origins:

  • Diet may exist a factor. High intake of dietary purine, loftier-fructose corn syrup, and sucrose can increase levels of uric acid.[33] [34]
  • Serum uric acid can be elevated past reduced excretion via the kidneys.[35]
  • Fasting or rapid weight loss can temporarily drag uric acid levels.[36]
  • Sure drugs, such as thiazide diuretics, tin increase claret uric acid levels past interfering with renal clearance.[37]
  • Tumor lysis syndrome, a metabolic complication of certain cancers or chemotherapy, due to nucleobase and potassium release into the plasma.[38]

Gout [edit]

Main article: Gout

A 2011 survey in the United States indicated that three.9% of the population had gout, whereas 21.four% had hyperuricemia without having symptoms.[39]

Backlog blood uric acid tin can induce gout,[40] a painful condition resulting from needle-similar crystals of uric acid precipitating in joints, capillaries, skin, and other tissues.[41] Gout can occur where serum uric acid levels are as depression as 6 mg per 100 mL (357 Î¼mol/Fifty), but an private can have serum values as loftier as 9.6 mg per 100 mL (565 Î¼mol/L) and not have gout.[eighteen]

In humans, purines are metabolized into uric acid, which is then excreted in the urine. Consumption of large amounts of some types of purine-rich foods, particularly meat and seafood, increases gout risk.[42] Purine-rich foods include liver, kidney, and sweetbreads, and certain types of seafood, including anchovies, herring, sardines, mussels, scallops, trout, haddock, mackerel, and tuna.[43] Moderate intake of purine-rich vegetables, all the same, is not associated with an increased risk of gout.[42]

One treatment for gout in the 19th century was administration of lithium salts;[44] lithium urate is more than soluble. Today, inflammation during attacks is more commonly treated with NSAIDs, colchicine, or corticosteroids, and urate levels are managed with allopurinol.[45] Allopurinol, which weakly inhibits xanthine oxidase, is an analog of hypoxanthine that is hydroxylated by xanthine oxidoreductase at the 2-position to give oxipurinol.[46]

Tumor lysis syndrome [edit]

Tumor lysis syndrome, an emergency condition that may result from blood cancers, produces high uric acid levels in blood when tumor cells release their contents into the claret, either spontaneously or post-obit chemotherapy.[38] Tumor lysis syndrome may atomic number 82 to acute kidney injury when uric acid crystals are deposited in the kidneys.[38] Treatment includes hyperhydration to dilute and excrete uric acrid via urine, rasburicase to reduce levels of poorly soluble uric acrid in blood, or allopurinol to inhibit purine catabolism from adding to uric acid levels.[38]

Lesch–Nyhan syndrome [edit]

Lesch–Nyhan syndrome, a rare inherited disorder, is as well associated with loftier serum uric acid levels.[47] Spasticity, involuntary motion, and cognitive retardation as well every bit manifestations of gout are seen in this syndrome.[48]

Cardiovascular disease [edit]

Hyperuricemia is associated with an increment in risk factors for cardiovascular affliction.[49] It is as well possible that high levels of uric acrid may have a causal role in the evolution of atherosclerotic cardiovascular disease, simply this is controversial and the data are conflicting.[50]

Blazon ii diabetes [edit]

Hyperuricemia may be a upshot of insulin resistance in diabetes rather than its precursor.[51] Ane study showed high serum uric acid was associated with higher risk of type 2 diabetes, independent of obesity, dyslipidemia, and hypertension.[52] Hyperuricemia is associated with components of metabolic syndrome, including in children.[53] [54]

Uric acrid rock germination [edit]

Kidney stones can form through deposits of sodium urate microcrystals.[55] [56]

Saturation levels of uric acid in blood may consequence in i form of kidney stones when the urate crystallizes in the kidney. These uric acrid stones are radiolucent, so do not announced on an intestinal apparently X-ray.[57] Uric acid crystals tin also promote the formation of calcium oxalate stones, acting every bit "seed crystals".[58]

Depression uric acid [edit]

Low uric acid (hypouricemia) can take numerous causes. Low dietary zinc intakes cause lower uric acid levels. This issue tin be even more pronounced in women taking oral contraceptive medication.[59] Sevelamer, a drug indicated for prevention of hyperphosphataemia in people with chronic kidney failure, can significantly reduce serum uric acid.[60]

Multiple sclerosis [edit]

Meta-analysis of 10 case-command studies plant that the serum uric acid levels of patients with multiple sclerosis were significantly lower compared to those of salubrious controls, perchance indicating a diagnostic biomarker for multiple sclerosis.[61]

Normalizing low uric acid [edit]

Correcting low or deficient zinc levels can assistance drag serum uric acid.[62]

See also [edit]

  • Theacrine or 1,3,7,9-tetramethyluric acrid, a purine alkaloid found in some teas
  • Uracil – purine nucleobase named by Robert Behrend who was attempting to synthesize derivatives of uric acid

References [edit]

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