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hydrogencarbonate |
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CHEBI:17544 |
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The carbon oxoanion resulting from the removal of a proton from carbonic acid. |
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This entity has been manually annotated by the ChEBI Team.
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CHEBI:22863, CHEBI:40961, CHEBI:5589, CHEBI:13363
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eMolecules:5747851 |
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In inorganic chemistry, bicarbonate (IUPAC-recommended nomenclature: hydrogencarbonate) is an intermediate form in the deprotonation of carbonic acid. It is a polyatomic anion with the chemical formula HCO−3.
Bicarbonate serves a crucial biochemical role in the physiological pH buffering system.
The term "bicarbonate" was coined in 1814 by the English chemist William Hyde Wollaston. The name lives on as a trivial name. |
Read full article at Wikipedia
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InChI=1S/CH2O3/c2-1(3)4/h(H2,2,3,4)/p-1 |
BVKZGUZCCUSVTD-UHFFFAOYSA-M |
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Mus musculus
(NCBI:txid10090)
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Source: BioModels - MODEL1507180067
See:
PubMed
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Saccharomyces cerevisiae
(NCBI:txid4932)
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Source: yeast.sf.net
See:
PubMed
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Escherichia coli
(NCBI:txid562)
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See:
PubMed
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Homo sapiens
(NCBI:txid9606)
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See:
DOI
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Escherichia coli metabolite
Any bacterial metabolite produced during a metabolic reaction in Escherichia coli.
Saccharomyces cerevisiae metabolite
Any fungal metabolite produced during a metabolic reaction in Baker's yeast (Saccharomyces cerevisiae ).
human metabolite
Any mammalian metabolite produced during a metabolic reaction in humans (Homo sapiens).
mouse metabolite
Any mammalian metabolite produced during a metabolic reaction in a mouse (Mus musculus).
cofactor
An organic molecule or ion (usually a metal ion) that is required by an enzyme for its activity. It may be attached either loosely (coenzyme) or tightly (prosthetic group).
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View more via ChEBI Ontology
hydrogen(trioxidocarbonate)(1−)
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hydrogencarbonate
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hydrogencarbonate(1−)
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hydrogentrioxocarbonate(1−)
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hydrogentrioxocarbonate(IV)
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hydroxidodioxidocarbonate(1−)
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[CO2(OH)]−
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IUPAC
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Acid carbonate
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KEGG COMPOUND
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Bicarbonate
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KEGG COMPOUND
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BICARBONATE ION
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PDBeChem
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HCO3−
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IUPAC
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HCO3-
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KEGG COMPOUND
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hydrogen carbonate
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PDBeChem
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Hydrogencarbonate
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KEGG COMPOUND
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hydrogencarbonate
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UniProt
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3903504
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Beilstein Registry Number
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Beilstein
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49249
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Gmelin Registry Number
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Gmelin
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71-52-3
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CAS Registry Number
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ChemIDplus
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Schiemsky T, Brandt I (2018) Bicarbonate interference on cobas 6000 c501 chloride ion-selective electrodes. Clinical chemistry and laboratory medicine 56, e214-e215 [PubMed:29466234] | Zhang Y, Li J, Liu F, Yan H, Li J (2018) Mediative mechanism of bicarbonate on anaerobic propionate degradation revealed by microbial community and thermodynamics. Environmental science and pollution research international 25, 12434-12443 [PubMed:29460248] [show Abstract] Syntrophic acetogenesis of volatile fatty acids (VFAs) such as propionate and butyrate is considered as the rate-limiting step of anaerobic digestion. Though being extensively researched, the mechanism is not well understood as the main constraint on developing effective solutions to the practical problem. In the present research work, the mediation of methanogenic propionate degradation by exogenous bicarbonate was evaluated, while the mechanism was revealed by microbial community and thermodynamics. It was found that the exogenous bicarbonate not more than 0.10 mol/L acted as a mediative role to enrich syntrophic acetogenic bacteria and decrease the actual Gibbs free energy change (ΔG) of syntrophic acetogenesis reaction, resulted in the increased degradation rate and methane production rate of propionate. The remarkably increased ΔG of methanogenic propionate degradation by the exogenous bicarbonate more than 0.15 mol/L decreased the degradation rate and methane production rate of propionate, though the ΔG of syntrophic acetogenesis reaction was also decreased by the exogenous bicarbonate. This research work provided a control strategy to enhance syntrophic acetogenesis, as well as the methanogenic VFAs degradation. | Beaume J, Braconnier A, Dolley-Hitze T, Bertocchio JP (2018) [Bicarbonate: From physiology to treatment for all clinicians]. Nephrologie & therapeutique 14, 13-23 [PubMed:29150416] [show Abstract] Acid-base regulation is essential to maintain homeostasis in humans. Carbonic acid/bicarbonate (H2CO3/HCO3-) couple is the most predominant extracellular buffer to keep plasma pH within a physiological range. The ability to (re)generate such a buffer is a key milestone that necessitates to understand a precise physiology of both renal tubule and digestive tract. Here, we first reviewed renal and digestive cycles of bicarbonate in physiology. We also reviewed pathological findings where acid-base disequilibrium is involved and nutritional and/or alkali therapy could be necessary. Secondly, data from clinical trials were synthesized. Alkali therapy, oral and parenteral, from mineral-based water, masterful preparations or pharmaceutics drugs, is regularly used in a wide range of clinical findings, even if supporting data are (often) of a low level of evidence. Bicarbonate is primarily used during contrast-induced nephropathy, metabolic acidosis in chronic kidney disease or nephrolithiasis in which alkaline urine is necessary. Cast nephropathy, rhabdomyolysis and tumor lysis syndrome make usually physicians prescribe alkali therapy even if this prescription is only supported by physiopathological data without any proven clinical results. Finally, bicarbonate is essential in the composition of dialysate in both hemodialysis and peritoneal dialysis. | Kunzelmann K, Schreiber R, Hadorn HB (2017) Bicarbonate in cystic fibrosis. Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society 16, 653-662 [PubMed:28732801] [show Abstract]
BackgroundCystic fibrosis (CF, mucoviscidosis) is caused by mutations in the gene encoding CF transmembrane conductance regulator (CFTR), which is a chloride and bicarbonate channel necessary for fluid secretion and extracellular alkalization. For a long time, research concentrated on abnormal Cl- and Na+ transport, but neglected bicarbonate as a crucial factor in CF.MethodsThe present short review reports early findings as well as recent insights into the role of CFTR for bicarbonate transport and its defects in CF.ResultsThe available data indicate impaired bicarbonate transport not only in pancreas, intestine, airways, and reproductive organs, but also in salivary glands, sweat duct and renal tubular epithelial cells. Defective bicarbonate transport is closely related to the impaired mucus properties and mucus blocking in secretory organs of CF patients, causing the life threatening lung disease.ConclusionsApart from the devastating lung disease, abrogated bicarbonate transport also leads to many other organ dysfunctions, which are outlined in the present review. | Shevela D, Su JH, Klimov V, Messinger J (2008) Hydrogencarbonate is not a tightly bound constituent of the water-oxidizing complex in photosystem II. Biochimica et biophysica acta 1777, 532-539 [PubMed:18439416] [show Abstract] Since the end of the 1950s hydrogencarbonate ('bicarbonate') is discussed as a possible cofactor of photosynthetic water-splitting, and in a recent X-ray crystallography model of photosystem II (PSII) it was displayed as a ligand of the Mn(4)O(x)Ca cluster. Employing membrane-inlet mass spectrometry (MIMS) and isotope labelling we confirm the release of less than one (~0.3) HCO(3)(-) per PSII upon addition of formate. The same amount of HCO(3)(-) release is observed upon formate addition to Mn-depleted PSII samples. This suggests that formate does not replace HCO(3)(-) from the donor side, but only from the non-heme iron at the acceptor side of PSII. The absence of a firmly bound HCO(3)(-) is corroborated by showing that a reductive destruction of the Mn(4)O(x)Ca cluster inside the MIMS cell by NH(2)OH addition does not lead to any CO(2)/HCO(3)(-) release. We note that even after an essentially complete HCO(3)(-)/CO(2) removal from the sample medium by extensive degassing in the MIMS cell the PSII samples retain > or =75% of their initial flash-induced O(2)-evolving capacity. We therefore conclude that HCO(3)(-) has only 'indirect' effects on water-splitting in PSII, possibly by being part of a proton relay network and/or by participating in assembly and stabilization of the water-oxidizing complex. | Medinas DB, Cerchiaro G, Trindade DF, Augusto O (2007) The carbonate radical and related oxidants derived from bicarbonate buffer. IUBMB life 59, 255-262 [PubMed:17505962] [show Abstract] The unequivocal demonstration that the carbonate radical (CO(3) (.-)) is produced from the reaction between the ubiquitous carbon dioxide and peroxynitrite, renewed the interest in the pathogenic roles of oxidants derived from the main physiological buffer, the bicarbonate-carbon dioxide pair. Here, we review the biochemical properties of both the carbonate radical and peroxymonocarbonate (HCO(4) (-)), and discuss the evidence of their formation under physiological conditions. Overall, the review emphasizes the recognition of the biological relevance of oxidants derived from the main physiological buffer as a crucial step into the understanding and control of numerous pathological states. | Casey JR (2006) Why bicarbonate? Biochemistry and cell biology = Biochimie et biologie cellulaire 84, 930-939 [PubMed:17215880] [show Abstract] Bicarbonate is a simple single carbon molecule that plays surprisingly important roles in diverse biological processes. Among these are photosynthesis, the Krebs cycle, whole-body and cellular pH regulation, and volume regulation. Since bicarbonate is charged it is not permeable to lipid bilayers. Mammalian membranes thus contain bicarbonate transport proteins to facilitate the specific transmembrane movement of HCO3(-). This review provides a wide-ranging view of the biochemistry of bicarbonate and its membrane transporters, revealing what makes the study of bicarbonate transport such a rewarding activity. | Assal JP, Aoki TT, Manzano FM, Kozak GP (1974) Metabolic effects of sodium bicarbonate in management of diabetic ketoacidosis. Diabetes 23, 405-411 [PubMed:4208463] |
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