Editing Uric acid (section)

=== Primates ===
In [[humans]] uric acid (actually hydrogen urate ion) is the final [[oxidation]] (breakdown) product of [[purine metabolism]] and is excreted in urine, whereas in most other [[mammal]]s, the enzyme [[uricase]] further oxidizes uric acid to [[allantoin]].<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 [[Vitamin C|ascorbic acid]], 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 [[reducing agent]]s ([[electron donor]]s) and potent [[antioxidant]]s. In humans, over half the antioxidant capacity of [[blood plasma]] 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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==== Humans ====
The normal concentration range of uric acid (or hydrogen urate ion) in human blood is 25 to 80&nbsp;mg/L for men and 15 to 60&nbsp;mg/L for women<ref>{{cite book|title=Harrison's Principles of Internal Medicine|publisher=[[McGraw-Hill Education|McGraw-Hill]]|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&nbsp;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 [[hyperuricemia]].<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&nbsp;mg per day (concentration of 270 to 360&nbsp;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 [[urea]].<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>