Levuglandin

Levuglandin D2
IUPAC name

(5Z,8R,9R,10E,12S)-9-acetyl-8-formyl-12- hydroxyheptadeca-5,10-dienoic acid
Identifiers
CAS number 91712-44-6 Y
PubChem 9548876
KEGG C13808 Y
Jmol-3D images Image 1
Properties
Molecular formula C20H32O5
Molar mass 352.465 g/mol
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Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa)
Infobox references
Levuglandin E2
IUPAC name

(5Z,8R,9R,10E,12S)-8-acetyl-9-formyl-12- hydroxyheptadeca-5,10-dienoic acid
Other names

LGE2
Identifiers
CAS number 91712-41-3
PubChem 5771742
KEGG C13807
Jmol-3D images Image 1
Properties
Molecular formula C20H32O5
Molar mass 352.465 g/mol
Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa)
Infobox references

Levuglandins are reactive aldehydes formed by the spontaneous rearrangement of prostaglandin H (PGH). Enantiomerically pure levuglandin (LG) E2 can also be formed through the cyclooxygenase (COX) pathway by a rearrangement of the prostaglandin (PG) endoperoxide PGH 2.[1] They are nonclassic eicosanoids. One species, levuglandin E2, (LGE2), forms neurotoxic adducts with amyloid beta.[2] Levuglandins and isolevuglandins can damage proteins by covalent adduction, thereby interfering with their normal functions. These lipid-derived protein modifications may serve as dosimeters of oxidative injury. Elevated plasma levels of isoLG-protein epitopes are associated with atherosclerosis but are independent of total cholesterol, a classical risk factor.

History

Though spontaneous rearrangements of PGH2 are known to generate prostaglandins (PG) PGD2 and PGE2.[3][4] Prof. Robert Salomon at Case Western Reserve University discovered that a novel alternative rearrangement also occurs that producing two γ-ketoaldehydes[5] and named them levuglandins LGD2 and LGE2 as they are derivatives of levulinaldehyde with prostanoid side chains.

References

  1. ^ Salomon RG (2005). "Isolevuglandins, oxidatively truncated phospholipids, and atherosclerosis". Ann. N. Y. Acad. Sci. 1043: 327–42. doi:10.1196/annals.1333.040. PMID 16037255. http://www.annalsnyas.org/cgi/pmidlookup?view=long&pmid=16037255. Retrieved 2008-01-16. 
  2. ^ Bautaud et al.; Brame, CJ; Salomon, RG; Roberts Lj, 2nd; Oates, JA (1999). "PGH -derived levuglandin adducts increase the neurotoxicity of Amyloid Β1–42" (pdf). Biochemistry 38 (29): 9389–9396. doi:10.1021/bi990470. PMID 10413514. http://www.blackwell-synergy.com/doi/pdf/10.1111/j.1471-4159.2005.03586.x. Retrieved 2007-10-02. 
  3. ^ M. Hamberg and B. Samuelsson, Detection and isolation of an endoperoxide intermediate in prostaglandin biosynthesis, Proc. Natl. Acad. Sci. U.S.A. 70 (1973), pp. 899–903.
  4. ^ D.H. Nugteren and E. Hazelhof, Isolation and properties of intermediates in prostaglandin biosynthesis, Biochim. Biophys. Acta 326 (1973) (3), pp. 448–461.
  5. ^ R.G. Salomon, D.B. Miller, M.G. Zagorski and D.J. Coughlin, Prostaglandin endoperoxides. 14. Solvent-induced fragmentation of prostaglandin endoperoxides. New aldehyde products from PGH2 and a novel intramolecular 1*2-hydride shift during endoperoxide fragmentation in aqueous solution, J. Am. Chem. Soc. 106 (1984) (20), pp. 6049–6060.