Fumarylacetoacetic acid

Fumarylacetoacetic acid
Names
Preferred IUPAC name
(2E)-4,6-Dioxooct-2-enedioic acid
Identifiers
3D model (JSmol)
ChemSpider
MeSH Fumarylacetoacetate
UNII
  • InChI=1S/C8H8O6/c9-5(1-2-7(11)12)3-6(10)4-8(13)14/h1-2H,3-4H2,(H,11,12)(H,13,14)/b2-1+
    Key: GACSIVHAIFQKTC-OWOJBTEDSA-N
  • O=C(\C=C\C(=O)O)CC(=O)CC(=O)O
Properties
C8H8O6
Molar mass 200.146 g·mol−1
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
Infobox references

Fumarylacetoacetic acid (fumarylacetoacetate) is an intermediate in the metabolism of tyrosine. It is formed through the conversion of 4-maleylacetoacetic acid into fumarylacetoacetic acid by the enzyme maleylacetoacetate isomerase. Fumarylacetoacetic acid is hydrolyzed by the enzyme fumarylacetoacetate hydrolase (FAH), producing acetoacetate and fumarate.[1] These compounds may then enter various other metabolic pathways.

Biosynthesis

The amino acid tyrosine is metabolised in a series of reactions, one of which is catalysed by homogentisate 1,2-dioxygenase. This converts the intermediate homogentisic acid into 4-maleylacetoacetic acid.[2][3]

The enzyme maleylacetoacetate isomerase subsequently converts 4-maleylacetoacetic acid to its geometric isomer, fumarylacetoacetic acid.[4]

Metabolism

The enzyme fumarylacetoacetate hydrolase (FAH) cleaves fumarylacetoacetic acid at its carbon-carbon bond during a hydrolysis reaction.[5] This is the final step in phenylalanine and tyrosine metabolism, yielding fumaric acid and acetoacetic acid. These hydrolytic reactions are essential during aromatic amino acid metabolism in humans.[6]

 
H2O
 
 
 
 
+
 

Clinical significance

Fumarylacetoacetate may accumulate in patients with Tyrosinemia type I, in which there is a deficiency of the FAH enzyme.[7] In this disease, fumarylacetoacetate and precursors in the catabolism of tyrosine, including maleylacetoacetic acid, succinylacetone, and homogentisic acid.

References

  1. ^ Bateman, Raynard L.; Bhanumoorthy, P.; Witte, John F.; McClard, Ronald W.; Grompe, Markus; Timm, David E. (2001-01-01). "Mechanistic Inferences from the Crystal Structure of Fumarylacetoacetate Hydrolase with a Bound Phosphorus-based Inhibitor *". Journal of Biological Chemistry. 276 (18): 15284–15291. doi:10.1074/jbc.M007621200. ISSN 0021-9258. PMID 11154690.
  2. ^ Borowski, Tomasz; Georgiev, Valentin; Siegbahn, Per E. M. (2005). "Catalytic Reaction Mechanism of Homogentisate Dioxygenase: A Hybrid DFT Study". Journal of the American Chemical Society. 127 (49): 17303–17314. doi:10.1021/ja054433j. PMID 16332080.
  3. ^ Timm, David E.; Titus, Greg P.; Mueller, Heather A.; Burgner, John; Rodríguez De Córdoba, Santiago; Peñalva, Miguel A. (2000). "Crystal structure of human homogentisate dioxygenase". Nature Structural Biology. 7 (7): 542–546. doi:10.1038/76756. PMID 10876237.
  4. ^ Polekhina, Galina; Board, Philip G.; Blackburn, Anneke C.; Parker, Michael W. (2001). "Crystal Structure of Maleylacetoacetate Isomerase/Glutathione Transferase Zeta Reveals the Molecular Basis for Its Remarkable Catalytic Promiscuity". Biochemistry. 40 (6): 1567–1576. doi:10.1021/bi002249z. PMID 11327815.
  5. ^ Timm DE, Mueller HA, Bhanumoorthy P, Harp JM, Bunick GJ (September 1999). "Crystal structure and mechanism of a carbon-carbon bond hydrolase". Structure. 7 (9): 1023–1033. doi:10.1016/s0969-2126(99)80170-1. PMID 10508789.
  6. ^ Universal protein resource accession number P16930 for "FAH - Fumarylacetoacetase - Homo sapiens (Human) - FAH gene & protein" at UniProt.
  7. ^ Chakrapani A, Holme E (2006). "Disorders of Tyrosine Metabolism". In Fernandes J, Saudubray JM, van den Berghe G, Walter JH (eds.). Inborn Metabolic Diseases. Springer. pp. 233–243. doi:10.1007/978-3-540-28785-8_18. ISBN 978-3-540-28785-8. PMC 1986449.