| Record Information |
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| Version | 5.0 |
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| Status | Detected and Quantified |
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| Creation Date | 2006-08-15 22:07:35 UTC |
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| Update Date | 2022-03-07 02:49:04 UTC |
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| HMDB ID | HMDB0000588 |
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| Secondary Accession Numbers | |
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| Metabolite Identification |
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| Common Name | Sodium |
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| Description | Sodium, also known as Na+ or sodium ion, belongs to the class of inorganic compounds known as homogeneous alkali metal compounds. These are inorganic compounds containing only metal atoms,with the largest atom being a alkali metal atom. Sodium is a weakly acidic compound (based on its pKa). Sodium exists in all living species, ranging from bacteria to humans. In humans, sodium is involved in the metabolic disorder called the triamterene action pathway. Outside of the human body, Sodium has been detected, but not quantified in, several different foods, such as cashew nuts, sugar apples, oregon yampahs, hazelnuts, and turnips. This could make sodium a potential biomarker for the consumption of these foods. Physiologically, it exists as an ion in the body. Sodium, with regard to humans, has been found to be associated with several diseases such as lipoid congenital adrenal hyperplasia, congenital secretory diarrhea, bartter syndrome, type 4b, neonatal, with sensorineural deafness, and adrenal hyperplasia, congenital, due to 3-beta-hydroxysteroid dehydrogenase 2 deficiency; sodium has also been linked to the inborn metabolic disorder primary hypomagnesemia. Sodium ions are necessary for regulation of blood and body fluids, transmission of nerve impulses, heart activity, and certain metabolic functions. Sodium is needed by animals, which maintain high concentrations in their blood and extracellular fluids, but the ion is not needed by plants. For certain people with salt-sensitive blood pressure, this extra intake may cause a negative effect on health. Most people consume far more sodium than is physiologically needed. |
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| Structure | |
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| Synonyms | | Value | Source |
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| Na(+) | ChEBI | | Na+ | ChEBI | | SODIUM ion | ChEBI | | Sodium(1+) | Kegg |
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| Chemical Formula | Na |
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| Average Molecular Weight | 22.9898 |
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| Monoisotopic Molecular Weight | 22.989769675 |
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| IUPAC Name | sodium(1+) ion |
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| Traditional Name | sodium(1+) ion |
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| CAS Registry Number | 7440-23-5 |
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| SMILES | [Na+] |
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| InChI Identifier | InChI=1S/Na/q+1 |
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| InChI Key | FKNQFGJONOIPTF-UHFFFAOYSA-N |
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| Chemical Taxonomy |
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| Description | Belongs to the class of inorganic compounds known as homogeneous alkali metal compounds. These are inorganic compounds containing only metal atoms,with the largest atom being a alkali metal atom. |
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| Kingdom | Inorganic compounds |
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| Super Class | Homogeneous metal compounds |
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| Class | Homogeneous alkali metal compounds |
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| Sub Class | Not Available |
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| Direct Parent | Homogeneous alkali metal compounds |
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| Alternative Parents | Not Available |
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| Substituents | |
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| Molecular Framework | Not Available |
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| External Descriptors | |
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| Ontology |
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| Not Available | Not Available |
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| Physical Properties |
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| State | Solid |
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| Experimental Molecular Properties | | Property | Value | Reference |
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| Melting Point | 97.82 °C | Not Available | | Boiling Point | Not Available | Not Available | | Water Solubility | Not Available | Not Available | | LogP | Not Available | Not Available |
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| Experimental Chromatographic Properties | Not Available |
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| Predicted Molecular Properties | |
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| Predicted Chromatographic Properties | Predicted Collision Cross SectionsPredicted Retention Times Underivatized| Chromatographic Method | Retention Time | Reference |
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| AjsUoB = Accucore 150 Amide HILIC with 10mM Ammonium Formate, 0.1% Formic Acid | 286.0 seconds | 40023050 | | Fem_Long = Waters ACQUITY UPLC HSS T3 C18 with Water:MeOH and 0.1% Formic Acid | 955.2 seconds | 40023050 | | Fem_Lipids = Ascentis Express C18 with (60:40 water:ACN):(90:10 IPA:ACN) and 10mM NH4COOH + 0.1% Formic Acid | 446.0 seconds | 40023050 | | Life_Old = Waters ACQUITY UPLC BEH C18 with Water:(20:80 acetone:ACN) and 0.1% Formic Acid | 201.4 seconds | 40023050 | | Life_New = RP Waters ACQUITY UPLC HSS T3 C18 with Water:(30:70 MeOH:ACN) and 0.1% Formic Acid | 368.2 seconds | 40023050 | | RIKEN = Waters ACQUITY UPLC BEH C18 with Water:ACN and 0.1% Formic Acid | 226.0 seconds | 40023050 | | Eawag_XBridgeC18 = XBridge C18 3.5u 2.1x50 mm with Water:MeOH and 0.1% Formic Acid | 336.9 seconds | 40023050 | | BfG_NTS_RP1 =Agilent Zorbax Eclipse Plus C18 (2.1 mm x 150 mm, 3.5 um) with Water:ACN and 0.1% Formic Acid | 428.1 seconds | 40023050 | | HILIC_BDD_2 = Merck SeQuant ZIC-HILIC with ACN(0.1% formic acid):water(16 mM ammonium formate) | 653.7 seconds | 40023050 | | UniToyama_Atlantis = RP Waters Atlantis T3 (2.1 x 150 mm, 5 um) with ACN:Water and 0.1% Formic Acid | 687.8 seconds | 40023050 | | BDD_C18 = Hypersil Gold 1.9µm C18 with Water:ACN and 0.1% Formic Acid | 198.4 seconds | 40023050 | | UFZ_Phenomenex = Kinetex Core-Shell C18 2.6 um, 3.0 x 100 mm, Phenomenex with Water:MeOH and 0.1% Formic Acid | 779.5 seconds | 40023050 | | SNU_RIKEN_POS = Waters ACQUITY UPLC BEH C18 with Water:ACN and 0.1% Formic Acid | 304.4 seconds | 40023050 | | RPMMFDA = Waters ACQUITY UPLC BEH C18 with Water:ACN and 0.1% Formic Acid | 394.4 seconds | 40023050 | | MTBLS87 = Merck SeQuant ZIC-pHILIC column with ACN:Water and :ammonium carbonate | 710.0 seconds | 40023050 | | KI_GIAR_zic_HILIC_pH2_7 = Merck SeQuant ZIC-HILIC with ACN:Water and 0.1% FA | 390.8 seconds | 40023050 | | Meister zic-pHILIC pH9.3 = Merck SeQuant ZIC-pHILIC column with ACN:Water 5mM NH4Ac pH9.3 and 5mM ammonium acetate in water | 312.5 seconds | 40023050 |
Predicted Kovats Retention IndicesUnderivatized |
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| Disease References | | Primary hypomagnesemia |
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- Jin-no Y, Kamiya Y, Okada M, Hirako M, Takada N, Kawaguchi M: Primary hypomagnesemia caused by isolated magnesium malabsorption: atypical case in adult. Intern Med. 1999 Mar;38(3):261-5. [PubMed:10337938 ]
| | 21-Hydroxylase deficiency |
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- Warinner SA, Zimmerman D, Thompson GB, Grant CS: Study of three patients with congenital adrenal hyperplasia treated by bilateral adrenalectomy. World J Surg. 2000 Nov;24(11):1347-52. [PubMed:11038205 ]
| | Bartter Syndrome, Type 4A, Neonatal, with Sensorineural Deafness |
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- Zaffanello M, Taranta A, Palma A, Bettinelli A, Marseglia GL, Emma F: Type IV Bartter syndrome: report of two new cases. Pediatr Nephrol. 2006 Jun;21(6):766-70. doi: 10.1007/s00467-006-0090-x. Epub 2006 Apr 1. [PubMed:16583241 ]
| | Bartter Syndrome, Type 1, Antenatal |
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- Adachi M, Asakura Y, Sato Y, Tajima T, Nakajima T, Yamamoto T, Fujieda K: Novel SLC12A1 (NKCC2) mutations in two families with Bartter syndrome type 1. Endocr J. 2007 Dec;54(6):1003-7. Epub 2007 Nov 12. [PubMed:17998760 ]
| | Adrenal insufficiency, congenital, with 46,XY sex reversal, partial or complete |
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- Kim CJ, Lin L, Huang N, Quigley CA, AvRuskin TW, Achermann JC, Miller WL: Severe combined adrenal and gonadal deficiency caused by novel mutations in the cholesterol side chain cleavage enzyme, P450scc. J Clin Endocrinol Metab. 2008 Mar;93(3):696-702. doi: 10.1210/jc.2007-2330. Epub 2008 Jan 8. [PubMed:18182448 ]
| | Bartter Syndrome, Type 2, Antenatal |
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- Chan WK, To KF, Tong JH, Law CW: Paradoxical hypertension and salt wasting in Type II Bartter syndrome. Clin Kidney J. 2012 Jun;5(3):217-20. doi: 10.1093/ckj/sfs026. Epub 2012 Mar 29. [PubMed:26069767 ]
| | Adrenal hyperplasia, congenital, due to 3-beta-hydroxysteroid dehydrogenase 2 deficiency |
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- Guven A, Polat S: Testicular Adrenal Rest Tumor in Two Brothers with a Novel Mutation in the 3-Beta-Hydroxysteroid Dehydrogenase-2 Gene. J Clin Res Pediatr Endocrinol. 2017 Mar 1;9(1):85-90. doi: 10.4274/jcrpe.3306. Epub 2016 Jul 29. [PubMed:27476613 ]
| | Bartter Syndrome, Type 3 |
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- Seys E, Andrini O, Keck M, Mansour-Hendili L, Courand PY, Simian C, Deschenes G, Kwon T, Bertholet-Thomas A, Bobrie G, Borde JS, Bourdat-Michel G, Decramer S, Cailliez M, Krug P, Cozette P, Delbet JD, Dubourg L, Chaveau D, Fila M, Jourde-Chiche N, Knebelmann B, Lavocat MP, Lemoine S, Djeddi D, Llanas B, Louillet F, Merieau E, Mileva M, Mota-Vieira L, Mousson C, Nobili F, Novo R, Roussey-Kesler G, Vrillon I, Walsh SB, Teulon J, Blanchard A, Vargas-Poussou R: Clinical and Genetic Spectrum of Bartter Syndrome Type 3. J Am Soc Nephrol. 2017 Aug;28(8):2540-2552. doi: 10.1681/ASN.2016101057. Epub 2017 Apr 5. [PubMed:28381550 ]
| | Bartter Syndrome, Type 4B, Neonatal, With Sensorineural Deafness |
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- Nozu K, Inagaki T, Fu XJ, Nozu Y, Kaito H, Kanda K, Sekine T, Igarashi T, Nakanishi K, Yoshikawa N, Iijima K, Matsuo M: Molecular analysis of digenic inheritance in Bartter syndrome with sensorineural deafness. J Med Genet. 2008 Mar;45(3):182-6. doi: 10.1136/jmg.2007.052944. [PubMed:18310267 ]
| | Lipoid Congenital Adrenal Hyperplasia |
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- Fujieda K, Tajima T, Nakae J, Sageshima S, Tachibana K, Suwa S, Sugawara T, Strauss JF 3rd: Spontaneous puberty in 46,XX subjects with congenital lipoid adrenal hyperplasia. Ovarian steroidogenesis is spared to some extent despite inactivating mutations in the steroidogenic acute regulatory protein (StAR) gene. J Clin Invest. 1997 Mar 15;99(6):1265-71. doi: 10.1172/JCI119284. [PubMed:9077535 ]
- Hauffa BP, Miller WL, Grumbach MM, Conte FA, Kaplan SL: Congenital adrenal hyperplasia due to deficient cholesterol side-chain cleavage activity (20, 22-desmolase) in a patient treated for 18 years. Clin Endocrinol (Oxf). 1985 Nov;23(5):481-93. [PubMed:3841304 ]
| | Corticosterone methyl oxidase I deficiency |
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- Ustyol A, Atabek ME, Taylor N, Yeung MC, Chan AO: Corticosterone Methyl Oxidase Deficiency Type 1 with Normokalemia in an Infant. J Clin Res Pediatr Endocrinol. 2016 Sep 1;8(3):356-9. doi: 10.4274/jcrpe.2824. Epub 2016 Apr 29. [PubMed:27125267 ]
| | Pseudohypoaldosteronism, type I, autosomal dominant |
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- Bowden SA, Cozzi C, Hickey SE, Thrush DL, Astbury C, Nuthakki S: Autosomal dominant pseudohypoaldosteronism type 1 in an infant with salt wasting crisis associated with urinary tract infection and obstructive uropathy. Case Rep Endocrinol. 2013;2013:524647. doi: 10.1155/2013/524647. Epub 2013 Dec 19. [PubMed:24455331 ]
| | Congenital secretory diarrhea |
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- Muller T, Wijmenga C, Phillips AD, Janecke A, Houwen RH, Fischer H, Ellemunter H, Fruhwirth M, Offner F, Hofer S, Muller W, Booth IW, Heinz-Erian P: Congenital sodium diarrhea is an autosomal recessive disorder of sodium/proton exchange but unrelated to known candidate genes. Gastroenterology. 2000 Dec;119(6):1506-13. [PubMed:11113072 ]
| | Congenital chloride diarrhea |
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- Lubani MM, Doudin KI, Sharda DC, Shaltout AA, al-Shab TS, Abdul Al YK, Said MA, Salhi MM, Ahmed SA: Congenital chloride diarrhoea in Kuwaiti children. Eur J Pediatr. 1989 Jan;148(4):333-6. [PubMed:2651131 ]
| | Wolfram syndrome 1 |
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- Valsalan R, Gonsalves H, Mailankot M, Mulamani N, Sheshadri S: Wolfram syndrome - clinical and diagnostic details. Indian J Clin Biochem. 2009 Oct;24(4):436-8. doi: 10.1007/s12291-009-0079-x. Epub 2009 Dec 30. [PubMed:23105875 ]
| | Bartter Syndrome, Type 5, Antenatal, Transient |
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- Laghmani K, Beck BB, Yang SS, Seaayfan E, Wenzel A, Reusch B, Vitzthum H, Priem D, Demaretz S, Bergmann K, Duin LK, Gobel H, Mache C, Thiele H, Bartram MP, Dombret C, Altmuller J, Nurnberg P, Benzing T, Levtchenko E, Seyberth HW, Klaus G, Yigit G, Lin SH, Timmer A, de Koning TJ, Scherjon SA, Schlingmann KP, Bertrand MJ, Rinschen MM, de Backer O, Konrad M, Komhoff M: Polyhydramnios, Transient Antenatal Bartter's Syndrome, and MAGED2 Mutations. N Engl J Med. 2016 May 12;374(19):1853-63. doi: 10.1056/NEJMoa1507629. Epub 2016 Apr 27. [PubMed:27120771 ]
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