| Revision as of 12:42, 15 February 2012 editBeetstra (talk | contribs)Edit filter managers, Administrators172,031 edits Saving copy of the {{chembox}} taken from revid 475819310 of page Uric_acid for the Chem/Drugbox validation project (updated: 'ChEBI', 'KEGG', 'StdInChI', 'StdInChIKey'). |
Latest revision as of 04:03, 21 December 2024 edit Preimage (talk | contribs)Extended confirmed users916 edits Remove Category:Triketones (reverting 02:13, 3 July 2017): ketones are RCOR' for R, R' organylTag: Undo |
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{{Short description|Organic compound}} |
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{{ambox | text = This page contains a copy of the infobox ({{tl|chembox}}) taken from revid of page ] with values updated to verified values.}} |
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{{distinguish|uronic acid|urea}} |
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{{Use dmy dates|date=February 2020}} |
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{{Chembox |
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{{Chembox |
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| Verifiedfields = changed |
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| Verifiedfields = changed |
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| Watchedfields = changed |
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| Watchedfields = changed |
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| verifiedrevid = 458280449 |
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| verifiedrevid = 476995734 |
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| ImageFileL1 = Harnsäure_Ketoform.svg |
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| ImageFileL1 = Harnsäure_Ketoform.svg |
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| ImageFileL1_Ref = {{chemboximage|correct|??}} |
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| ImageFileL1_Ref = {{chemboximage|correct|??}} |
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| ImageNameL1 = Kekulé, keletal formula of a minor uric acid tautomer |
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| ImageFileR1 = Uric_acid3D.png |
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| ImageFileR1 = Uric_acid3D.png |
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| ImageFileR1_Ref = {{chemboximage|correct|??}} |
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| ImageFileR1_Ref = {{chemboximage|correct|??}} |
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| ImageNameR1 = Spacefill model of a minor uric acid tautomer |
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| PIN = 7,9-Dihydro-1''H''-purine-2,6,8(3''H'')-trione{{Citation needed|date = October 2011}} |
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| PIN = 7,9-Dihydro-1''H''-purine-2,6,8(3''H'')-trione |
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| OtherNames = 2,6,8-Trioxypurine{{Citation needed|date = October 2011}} |
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| OtherNames = 2,6,8-Trioxypurine; 2,6,8-Trihydroxypurine; 2,6,8-Trioxopurine; 1''H''-Purine-2,6,8-trione |
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| Section1 = {{Chembox Identifiers |
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|Section1={{Chembox Identifiers |
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| IUPHAR_ligand = 4731 |
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| CASNo = 69-93-2 |
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| CASNo_Ref = {{cascite|correct|CAS}} |
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| CASNo = 69-93-2 |
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| CASNo_Ref = {{cascite|correct|CAS}} |
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| PubChem = 1175 |
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| PubChem = 1175 |
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| ChemSpiderID = 1142 |
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| PubChem_Ref = {{Pubchemcite|correct|Pubchem}} |
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| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}} |
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| ChemSpiderID = 1142 |
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| UNII = 268B43MJ25 |
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| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}} |
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| UNII_Ref = {{fdacite|correct|FDA}} |
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| UNII = 268B43MJ25 |
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| EINECS = 200-720-7 |
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| UNII_Ref = {{fdacite|correct|FDA}} |
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| EINECS = 200-720-7 |
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| DrugBank = DB01696 |
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| DrugBank_Ref = {{drugbankcite|correct|drugbank}} |
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| DrugBank = DB01696 |
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| KEGG = C00366 |
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| DrugBank_Ref = {{drugbankcite|correct|drugbank}} |
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| KEGG_Ref = {{keggcite|changed|kegg}} |
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| KEGG = <!-- blanked - oldvalue: C00366 --> |
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| MeSHName = Uric+Acid |
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| KEGG_Ref = {{keggcite|changed|kegg}} |
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| MeSHName = Uric+Acid |
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| ChEBI = 27226 |
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| ChEBI_Ref = {{ebicite|changed|EBI}} |
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| ChEBI = 62589 |
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| ChEMBL = 792 |
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| ChEBI_Ref = {{ebicite|changed|EBI}} |
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| ChEMBL_Ref = {{ebicite|correct|EBI}} |
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| ChEMBL = 792 |
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| SMILES = O=C1Nc2nc(=O)nc2C(=O)N1 |
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| ChEMBL_Ref = {{ebicite|correct|EBI}} |
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| SMILES_Comment = ] form |
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| SMILES = OC1Nc2nc(=O)nc2C(=O)N1 |
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| SMILES1 = OC1NC2=NC(=O)N=C2C(=O)N1 |
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| SMILES1 = Oc0nc(O)nc1c0NC(=O)N1 |
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| SMILES1_Comment = intermediate form |
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| Beilstein = 156158 |
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| SMILES2 = Oc0nc(O)nc1c0N=C(O)N1 |
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| 3DMet = B00094 |
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| SMILES2_Comment = ] form |
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| StdInChI = 1S/C5H4N4O3/c10-3-1-2(7-4(11)6-1)8-5(12)9-3/h(H4,6,7,8,9,10,11,12) |
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| SMILES3 = Oc0nc(O)nc1c0N=C()N1 |
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| StdInChI_Ref = {{stdinchicite|changed|chemspider}} |
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| SMILES3_Comment = urate monoanion |
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| InChI = 1/C5H4N4O3/c10-3-1-2(7-4(11)6-1)8-5(12)9-3/h(H4,6,7,8,9,10,11,12)/f/h6-9H |
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| Beilstein = 156158 |
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| StdInChIKey = LEHOTFFKMJEONL-UHFFFAOYSA-N |
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| 3DMet = B00094 |
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| StdInChIKey_Ref = {{stdinchicite|changed|chemspider}} |
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| StdInChI = 1S/C5H4N4O3/c10-3-1-2(7-4(11)6-1)8-5(12)9-3/h5,12H,(H,9,10)(H,7,8,11) |
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| InChIKey = LEHOTFFKMJEONL-UHFFFAOYAN |
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| StdInChI_Ref = {{stdinchicite|changed|chemspider}} |
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}} |
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| StdInChIKey = DZGSAURIFGGOJK-UHFFFAOYSA-N |
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| Section2 = {{Chembox Properties |
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| StdInChIKey_Ref = {{stdinchicite|changed|chemspider}} |
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| Formula = {{Chem|C|5|H|4|N|4|O|3}} |
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| MolarMass = 168.1103 g mol<sup>-1</sup> |
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| ExactMass = 168.028340014 g mol<sup>-1</sup> |
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| Appearance = White crystals |
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| Solubility = 60 mg dm<sup>-3</sup> (at 20 °C) |
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| MeltingPtCL = 300 |
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| LogP = -1.107 |
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| pKa = 5.6 |
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| pKb = 8.4 |
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}} |
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| Section3 = {{Chembox Thermochemistry |
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| DeltaHf = -619.69--617.93 kJ mol<sup>-1</sup> |
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| DeltaHc = -1.9212--1.91956 MJ mol<sup>-1</sup> |
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| Entropy = 173.2 J K<sup>-1</sup> mol<sup>-1</sup> |
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| HeatCapacity = 166.15 J K<sup>-1</sup> mol<sup>-1</sup> (at 24.0 °C) |
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}} |
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}} |
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|Section2={{Chembox Properties |
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| C=5 | H=4 | N=4 | O=3 |
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| Appearance = White crystals |
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| Solubility = 6 mg/100 mL (at 20 °C) |
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| MeltingPtC = 300 |
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| LogP = −1.107 |
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| pKa = 5.6 |
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| pKb = 8.4 |
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| MagSus = {{val|-6.62|e=-5|u=cm<sup>3</sup> mol<sup>−1</sup>}} |
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}} |
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}} |
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|Section3={{Chembox Thermochemistry |
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| DeltaHf = −619.69 to −617.93 kJ mol<sup>−1</sup> |
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| DeltaHc = −1921.2 to −1919.56 kJ mol<sup>−1</sup> |
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| Entropy = 173.2 J K<sup>−1</sup> mol<sup>−1</sup> |
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| HeatCapacity = 166.15 J K<sup>−1</sup> mol<sup>−1</sup> (at 24.0 °C) |
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}} }} |
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'''Uric acid''' is a ] of ], ], ], and ] with the ] C<sub>5</sub>H<sub>4</sub>N<sub>4</sub>O<sub>3</sub>. 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 ] ]s, and it is a normal component of ].<ref>{{Cite web |title=Uric Acid |url=https://pubchem.ncbi.nlm.nih.gov/compound/Uric-Acid |website=PubChem}}</ref> ] can lead to ] and are associated with other medical conditions, including ] and the formation of ammonium acid urate ]. |
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==Chemistry== |
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Uric acid was first isolated from ]s in 1776 by Swedish chemist ].<ref name="Scheele">{{cite journal|author-link=Carl Wilhelm Scheele|last=Scheele|first=C. W.|title=Examen Chemicum Calculi Urinari|trans-title=A chemical examiniation of kidney stones|journal=Opuscula|date=1776|volume=2|page=73}}</ref> In 1882, the Ukrainian chemist ] first synthesized uric acid by melting ] with ].<ref>{{cite journal|first=J.|last=Horbaczewski|date=1882|url=https://books.google.com/books?id=b448AAAAIAAJ&pg=PA796|title=Synthese der Harnsäure|trans-title=Synthesis of uric acid|journal=Monatshefte für Chemie und Verwandte Teile Anderer Wissenschaften|volume=3|pages=796–797|doi=10.1007/BF01516847|s2cid=92323943}}</ref> |
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Uric acid displays lactam–lactim ].<ref name="LiebermanMarks2007">{{cite book|last1=Lieberman|first1=M.|url=https://archive.org/details/marksessentialme0000lieb|title=Marks' Essential Medical Biochemistry|last2=Marks|first2=A. D.|last3=Smith|first3=C. M.|last4=Marks|first4=D. B.|publisher=Lippincott Williams & Wilkins|year=2007|isbn=978-0-7817-9340-7|location=Philadelphia|pages=–|url-access=registration}}</ref> Uric acid crystallizes in the lactam form,<ref>{{cite journal |last1=Ringertz |first1=H. |title=The molecular and crystal structure of uric acid |journal=Acta Crystallographica |date=1 March 1966 |volume=20 |issue=3 |pages=397–403 |doi=10.1107/S0365110X66000914|doi-access=free |bibcode=1966AcCry..20..397R }}</ref> with ] also indicating that tautomer to be the most stable.<ref>{{cite journal |last1=Jiménez |first1=V. |last2=Alderete |first2=J. B. |title=Theoretical calculations on the tautomerism of uric acid in gas phase and aqueous solution |journal=Journal of Molecular Structure: THEOCHEM |date=November 2005 |volume=755 |issue=1–3 |pages=209–214 |doi=10.1016/j.theochem.2005.08.001}}</ref> Uric acid is a ] with ] = 5.4 and p''K''<sub>a2</sub> = 10.3.<ref>{{cite book|last=McCrudden|first=F. H.|title=Uric Acid: The Chemistry, Physiology and Pathology of Uric Acid and the Physiologically Important Purin Bodies, with a Discussion of the Metabolism in Gout|publisher=BiblioBazaar|year=2008|isbn=978-0-554-61991-0|location=Charleston, SC|orig-year=1905}}</ref> At physiological pH, urate predominates in solution.{{medical citation needed|date=August 2024}} |
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] |
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] |
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==Biochemistry== |
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The enzyme ] (XO) ] the formation of uric acid from ] and ]. XO, which is found in mammals, functions primarily as a dehydrogenase and rarely as an oxidase, despite its name.<ref>{{Cite journal |first1=K. |last1=Ichida |first2=Y. |last2=Amaya |first3=K. |last3=Noda |first4=S. |last4=Minoshima |first5=T. |last5=Hosoya |first6=O. |last6=Sakai |first7=N. |last7=Shimizu |first8=T. |last8=Nishino |date=November 1993 |title=Cloning of the cDNA encoding human xanthine dehydrogenase (oxidase): Structural analysis of the protein and chromosomal location of the gene |url=https://linkinghub.elsevier.com/retrieve/pii/037811199390652J |journal=Gene |language=en |volume=133 |issue=2 |pages=279–284 |doi=10.1016/0378-1119(93)90652-J |pmid=8224915 |access-date=1 January 2022 |archive-date=15 June 2022 |archive-url=https://web.archive.org/web/20220615142523/https://linkinghub.elsevier.com/retrieve/pii/037811199390652J |url-status=live }}</ref> Xanthine in turn is produced from other ]s. Xanthine oxidase is a large enzyme whose ] consists of the metal ] bound to ] and oxygen.<ref name="Hille">{{cite journal | pmid = 15581570 | year = 2005 | last1 = Hille | first1 = R. | title = Molybdenum-containing hydroxylases | volume = 433 | issue = 1 | pages = 107–116 | doi = 10.1016/j.abb.2004.08.012 | journal = Archives of Biochemistry and Biophysics}}</ref> <!--tangential: Within cells, xanthine oxidase can exist as xanthine dehydrogenase and xanthine oxireductase, which has also been purified from ] milk and ] extracts.<ref name="Hori">{{cite journal |last1=Hori |first1=N. |last2=Uehara |first2=K. |last3=Mikami |first3=Y. | journal = Bioscience, Biotechnology, and Biochemistry | year = 1992 | volume = 56 | pages = 580–582 | doi = 10.1271/bbb.56.580 |pmid=27280651 | title = Enzymatic Synthesis of 5-Methyluridine from Adenosine and Thymine with High Efficiency | issue = 4|doi-access=free }}</ref>--> Uric acid is released in ] conditions (low oxygen saturation).<ref name="Baillie 1473-1478">{{Cite journal| volume = 131| issue = 5| pages = 1473–1478| last1 = Baillie| first1 = J. K. |first2=M. G. |last2=Bates |first3=A. A. |last3=Thompson |first4=W. S. |last4=Waring |first5=R. W. |last5=Partridge |first6=M. F. |last6=Schnopp |first7=A. |last7=Simpson |first8=F. |last8=Gulliver-Sloan |first9=S. R. |last9=Maxwell |first10=D. J. |last10=Webb | title = Endogenous urate production augments plasma antioxidant capacity in healthy lowland subjects exposed to high altitude| journal = Chest| date = May 2007| doi = 10.1378/chest.06-2235| pmid = 17494796}}</ref> |
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===Water solubility=== |
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In general, the water ] of uric acid and its ] and ] ] is rather low. All these salts exhibit greater solubility in hot water than cold, allowing for easy recrystallization. This low solubility is significant for the ] of gout. The solubility of the acid and its salts in ] is very low or negligible. In ethanol/water mixtures, the solubilities are somewhere between the end values for pure ethanol and pure water.{{medical citation needed|date=August 2024}} |
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:{| class="wikitable sortable" |
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|+ Solubility of urate salts (grams of water per gram of compound) |
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! data-sort-type="text" | Compound |
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! data-sort-type="number" | Cold water |
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! data-sort-type="number" | Boiling water |
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|- |
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| Uric acid |
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| align=right | 15,000 |
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| align=right | 2,000 |
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|- |
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| Ammonium hydrogen urate |
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| align=center | — |
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| align=right | 1,600 |
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|- |
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| Lithium hydrogen urate |
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| align=right | 370 |
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| align=right | 39 |
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|- |
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| Sodium hydrogen urate |
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| align=right | 1,175 |
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| align=right | 124 |
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|- |
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| Potassium hydrogen urate |
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| align=right | 790 |
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| align=right | 75 |
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|- |
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| Magnesium dihydrogen diurate |
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| align=right | 3,750 |
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| align=right | 160 |
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|- |
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| Calcium dihydrogen diurate |
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| align=right | 603 |
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| align=right | 276 |
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|- |
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| Disodium urate |
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| align=right | 77 |
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| align=center | — |
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|- |
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| Dipotassium urate |
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| align=right | 44 |
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| align=right | 35 |
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|- |
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| Calcium urate |
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| align=right | 1,500 |
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| align=right | 1,440 |
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|- |
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| Strontium urate |
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| align=right | 4,300 |
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| align=right | 1,790 |
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|- |
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| Barium urate |
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| align=right | 7,900 |
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| align=right | 2,700 |
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|} |
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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.<ref>{{cite book|title=CRC Handbook of Chemistry and Physics|title-link=CRC Handbook of Chemistry and Physics|publisher=]|year=1981|editor-last=Weast|editor-first=R. C.|edition=62nd|location=Boca Raton, FL|oclc=7842683}}</ref><ref>{{cite book|title=Merck Index|publisher=Merck|year=1976|isbn=978-0-911910-26-1|editor-last=Windholz|editor-first=M.|edition=9th}}</ref><ref>{{cite book | title = Uric acid | first = Francis H. | last = McCrudden | page = 58}}</ref> |
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== Genetic and physiological diversity == |
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=== Primates === |
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In ] uric acid (actually hydrogen urate ion) is the final ] (breakdown) product of ] and is excreted in urine, whereas in most other ]s, the enzyme ] further oxidizes uric acid to ].<ref>{{cite web |last=Angstadt |first=C. N. |title=Purine and Pyrimidine Metabolism: Purine Catabolism |website=NetBiochem |date=4 December 1997 |url=http://library.med.utah.edu/NetBiochem/pupyr/pp.htm#Pu%20Catab |access-date=28 December 2006 |archive-date=27 November 2020 |archive-url=https://web.archive.org/web/20201127012354/http://library.med.utah.edu/NetBiochem/pupyr/pp.htm#Pu%20Catab |url-status=live }}</ref> The loss of uricase in higher primates parallels the similar loss of the ability to synthesize ], leading to the suggestion that urate may partially substitute for ascorbate in such species.<ref name="Proct">{{cite journal |last=Proctor |first=P. |title=Similar functions of uric acid and ascorbate in man? |journal=Nature |volume=228 |issue=5274 |pages=868 |date=November 1970 |pmid=5477017 |doi= 10.1038/228868a0|bibcode=1970Natur.228..868P |s2cid=4146946 |doi-access=free }}</ref> Both uric acid and ascorbic acid are strong ]s (]s) and potent ]s. In humans, over half the antioxidant capacity of ] comes from hydrogen urate ion.<ref>{{cite journal | doi = 10.1046/j.1365-2362.1997.1390687.x | title = Antioxidant status in patients with uncomplicated insulin-dependent and non-insulin-dependent diabetes mellitus | year = 1997 | last1 = Maxwell | first1 = S. R. J. | last2 = Thomason | first2 = H. | last3 = Sandler | first3 = D. | last4 = Leguen | first4 = C. | last5 = Baxter | first5 = M. A. | last6 = Thorpe | first6 = G. H. G. | last7 = Jones | first7 = A. F. | last8 = Barnett | first8 = A. H. | journal = European Journal of Clinical Investigation | volume = 27 | issue = 6 | pages = 484–490 | pmid = 9229228| s2cid = 11773699 }} |
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</ref> |
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==== Humans ==== |
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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 60 mg/L for women<ref>{{cite book|title=Harrison's Principles of Internal Medicine|publisher=]|year=1987|isbn=978-0-07-079454-2|editor-last=Braunwald|editor-first=E.|edition=11th|location=New York|page=A-3}}</ref> (but see below for slightly different values). An individual can have serum values as high as 96 mg/L and not have gout.<ref name="hyperuricemia" /> In humans, about 70% of daily uric acid disposal occurs via the kidneys, and in 5–25% of humans, impaired renal (kidney) excretion leads to ].<ref name="Vitart_2008">{{cite journal |last1=Vitart |first1=V. |last2=Rudan |first2=I. |last3=Hayward |first3=C. |display-authors=etal |title=SLC2A9 is a newly identified urate transporter influencing serum urate concentration, urate excretion and gout |journal=Nature Genetics |volume=40 |issue=4 |pages=437–442 |date=April 2008 |pmid=18327257 |doi=10.1038/ng.106 |s2cid=6720464 }}</ref> Normal excretion of uric acid in the urine is 270 to 360 mg per day (concentration of 270 to 360 mg/L if one litre of urine is produced per day – higher than the solubility of uric acid because it is in the form of dissolved acid urates), roughly 1% as much as the daily excretion of ].<ref>{{Cite book | url=https://www.ncbi.nlm.nih.gov/books/NBK562201/ | pmid=32965872 | title=StatPearls | chapter=Hyperuricosuria | year=2022 | publisher=StatPearls | last1=Kaur | first1=P. | last2=Bhatt | first2=H. | access-date=21 March 2022 | archive-date=26 October 2022 | archive-url=https://web.archive.org/web/20221026085112/https://www.ncbi.nlm.nih.gov/books/NBK562201/ | url-status=live }}</ref> |
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=== Dogs === |
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The ] has a genetic defect in uric acid uptake by the ] and ]s, resulting in decreased conversion to ], so this breed excretes uric acid, and not allantoin, in the urine.<ref>{{cite journal |last1=Friedman |first1=M. |last2=Byers |first2=S. O. |name-list-style=amp |title=Observations concerning the causes of the excess excretion of uric acid in the Dalmatian dog |journal=The Journal of Biological Chemistry |volume=175 |issue=2 |pages=727–735 |date=1 September 1948 |doi=10.1016/S0021-9258(18)57191-X |pmid=18880769 |doi-access=free }}</ref> |
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=== Birds, reptiles and desert-dwelling mammals === |
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In ]s and ]s, and in some desert-dwelling mammals (such as the ]), uric acid also is the end product of purine metabolism, but it is excreted in ] as a dry mass. This involves a complex ] that is energetically costly in comparison to processing of other nitrogenous wastes such as ] (from the ]) or ], but has the advantages of reducing water loss and preventing dehydration.<ref name="Hazard">{{cite book | last = Hazard | first = L. C. | title = Sodium and Potassium Secretion by Iguana Salt Glands | series = Iguanas: Biology and Conservation | publisher = University of California Press | pages = 84–85 | year = 2004 | isbn = 978-0-520-23854-1 | url = https://books.google.com/books?id=Dyb8bNBh5nwC }}</ref> |
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=== Invertebrates === |
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'']'', a marine ] worm, uses uric acid as a sexual ]. The female of the species releases uric acid into the water during ], which induces males to release sperm.<ref>{{cite journal|last1=Zeeck|first1=E.|last2=Harder|first2=T.|last3=Beckmann|first3=M.|title= Uric acid: the sperm-release pheromone of the marine polychaete ''Platynereis dumerilii'' |journal=Journal of Chemical Ecology|date=1998|volume=24|issue=1|pages=13–22|doi=10.1023/A:1022328610423|s2cid=42318049}}</ref> |
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=== Bacteria === |
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Uric acid metabolism is done in the human gut by ∼1/5 of bacteria species that come from 4 of 6 major phyla. Such metabolism is anaerobic involving uncharacterized ammonia lyase, peptidase, carbamoyl transferase, and oxidoreductase enzymes. The result is that uric acid is converted into ] or ] and the ] such as ] and ].<ref name="v435">{{cite journal |last1=Liu |first1=Yuanyuan |last2=Jarman |first2=J. Bryce |last3=Low |first3=Yen S. |last4=Augustijn |first4=Hannah E. |last5=Huang |first5=Steven |last6=Chen |first6=Haoqing |last7=DeFeo |first7=Mary E. |last8=Sekiba |first8=Kazuma |last9=Hou |first9=Bi-Huei |last10=Meng |first10=Xiandong |last11=Weakley |first11=Allison M. |last12=Cabrera |first12=Ashley V. |last13=Zhou |first13=Zhiwei |last14=van Wezel |first14=Gilles |last15=Medema |first15=Marnix H. |year=2023 |title=A widely distributed gene cluster compensates for uricase loss in hominids |journal=Cell |volume=186 |issue=16 |pages=3400–3413.e20 |doi=10.1016/j.cell.2023.06.010 |issn=0092-8674 |doi-access=free |last16=Ganesan |first16=Calyani |last17=Pao |first17=Alan C. |last18=Gombar |first18=Saurabh |last19=Dodd |first19=Dylan|pmid=37541197 |pmc=10421625 |hdl=1887/3719494 |hdl-access=free }}</ref> Radioisotope studies suggest about 1/3 of uric acid is removed in healthy people in their gut with this being roughly 2/3 in those with kidney disease.<ref name="l551">{{cite journal |last=Sorensen |first=Leif B. |year=1965 |title=Role of the intestinal tract in the elimination of uric acid |journal=Arthritis & Rheumatism |publisher=Wiley |volume=8 |issue=4 |pages=694–706 |doi=10.1002/art.1780080429 |pmid=5859543 |issn=0004-3591}}</ref> In mouse models, such bacteria compensate for the loss of uricase leading researchers to raise the possibility "that antibiotics targeting anaerobic bacteria, which would ablate gut bacteria, increase the risk for developing gout in humans".<ref name="v435" /> |
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==Genetics== |
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Although foods such as meat and seafood can elevate serum urate levels, genetic variation is a much greater contributor to high serum urate.<ref name="pmid30305269">{{cite journal | last1=Major |first1=T. J. |last2=Topless |first2=R. K. |last3=Merriman |first3=T. R. | title=Evaluation of the diet wide contribution to serum urate levels: meta-analysis of population based cohorts | journal=] | volume=363 | pages=k3951 | year=2018 | doi = 10.1136/bmj.k3951 | pmc=6174725 | pmid=30305269}}</ref><ref name="pmid32620198">{{cite journal | author=Keenan |first=R. T. | title=The biology of urate | journal=Seminars in Arthritis and Rheumatism | volume=50 | issue=35| pages=S2–S10 | year=2020 | doi = 10.1016/j.semarthrit.2020.04.007 | pmid=32620198 |doi-access=free }}</ref> A proportion of people have mutations in the urate transport proteins responsible for the excretion of uric acid by the kidneys. Variants of a number of genes, linked to serum urate, have so far been identified: '']''; '']''; '']''; '']''; '']''; '']''; '']''; '']''; and '']''.<ref>{{cite journal |last1=Aringer |first1=M. |last2=Graessler |first2=J. |title=Understanding deficient elimination of uric acid |journal=Lancet |volume=372 |issue=9654 |pages=1929–1930 |date=December 2008 |pmid=18834627 |doi=10.1016/S0140-6736(08)61344-6|s2cid=1839089 }}</ref><ref name="Kolz_2009">{{cite journal |last1=Kolz |first1=M. |last2=Johnson |first2=T. |display-authors=etal | editor1-last=Allison | editor1-first=David B. |title=Meta-analysis of 28,141 individuals identifies common variants within five new loci that influence uric acid concentrations | journal=PLOS Genet. |date=June 2009 | volume=5 | issue=6 | pmid=19503597 | doi=10.1371/journal.pgen.1000504 | pages=e1000504 | pmc=2683940 |doi-access=free }}</ref><ref>{{cite journal|last=Köttgen|first=A.|title=Genome-wide association analyses identify 18 new loci associated with serum urate concentrations|journal=Nature Genetics|date=February 2013|volume=45|issue=2|pages=145–154|pmid=23263486|doi=10.1038/ng.2500|pmc=3663712|display-authors=etal|url=https://www.pure.ed.ac.uk/ws/files/8739767/Genome_wide_association_analyses_identify_18_new_loci_associated_with_serum_urate_concentrations.pdf}}</ref> GLUT9, encoded by the ''SLC2A9'' gene, is known to transport both uric acid and ].<ref name="Vitart_2008"/><ref name="Döring_2008">{{cite journal |last1=Döring |first1=A. |last2=Gieger |first2=C. |last3=Mehta |first3=D. |display-authors=etal |title=SLC2A9 influences uric acid concentrations with pronounced sex-specific effects |journal=Nature Genetics |volume=40 |issue=4 |pages=430–436 |date=April 2008 |pmid=18327256 |doi=10.1038/ng.107|s2cid=29751482 }}</ref><ref>{{Cite journal|last1=Mandal|first1=Asim K.|last2=Mount|first2=David B.|date=February 2015|title=The molecular physiology of uric acid homeostasis|url=https://pubmed.ncbi.nlm.nih.gov/25422986/|journal=]|volume=77|pages=323–345|doi=10.1146/annurev-physiol-021113-170343|pmid=25422986}}</ref> |
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Myogenic ], as a result of the ] running when ATP reservoirs in muscle cells are low, is a common pathophysiologic feature of ], such as ], which is a ] impairing the ability of ATP (energy) production for muscle cells.<ref name=":0">{{cite journal | doi=10.1056/NEJM198707093170203 | title=Myogenic Hyperuricemia | year=1987 | last1=Mineo | first1=Ikuo | last2=Kono | first2=Norio | last3=Hara | first3=Naoko | last4=Shimizu | first4=Takao | last5=Yamada | first5=Yuya | last6=Kawachi | first6=Masanori | last7=Kiyokawa | first7=Hiroaki | last8=Wang | first8=Yan Lin | last9=Tarui | first9=Seiichiro | journal=New England Journal of Medicine | volume=317 | issue=2 | pages=75–80 | pmid=3473284 }}</ref> In these metabolic myopathies, myogenic hyperuricemia is exercise-induced; inosine, hypoxanthine and uric acid increase in plasma after exercise and decrease over hours with rest.<ref name=":0" /> Excess AMP (adenosine monophosphate) is converted into uric acid.<ref name=":0" /> |
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AMP → IMP → Inosine → Hypoxanthine → Xanthine → Uric Acid<ref name=":0" /> |
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==Clinical significance and research== |
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In human ], the ] of uric acid is typically 3.4–7.2 mg per 100 mL(200–430 μmol/L) for men, and 2.4–6.1 mg per 100 mL for women (140–360 μmol/L).<ref>{{cite web|title=Harmonisation of Reference Intervals|url=http://www.acb.org.uk/docs/Pathology%20Harmony%20for%20web.pdf|website=Pathology Harmony (UK)|access-date=13 August 2013|url-status=dead|archive-url=https://web.archive.org/web/20130802082027/http://www.acb.org.uk/docs/Pathology%20Harmony%20for%20web.pdf|archive-date=2 August 2013}}</ref> Uric acid concentrations in blood plasma above and below the normal range are known as, respectively, ] and ]. Likewise, uric acid concentrations in urine above and below normal are known as ] and hypouricosuria. Uric acid levels in saliva may be associated with blood uric acid levels.<ref>{{Cite journal|pmid=26276048|year=2015|last1=Zhao|first1=J|title=Salivary uric acid as a noninvasive biomarker for monitoring the efficacy of urate-lowering therapy in a patient with chronic gouty arthropathy|journal=Clinica Chimica Acta|volume=450|pages=115–20|last2=Huang|first2=Y|doi=10.1016/j.cca.2015.08.005}}</ref> |
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===High uric acid=== |
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] (high levels of uric acid), which induces ], has various potential origins: |
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* Diet may be a factor. High intake of dietary ], ], and ] can increase levels of uric acid.<ref name="Cirillo">{{cite journal |pmid=17130256 |doi=10.1681/ASN.2006080909 |volume=17 |issue=12 Suppl. 3 |title=Uric acid, the metabolic syndrome, and renal disease |date=December 2006 |last1=Cirillo |first1=P. |last2=Sato |first2=W. |last3=Reungjui |first3=S. |display-authors=etal |journal=Journal of the American Society of Nephrology |pages=S165–S168 |s2cid=28722975 |url=http://jasn.asnjournals.org/content/17/12_suppl_3/S165.full.pdf |access-date=20 April 2018 |archive-date=15 May 2013 |archive-url=https://web.archive.org/web/20130515003345/http://jasn.asnjournals.org/content/17/12_suppl_3/S165.full.pdf |url-status=live }}</ref><ref name="Theodore">{{cite journal | pmid = 19403709 | doi=10.3945/jn.108.098194 | volume=139 | issue=6 | title=The Effect of High-Fructose Corn Syrup Consumption on Triglycerides and Uric Acid |date=June 2009 | first1=T. J. |last1=Angelopoulos |first2=J. |last2=Lowndes |first3=L. |last3=Zukley |first4=K. J. |last4=Melanson |first5=V. |last5=Nguyen |first6=A. |last6=Huffman |first7=J. M. |last7=Rippe | journal=The Journal of Nutrition | pages=1242S–1245S|doi-access=free }}</ref> |
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* Serum uric acid can be elevated by reduced excretion via the ]s.<ref name="Mayo">{{cite web |date=11 September 2010 |url=http://www.mayoclinic.com/health/high-uric-acid-level/MY00160 |title=High uric acid level |website=Mayo Clinic |access-date=24 April 2011 |archive-date=25 August 2011 |archive-url=https://web.archive.org/web/20110825234358/http://www.mayoclinic.com/health/high-uric-acid-level/MY00160 |url-status=live }}</ref> |
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* Fasting or rapid weight loss can temporarily elevate uric acid levels.<ref name="pmid7024153">{{cite journal| last = Howard | first = A. N. | title = The historical development, efficacy and safety of very-low-calorie diets| journal = International Journal of Obesity| volume = 5| issue = 3| pages = 195–208| year = 1981| pmid = 7024153}}</ref> |
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* Certain drugs, such as ] diuretics, can increase blood uric acid levels by interfering with ].<ref>{{cite web|title=Diuretic-Related Side Effects: Development and Treatment|url=http://www.medscape.com/viewarticle/489521_7|publisher=Medscape|access-date=17 May 2013|archive-date=4 May 2013|archive-url=https://web.archive.org/web/20130504004901/http://www.medscape.com/viewarticle/489521_7|url-status=live}}</ref> |
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* ], a metabolic complication of certain cancers or chemotherapy, due to ] and potassium release into the plasma.<ref name="howard"/> |
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* ] (disrupted NADH/NAD<sup>+</sup> ratio) caused by diabetic hyperglycemia and excessive alcohol consumption.<ref>{{Cite book |last=Coffee |first=Carole J. |title=Quick Look Medicine: Metabolism |publisher=Hayes Barton Press |year=1999 |isbn=1-59377-192-4 |pages=176–177}}</ref> |
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====Gout==== |
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{{main|Gout}} |
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A 2011 survey in the United States indicated that 3.9% of the population had gout, whereas 21.4% had hyperuricemia without having symptoms.<ref name="pmid30485934">{{cite journal | last1=Li |first1=R. |last2=Yu |first2=K. |last3=Li |first3=C. | title=Dietary factors and risk of gout and hyperuricemia: a meta-analysis and systematic review | journal=Asia Pacific Journal of Clinical Nutrition | volume=27 | issue=6 | pages=1344–1356 | year=2018 | doi = 10.6133/apjcn.201811_27(6).0022 | pmid=30485934}}</ref> |
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Excess blood uric acid (serum urate) can induce ],<ref name="Heinig M, Johnson RJ 2006 1059–64">{{cite journal |last1=Heinig |first1=M. |last2=Johnson |first2=R. J. |title=Role of uric acid in hypertension, renal disease, and metabolic syndrome |journal=Cleveland Clinic Journal of Medicine |volume=73 |issue=12 |pages=1059–1064 |date=December 2006 |pmid=17190309 |doi=10.3949/ccjm.73.12.1059|doi-broken-date=29 November 2024 |s2cid=45409308 }}</ref> a painful condition resulting from needle-like crystals of uric acid termed ''monosodium urate crystals''<ref name="Abhishek">{{cite journal |last1=Abhishek |first1=A |last2=Roddy |first2=E |last3=Doherty |first3=M |title=Gout - a guide for the general and acute physicians. |journal=Clinical Medicine |date=February 2017 |volume=17 |issue=1 |pages=54–59 |doi=10.7861/clinmedicine.17-1-54 |pmid=28148582|pmc=6297580 }}</ref> precipitating in ]s, ], ], and other tissues.<ref name=Lancet2010>{{cite journal |last1=Richette |first1=P. |last2=Bardin |first2=T. |title=Gout |journal=Lancet |volume=375 |issue=9711 |pages=318–328 |date=January 2010 |pmid=19692116 |doi=10.1016/S0140-6736(09)60883-7 |s2cid=208793280 }}</ref> Gout can occur where serum uric acid levels are as low as 6 mg per 100 mL (357 μmol/L), but an individual can have serum values as high as 9.6 mg per 100 mL (565 μmol/L) and not have gout.<ref name=hyperuricemia>{{cite journal |last1=Tausche |first1=A. K. |last2=Unger |first2=S. |last3=Richter |first3=K. |display-authors=etal |trans-title=Hyperuricemia and gout: diagnosis and therapy |language=de |journal=Der Internist |volume=47 |issue=5 |pages=509–521 |date=May 2006 |pmid=16586130 |doi=10.1007/s00108-006-1578-y |title=Hyperurikämie und Gicht|s2cid=11480796 }}</ref> |
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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.<ref name=Choi>{{cite journal |last1=Choi |first1=H. K. |last2=Atkinson |first2=K. |last3=Karlson |first3=E. W. |last4=Willett |first4=W. |last5=Curhan |first5=G. |title=Purine-rich foods, dairy and protein intake, and the risk of gout in men |journal=The New England Journal of Medicine |volume=350 |issue=11 |pages=1093–1103 |date=March 2004 |pmid=15014182 |doi=10.1056/NEJMoa035700|doi-access=free }}</ref> Purine-rich foods include liver, kidney, and ], and certain types of seafood, including anchovies, herring, sardines, mussels, scallops, trout, haddock, mackerel, and tuna.<ref>{{Cite web|date=July 2, 2020|title=Gout diet: What's allowed, what's not|url=http://www.mayoclinic.org/healthy-lifestyle/nutrition-and-healthy-eating/in-depth/gout-diet/art-20048524|website=]|publisher=|access-date=13 January 2017|archive-date=7 January 2017|archive-url=https://web.archive.org/web/20170107022952/http://www.mayoclinic.org/healthy-lifestyle/nutrition-and-healthy-eating/in-depth/gout-diet/art-20048524|url-status=live}}</ref> Moderate intake of purine-rich vegetables, however, is not associated with an increased risk of gout.<ref name=Choi/> |
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One treatment for gout in the 19th century was administration of ] salts;<ref>{{cite journal |first= Gerhard N. |last=Schrauzer |journal=Journal of the American College of Nutrition |volume=21 |issue=1 |pages=14–21 |year=2002 |title= Lithium: Occurrence, Dietary Intakes, Nutritional Essentiality |pmid= 11838882 |doi= 10.1080/07315724.2002.10719188|s2cid=25752882 }}</ref> lithium urate is more soluble. Today, inflammation during attacks is more commonly treated with ]s, ], or ]s, and urate levels are managed with ].<ref>{{cite web|title=NHS Clinical Knowledge Summaries |url=http://www.cks.nhs.uk/gout/background_information/causes_and_risk_factors#-291124 |url-status=dead |archive-url=https://web.archive.org/web/20120304060453/http://www.cks.nhs.uk/gout/background_information/causes_and_risk_factors |archive-date=4 March 2012 |publisher=UK ]}}</ref> Allopurinol, which weakly inhibits xanthine oxidase, is an analog of hypoxanthine that is hydroxylated by ] at the 2-position to give oxipurinol.<ref>{{cite journal|pmid=16507884|pmc=2233605|year=2006|last1=Pacher|first1=P.|title=Therapeutic effects of xanthine oxidase inhibitors: Renaissance half a century after the discovery of allopurinol|journal=Pharmacological Reviews|volume=58|issue=1|pages=87–114|last2=Nivorozhkin|first2=A.|last3=Szabó|first3=C.|doi=10.1124/pr.58.1.6}}</ref> |
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====Tumor lysis syndrome==== |
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], an emergency condition that may result from ]s, produces high uric acid levels in blood when tumor cells release their contents into the blood, either spontaneously or following ].<ref name="howard">{{Cite journal|last1=Howard|first1=S. C.|last2=Jones|first2=D. P.|last3=Pui|first3=C.-H.|date=12 May 2011|title=The Tumor Lysis Syndrome|journal=The New England Journal of Medicine|volume=364|issue=19|pages=1844–1854|doi=10.1056/NEJMra0904569|issn=0028-4793|pmc=3437249|pmid=21561350}}</ref> Tumor lysis syndrome may lead to ] when uric acid crystals are deposited in the kidneys.<ref name=howard/> Treatment includes ] to dilute and excrete uric acid via ], ] to reduce levels of poorly soluble uric acid in blood, or ] to inhibit ] ] from adding to uric acid levels.<ref name=howard/> |
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====Lesch–Nyhan syndrome==== |
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], a rare inherited disorder, is also associated with high serum uric acid levels.<ref>{{cite journal |last1=Luo |first1=Y. C. |last2=Do |first2=J. S. |last3=Liu |first3=C. C. |title=An amperometric uric acid biosensor based on modified Ir–C electrode |journal=Biosensors & Bioelectronics |volume=22 |issue=4 |pages=482–488 |date=October 2006 |pmid=16908130 |doi=10.1016/j.bios.2006.07.013}}</ref> Spasticity, involuntary movement, and cognitive retardation as well as manifestations of gout are seen in this syndrome.<ref>{{cite journal |last=Nyhan |first=W. L. |title=Lesch-Nyhan Disease |journal=Journal of the History of the Neurosciences |volume=14 |issue=1 |pages=1–10 |date=March 2005 |pmid=15804753 |doi=10.1080/096470490512490|s2cid=37934468 }}</ref> |
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====Cardiovascular disease==== |
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Hyperuricemia is associated with an increase in ] for ].<ref>{{cite journal|journal=Expert Review of Cardiovascular Therapy |year=2014 |volume=12 |issue=10 |pages=1219–1225 |doi=10.1586/14779072.2014.957675 |pmid=25192804|title=Hyperuricemia and cardiovascular disease risk |last1=Borghi |first1=C. |last2=Verardi |first2=F. M. |last3=Pareo |first3=I. |last4=Bentivenga |first4=C. |last5=Cicero |first5=A. F.|s2cid=42023170 }}</ref> It is also possible that high levels of uric acid may have a causal role in the development of atherosclerotic cardiovascular disease, but this is controversial and the data are conflicting.<ref>{{Cite journal |last1=Saito |first1=Yuichi |last2=Tanaka |first2=Atsushi |last3=Node |first3=Koichi |last4=Kobayashi |first4=Yoshio |date=July 2021 |title=Uric acid and cardiovascular disease: A clinical review |journal=Journal of Cardiology |volume=78 |issue=1 |pages=51–57 |doi=10.1016/j.jjcc.2020.12.013 |issn=1876-4738 |pmid=33388217|s2cid=230482803 |doi-access=free }}</ref> |
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====Uric acid stone formation==== |
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] |
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]s can form through deposits of sodium urate microcrystals.<ref name="Banach">{{cite journal |last1=Banach |first1=K. |last2=Bojarska |first2=E. |last3=Kazimierczuk |first3=Z. |last4=Magnowska |first4=L. |last5=Bzowska |first5=A. |date=2005 |title=Kinetic Model of Oxidation Catalyzed by Xanthine Oxidase—The Final Enzyme in Degradation of Purine Nucleosides and Nucleotides |journal=Nucleic Acids |volume=24 |issue=5–7 |pages=465–469 |doi=10.1081/ncn-200060006 |pmid=16247972 |s2cid=42906456}}</ref> |
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Saturation levels of uric acid in blood may result in one form of ]s when the urate crystallizes in the kidney. These uric acid stones are ], so do not appear on an abdominal plain ].<ref>{{Cite journal |last1=Worcester |first1=E. M. |last2=Coe |first2=F. L. |date=2008 |title=Nephrolithiasis |journal=Primary Care: Clinics in Office Practice |language=en |volume=35 |issue=2 |pages=369–391 |doi=10.1016/j.pop.2008.01.005 |pmc=2518455 |pmid=18486720}}</ref> Uric acid crystals can also promote the formation of ] stones, acting as "seed crystals".<ref>{{cite journal |last=Pak |first=C. Y. |date=September 2008 |title=Medical stone management: 35 years of advances |journal=The Journal of Urology |volume=180 |issue=3 |pages=813–819 |doi=10.1016/j.juro.2008.05.048 |pmid=18635234}}</ref> |
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====Diabetes==== |
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Hyperuricemia is associated with components of ], including in children.<ref>{{Cite journal|last=De Oliveira|first=E. P. |display-authors=etal |date=2012|title=High plasma uric acid concentration: Causes and consequences|journal=Diabetology & Metabolic Syndrome|volume=4|pages=12|pmid=22475652|pmc=3359272|doi=10.1186/1758-5996-4-12 |doi-access=free }}</ref><ref>{{Cite journal|last=Wang|first=J. Y.|display-authors=etal|date=2012|title=Predictive value of serum uric acid levels for the diagnosis of metabolic syndrome in adolescents|journal=The Journal of Pediatrics|volume=161 |issue=4|pages=753–6.e2|pmid=22575243|doi=10.1016/j.jpeds.2012.03.036}}</ref> |
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===Low uric acid=== |
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Low uric acid (]) can have numerous causes. Low dietary ] intakes cause lower uric acid levels. This effect can be even more pronounced in women taking oral contraceptive medication.<ref>{{cite journal |last1=Hess |first1=F. M. |last2=King |first2=J. C. |last3=Margen |first3=S. |title=Effect of low zinc intake and oral contraceptive agents on nitrogen utilization and clinical findings in young women |journal=The Journal of Nutrition |volume=107 |issue=12 |pages=2219–2227 |date=1 December 1977|pmid=925768 |doi=10.1093/jn/107.12.2219}}</ref> ], a drug indicated for prevention of ] in people with ], can significantly reduce serum uric acid.<ref>{{cite journal |last1=Garg |first1=J. P. |last2=Chasan-Taber |first2=S. |last3=Blair |first3=A. |display-authors=etal |title=Effects of sevelamer and calcium-based phosphate binders on uric acid concentrations in patients undergoing hemodialysis: a randomized clinical trial |journal=Arthritis and Rheumatism |volume=52 |issue=1 |pages=290–295 |date=January 2005 |pmid=15641045 |doi=10.1002/art.20781|doi-access=free }}</ref> |
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====Multiple sclerosis==== |
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] of 10 case-control studies found that the serum uric acid levels of patients with ] were significantly lower compared to those of healthy controls, possibly indicating a diagnostic ] for multiple sclerosis.<ref>{{cite journal |last1=Wang |first1=L. |last2=Hu |first2=W. |last3=Wang |first3=J. |last4=Qian |first4=W. |last5=Xiao |first5=H. |year=2016 |title=Low serum uric acid levels in patients with multiple sclerosis and neuromyelitis optica: An updated meta-analysis |pmid=27645338 |journal=Multiple Sclerosis and Related Disorders |volume=9 |pages=17–22 |doi=10.1016/j.msard.2016.05.008}}</ref> |
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====Normalizing low uric acid==== |
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Correcting low or deficient zinc levels can help elevate ] uric acid.<ref>{{cite journal |last1=Umeki |first1=S. |last2=Ohga |first2=R. |last3=Konishi |first3=Y. |last4=Yasuda |first4=T. |last5=Morimoto |first5=K. |last6=Terao |first6=A. |title=Oral zinc therapy normalizes serum uric acid level in Wilson's disease patients |journal=The American Journal of the Medical Sciences |volume=292 |issue=5 |pages=289–292 |date=November 1986 |pmid=3777013 |doi=10.1097/00000441-198611000-00007|s2cid=39995735 |doi-access=free }}</ref> |
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== See also == |
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* ] or 1,3,7,9-tetramethyluric acid, a purine alkaloid found in some teas |
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* ] – ] ] named by Robert Behrend who was attempting to synthesize derivatives of uric acid |
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* ] |
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* ] |
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==References== |
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{{Reflist|30em}} |
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==External links== |
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{{Commons category}} |
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* |
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{{Nucleotide metabolism intermediates}} |
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{{Antioxidants}} |
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{{Purinergics}} |
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{{Authority control}} |
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{{DEFAULTSORT:Uric Acid}} |
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