n.

(化合物)尿酸塩、尿酸

関: uric、uric acid

WordNet

a salt of uric acid
acting to increase the excretion of uric acid in the urine
in or relating to or obtained from urine; "uric acid"

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尿の,尿に関する(含まれている),尿から得られる

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/10/20 19:31:29」(JST)

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Uric acid is a heterocyclic compound of carbon, nitrogen, oxygen, and hydrogen with the formula C₅H₄N₄O₃. 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. High blood concentrations of uric acid can lead to gout. The chemical is associated with other medical conditions including diabetes and the formation of ammonium acid urate kidney stones.

1 Chemistry
- 1.1 Solubility
2 Biology
- 2.1 Other animals
3 Genetics
4 Medicine
- 4.1 High uric acid
  - 4.1.1 Causes of high uric acid
  - 4.1.2 Gout
  - 4.1.3 Lesch-Nyhan syndrome
  - 4.1.4 Cardiovascular disease
  - 4.1.5 Type 2 diabetes
  - 4.1.6 Metabolic syndrome
  - 4.1.7 Uric acid stone formation
- 4.2 Low Uric Acid
  - 4.2.1 Causes of low uric acid
  - 4.2.2 Multiple sclerosis
  - 4.2.3 Normalizing low uric acid
- 4.3 Oxidative stress
5 Sources
6 Correlations with creative output
7 See also
8 References
9 Further reading
10 External links

Chemistry

Uric acid is a diprotic acid with pKa₁=5.4 and pKa₂=10.3.^[1] Thus in strong alkali at high pH, it forms the dually charged full urate ion, but at biological pH or in the presence of carbonic acid or carbonate ions, it forms the singly charged hydrogen or acid urate ion, as its pKa₁ is lower than the pKa₁ of carbonic acid. As its second ionization is so weak, the full urate salts tend to hydrolyze back to hydrogen urate salts and free base at pH values around neutral. It is aromatic because of the purine functional group.

As a bicyclic, heterocyclic purine derivative, uric acid does not protonate as an oxygen [-OH] like carboxylic acids do. X-ray diffraction studies on the hydrogen urate ion in crystals of ammomium hydrogen urate, formed in vivo as gouty deposits, reveal the keto-oxygen in the 2 position of a tautomer of the purine structure exists as a hydroxyl group and the two flanking nitrogen atoms at the 1 and 3 positions share the ionic charge in the six-membered pi-resonance-stabilized ring.^[2]

Thus, while most organic acids are deprotonated by the ionization of a polar hydrogen-to-oxygen bond, usually accompanied by some form of resonance stabilization (resulting in a carboxylate ion), uric acid is deprotonated at a nitrogen atom and uses a tautomeric keto/hydroxy group as an electron-withdrawing group to increase the pK₁ value. The five-membered ring also possesses a keto group (in the 8 position), flanked by two secondary amino groups (in the 7 and 9 positions), and deprotonation of one of these at high pH could explain the pK₂ and behavior as a diprotic acid. Similar tautomeric rearrangement and pi-resonance stabilization would then give the ion some degree of stability. (On the structure shown at the upper-right, the NH at the upper-right on the six-membered ring is "1", counting clockwise around the six-membered ring to "6" for the keto carbon at the top of the six-membered ring. The uppermost NH on the five-membered ring is "7", counting counter-clockwise around this ring to the lower NH, which is "9".)

Uric acid was first isolated from kidney stones in 1776 by Scheele.^[3] As far as laboratory synthesis is concerned, in 1882, Ivan Horbaczewski claimed to have prepared uric acid by melting urea hydrogen peroxide with glycine, trichlorolactic acid, and its amide.^{[citation needed]} Soon after, repetition by Eduard Hoffmann shows that this preparation with glycine gives no trace of uric acid, but trichlorolacetamide produces some uric acid. Thus, Hoffmann was the first to synthesize uric acid.^[4]

Solubility

In general, the water solubility of uric acid and its alkali metal and alkaline earth salts 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 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 water.

Compound	Cold water	Boiling water
Uric Acid	15000	2000
NH₄HUrate	-	1600
LiHUrate	370	39
NaHUrate	1175	124
KHUrate	790	75
Mg(HUrate)₂	3750	160
Ca(HUrate)₂	603	276
Na₂Urate	77	-
K₂Urate	44	35
CaUrate	1500	1440
SrUrate	4300	1790
BaUrate	7900	2700

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.^[5]^[6]^[7]

Biology

The enzyme xanthine oxidase makes uric acid 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.^[8] Within cells, xanthine oxidase can exist as xanthine dehydrogenase and xanthine oxireductase, which has also been purified from bovine milk and spleen extracts.^[9] Uric acid is released in hypoxic conditions.^[10]

In humans and higher primates, uric acid is the final oxidation (breakdown) product of purine metabolism and is excreted in urine. In most other mammals, the enzyme uricase further oxidizes uric acid to allantoin.^[11] 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.^[12] 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 uric acid.^[13]

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.^[14]

Other animals

The Dalmatian dog has a genetic defect in uric acid uptake by the liver and kidneys, resulting in decreased conversion to allantoin, so this breed excretes uric acid, and not allantoin, in the urine.^[15]

In birds and reptiles, and in some desert dwelling mammals (e.g., the kangaroo rat), uric acid also is the end-product of purine metabolism, but it is excreted in feces as a dry mass. This involves a complex metabolic pathway that is energetically costly in comparison to processing of other nitrogenous wastes such as urea (from urea cycle) or ammonia, but has the advantages of reducing water loss and, hence, reducing the need for water.^[16]

Genetics

A proportion of people have mutations in the proteins responsible for the excretion of uric acid by the kidneys. Variants within a number of genes have so far been identified: SLC2A9; ABCG2; SLC17A1; SLC22A11; SLC22A12; SLC16A9; GCKR; LRRC16A; and PDZK1.^[17]^[18] ^[19] SLC2A9 is known to transport both uric acid and fructose.^[14]^[20]

Medicine

In human blood plasma, the reference range of uric acid is typically 3.4-7.2 mg/dL (200-430 µmol/L) for men (1 mg/dL=59.48 µmol/L), and 2.4-6.1 mg/dL for women (140-360 µmol/L).^[21] However, blood test results should always be interpreted using the range provided by the laboratory that performed the test. Uric acid concentrations in blood plasma above and below the normal range are known, respectively, as hyperuricemia and hypouricemia. Likewise, uric acid concentrations in urine above and below normal are known as hyperuricosuria and hypouricosuria. Such abnormal concentrations of uric acid are not medical conditions, but are associated with a variety of medical conditions.^{[citation needed]}

High uric acid

High levels of uric acid is called hyperuricemia and can lead to gout.

Causes of high uric acid

Diet may be a factor. High intake of dietary purine, high-fructose corn syrup, and table sugar can cause increased levels of uric acid.^[22]^[23]

Serum uric acid can be elevated due to reduced excretion by the kidneys.^[24]

Fasting or rapid weight loss can temporarily elevate uric acid levels.

Certain drugs, such as thiazide diuretics, can increase uric acid levels in the blood by interfering with renal clearance.^[25]

Gout

Excess serum accumulation of uric acid in the blood can lead to a type of arthritis known as gout.^[26] This painful condition is the result of needle-like crystals of uric acid precipitating in joints, capillaries, skin, and other tissues.^[27] Kidney stones can also form through the process of formation and deposition of sodium urate microcrystals.^[28]^[29]

A study found that men who drink two or more sugar-sweetened beverages a day have an 85% higher chance of developing gout than those who drank such beverages infrequently.^[30]

Gout can occur where serum uric acid levels are as low as 6 mg/dL (~357 µmol/L), but an individual can have serum values as high as 9.6 mg/dL (~565 µmol/L) and not have gout.^[31]

One treatment for gout, in the 19th century, had been administration of lithium salts;^[32] lithium urate is more soluble. Today, inflammation during attacks is more commonly treated with NSAIDs or corticosteroids, and urate levels are managed with allopurinol.^[33] Allopurinol, developed over 30 years ago by Elion et al., weakly inhibits xanthine oxidase. It is an analog of hypoxanthine that is hydroxylated by xanthine oxidoreductase at the 2-position to give oxipurinol. Oxipurinol has been supposed to bind tightly to the reduced molybdenum ion in the enzyme and, thus, inhibits uric acid synthesis.^[34]

Lesch-Nyhan syndrome

Lesch-Nyhan syndrome, an extremely rare inherited disorder, is also associated with very high serum uric acid levels.^[35] Spasticity, involuntary movement, and cognitive retardation as well as manifestations of gout are seen in cases of this syndrome.^[36]

Cardiovascular disease

Hyperuricemia may be associated with an increase in risk factors for cardiovascular disease.^[37]

Type 2 diabetes

The association of high serum uric acid with insulin resistance has been known since the early part of the 20th century, but the hypothesis that high serum uric acid is a risk factor for diabetes has long been a matter of debate. In fact, hyperuricemia was presumed to be a consequence of insulin resistance rather than its precursor.^[38] However, a prospective follow-up study showed high serum uric acid is associated with higher risk of type 2 diabetes, independent of obesity, dyslipidemia, and hypertension.^[39]

Metabolic syndrome

Hyperuricemia is associated with components of metabolic syndrome. A study has suggested fructose-induced hyperuricemia may play a pathogenic role in the metabolic syndrome.^[40] This is consistent with the increased consumption in recent decades of fructose-containing beverages (such as fruit juices and soft drinks sweetened with sugar and high-fructose corn syrup) and the epidemic of diabetes and obesity.^[30]

Uric acid stone formation

Saturation levels of uric acid in blood may result in one form of kidney stones when the urate crystallizes in the kidney. These uric acid stones are radiolucent and so do not appear on an abdominal plain X-ray, and thus their presence must be diagnosed by ultrasound for this reason or stone protocol CT. Very large stones may be detected on X-ray by their displacement of the surrounding kidney tissues.

Uric acid stones, which form in the absence of secondary causes such as chronic diarrhea, vigorous exercise, dehydration, and animal protein loading, are felt to be secondary to obesity and insulin resistance seen in metabolic syndrome. Increased dietary acid leads to increased endogenous acid production in the liver and muscles, which in turn leads to an increased acid load to the kidneys. This load is handled more poorly because of renal fat infiltration and insulin resistance, which are felt to impair ammonia excretion (a buffer). The urine is, therefore, quite acidic, and uric acid becomes insoluble, crystallizes and stones form. In addition, naturally present promoter and inhibitor factors may be affected. This explains the high prevalence of uric stones and unusually acidic urine seen in patients with type 2 diabetes. Uric acid crystals can also promote the formation of calcium oxalate stones, acting as "seed crystals" (heterogeneous nucleation).^[41]

Low Uric Acid

Causes of low uric acid

Low uric acid (hypouricemia) can have numerous causes.

Low dietary zinc intakes cause lower uric acid levels. This effect can be even more pronounced in women taking oral contraceptive medication.^[42]

Xanthine oxidase is an Fe-Mo enzyme, so people with Fe deficiency (the most common cause of anemia in young women) or Mo deficiency can experience hypouricemia.

Xanthine oxidase loses its function and gains ascorbase function when some of the Fe atoms in XO are replaced with Cu atoms. As such, people with high Cu/Fe can experience hypouricemia and vitamin C deficiency, resulting in oxidative damage. Since estrogen increases the half-life of Cu, women with very high estrogen levels and intense blood loss during menstruation are likely to have a high Cu/Fe and present with hypouricemia.

Sevelamer, a drug indicated for prevention of hyperphosphataemia in patients with chronic renal failure, can significantly reduce serum uric acid.^[43]

But the main cause of congenitally low uric acid, sometimes as low as zero, remains the Molybdenum cofactor deficiency.

Multiple sclerosis

Lower serum values of uric acid have been associated with multiple sclerosis (MS). MS patients have been found to have serum levels ~194 µmol/L, with patients in relapse averaging ~160 µmol/L and patients in remission averaging ~230 µmol/L. Serum uric acid in healthy controls was ~290 µmol/L.^[44] Conversion factor: 1 mg/dL=59.48 µmol/L^[45]

A 1998 study completed a statistical analysis of 20 million patient records, comparing serum uric acid values in patients with gout and patients with multiple sclerosis. Almost no overlap between the groups was found.^[46]

Uric acid has been successfully used in the treatment and prevention of the animal (murine) model of MS. A 2006 study found elevation of serum uric acid values in multiple sclerosis patients, by oral supplementation with inosine, resulted in lower relapse rates, and no adverse effects.^[47]

Normalizing low uric acid

Correcting low or deficient zinc levels can help elevate serum uric acid.^[48] Inosine can be used to elevate uric acid levels.^[44] Zn inhibits Cu absorption, helping to reduce the high Cu/Fe in some people with hypouricemia. Fe supplements can ensure adequate Fe reserves (ferritin above 25 ng/dl), also correcting the high Cu/Fe.

Oxidative stress

Uric acid may be a marker of oxidative stress,^[49] and may have a potential therapeutic role as an antioxidant.^[50] On the other hand, like other strong reducing substances such as ascorbate, uric acid can also act as a prooxidant. Thus, it is unclear whether elevated levels of uric acid in diseases associated with oxidative stress such as stroke and atherosclerosis are a protective response or a primary cause.^[51]

For example, some researchers propose hyperuricemia-induced oxidative stress is a cause of metabolic syndrome.^[40]^[52] On the other hand, plasma uric acid levels correlate with longevity in primates and other mammals.^[53] This is presumably a function of urate's antioxidant properties.^[54]

Sources

In humans, purines are excreted as uric acid. Purines are found in high amounts in animal food products, such as liver and sardines.^[55] A moderate amount of purine is also contained in beef, pork, poultry, fish and seafood, asparagus, cauliflower, spinach, mushrooms, green peas, lentils, dried peas, beans, oatmeal, wheat bran, and wheat germ.^[56]

Examples of high purine and Fe sources include: sweetbreads, anchovies, sardines, liver, beef kidneys, brains, meat extracts (e.g., Oxo, Bovril), herring, mackerel, scallops, game meats, beer, and gravy.

Moderate and even high intake of purine-containing vegetables is not associated with an increased risk of gout. One serving of meat or seafood (3 oz = 85 g) mildly increases risk of gout, while two servings increase risk by at least 40%. Milk products reduce the risk of gout notably, whereas total protein intake has no effect.^[57]

Correlations with creative output

Havelock Ellis found in his A Study of British Genius (1904) that there was an unusually high rate of gout among eminent men in his study, and gout is associated with higher volumes of uric acid in the blood. He therefore suggested that it might have something to do with it. Later investigators have examined this relationship, and there is indeed a correlation.^[58] A review is Jensen & Sinha (1993),^[59] which found only a slight correlation between IQ and serum urate level (SUL), however there was a stronger correlation between SUL and scholastic achievement, even after controlling for IQ. Another study found a correlation of +.37 between serum urate level and publication rates of university professors. Jensen speculates that it may be due to uric acid's having a similar chemical structure to that of caffeine, and thus acting as a natural stimulant.^[59]

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^ Choi HK, Atkinson K, Karlson EW, Willett W, Curhan G (March 2004). "Purine-rich foods, dairy and protein intake, and the risk of gout in men". The New England Journal of Medicine 350 (11): 1093–103. doi:10.1056/NEJMoa035700. PMID 15014182.
^ Arthur Jensen (1996). "Giftedness ≠ Genius". In Camilla Perrson Benbow, David Lubinski. Intellectual talent: From Psychometrics to Giftedness. Hopkins. pp. 403–404. ISBN 9780801853012.
^ ^a ^b Arthur Jensen; SN Sinha (1993). "Physical correlates of human intelligence". In Philip A. Vernon. Biological approaches to the study of human intelligence. Norwood, NJ: Ablex Publ. Corp. ISBN 9780893917982.

External links

Uric acid - Lab Tests Online
Uric acid blood test - MedlinePlus
International Kidney Stone Institute
NHS Clinical Knowledge Summaries^{[dead link]}
Uric acid: analyte monograph - the Association for Clinical Biochemistry and Laboratory Medicine

UpToDate Contents

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1. 尿酸のバランス uric acid balance
2. 無症候性高尿酸血症 asymptomatic hyperuricemia
3. 痛風の臨床症状および診断 clinical manifestations and diagnosis of gout
4. 尿酸による腎疾患 uric acid renal diseases
5. 低尿酸血症：原因および臨床的意義 hypouricemia causes and clinical significance

English Journal

Effects of garlic extract on TNF-α expression and oxidative stress status in the kidneys of rats with STZ + nicotinamide-induced diabetes.

Ziamajidi N1,2, Nasiri A1, Abbasalipourkabir R1, Sadeghi Moheb S1,2.
Pharmaceutical biology.Pharm Biol.2017 Dec;55(1):526-531.
CONTEXT: Allium sativum L. (Liliaceae) (garlic) is a medicinal plant that is widely used in herbal medicine. Nephropathy is a complication of diabetes that is induced by long-term hyperglycaemia.OBJECTIVE: The effects of aqueous extract of garlic (AGE) on the expression of tumour necrosis factor-alp
PMID 27937047

Effect of Cichorium intybus L. seed extract on renal parameters in experimentally induced early and late diabetes type 2 in rats.

Pourfarjam Y1, Rezagholizadeh L1, Nowrouzi A1,2,3, Meysamie A4, Ghaseminejad S1, Ziamajidi N5, Norouzi D6.
Renal failure.Ren Fail.2017 Nov;39(1):211-221. doi: 10.1080/0886022X.2016.1256317. Epub 2016 Nov 16.
Blood and urine biochemistry screening tests are important for initial detection of diabetes, determination of severity of its complications, and monitoring of therapy. We evaluated the effects of aqueous chicory seed extract (CSE), on renal biochemical parameters, histology, and Na+/glucose cotansp
PMID 27846769

Olive oil abrogates acrylamide induced nephrotoxicity by modulating biochemical and histological changes in rats.

Ghorbel I1, Elwej A1, Fendri N2, Mnif H3, Jamoussi K2, Boudawara T3, Grati Kamoun N4, Zeghal N1.
Renal failure.Ren Fail.2017 Nov;39(1):236-245. doi: 10.1080/0886022X.2016.1256320. Epub 2016 Nov 15.
Acrylamide (ACR) is one of the most important contaminants occurring in foods heated at high temperatures. The aim of this study is to investigate the protective efficacy of extra virgin olive oil (EVOO), a main component of the Mediterranean diet, against nephrotoxicity induced by ACR. Rats have re
PMID 27846768

Japanese Journal

5) 妊娠高血圧症候群ならびに関連疾患の発症予知 : リスク因子の解明をめざして(シンポジウム2:周産期「妊娠高血圧症候群の基礎と臨床-予防・治療の新戦略に向けて」,第65回日本産科婦人科学会・学術講演会)

森川守
日本産科婦人科學會雜誌 65(11), 2616-2624, 2013-11-01
… AT activity significantly correlates negatively with D-dimer, serum creatinine, and urate. …
NAID 110009674985

5) 妊娠高血圧症候群ならびに関連疾患の発症予知 : リスク因子の解明をめざして(シンポジウム2:周産期「妊娠高血圧症候群の基礎と臨床-予防・治療の新戦略に向けて」,第65回日本産科婦人科学会・学術講演会)

森川守
日本産科婦人科學會雜誌 65(11), 2616-2624, 2013-11-01
… AT activity significantly correlates negatively with D-dimer, serum creatinine, and urate. …
NAID 110009661873

酸性尿酸アンモニウム結石の1例

山尾裕,福原恒,桑原元 [他]
西日本泌尿器科 = The Nishinihon journal of urology 75(7), 369-371, 2013-07
NAID 40019705106

Related Pictures

★リンクテーブル★

リンク元	「uricosuric」「uric」
拡張検索	「suppurate」「polyunsaturated alkamide」

「uricosuric」

Uric acid
	; Crystals of urate in polarized light
Names
	Systematic IUPAC name 7,9-Dihydro-1H-purine-2,6,8(3H)-trione
	Other names 2,6,8-Trioxypurine; 2,6,8-Trihydroxypurine; 2,6,8-Trioxopurine; 1H-Purine-2,6,8-triol
Identifiers
CAS Registry Number	69-93-2
3DMet	B00094
Beilstein Reference	156158
ChEBI	CHEBI:27226
ChEMBL	ChEMBL792
ChemSpider	1142
DrugBank	DB01696
EC number	200-720-7
	InChI InChI=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) ; Key: DZGSAURIFGGOJK-UHFFFAOYSA-N ; 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; Key: LEHOTFFKMJEONL-UHFFFAOYAN ;
IUPHAR/BPS	4731
Jmol-3D images	Image; Image
KEGG	C00366
MeSH	Uric+Acid
PubChem	1175
	SMILES OC1Nc2nc(=O)nc2C(=O)N1 ; OC1NC2=NC(=O)N=C2C(=O)N1 ;
UNII	268B43MJ25
Properties
Chemical formula	C5H4N4O3
Molar mass	168.11 g·mol−1
Appearance	White crystals
Melting point	300 °C (572 °F; 573 K)
Solubility in water	0.0006g/100 mL (at 20 °C)
log P	-1.107
Acidity (pKa)	5.6
Basicity (pKb)	8.4
Thermochemistry
Specific; heat capacity (C)	166.15 J K−1 mol−1 (at 24.0 °C)
Std molar; entropy (So298)	173.2 J K−1 mol−1
Std enthalpy of; formation (ΔfHo298)	-619.69–617.93 kJ mol−1
Std enthalpy of; combustion (ΔcHo298)	-1.9212–1.91956 MJ mol−1
	Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
	verify (what is: /?)
	Infobox references

　　[★]

adj.

(医)(尿酸中の)尿酸排泄の、尿酸排泄を促進する

n.

尿酸排泄促進剤

関: uricotelic

関: uricosuria 尿酸尿; uric acid urate 尿酸; urico-,uric- (語を連結して)尿酸

「uric」

　　[★]

adj.

尿酸の

comb form.

尿酸 (=urico)

関: urate、uric acid

「suppurate」

　　[★]

vi

化膿する

関: (adj.)suppurative

「polyunsaturated alkamide」

　　[★]

多価不飽和アルカミド

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[2] European Powder Diffraction Conference, EPDIC-9^{[full citation needed]}

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[SI_Units_for_Clinical_Data-45] SI Units for Clinical Data

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[55] Gout Causes: List of Diet/Food Sources High or Low in Purine Content

[56] Gout Diet / Low Purine Diet - Limit High Purine foods

[57] Choi HK, Atkinson K, Karlson EW, Willett W, Curhan G (March 2004). "Purine-rich foods, dairy and protein intake, and the risk of gout in men". The New England Journal of Medicine 350 (11): 1093–103. doi:10.1056/NEJMoa035700. PMID 15014182.

[intellectualtalent-58] Arthur Jensen (1996). "Giftedness ≠ Genius". In Camilla Perrson Benbow, David Lubinski. Intellectual talent: From Psychometrics to Giftedness. Hopkins. pp. 403–404. ISBN 9780801853012.

[jensensinha-59] Arthur Jensen; SN Sinha (1993). "Physical correlates of human intelligence". In Philip A. Vernon. Biological approaches to the study of human intelligence. Norwood, NJ: Ablex Publ. Corp. ISBN 9780893917982.

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