Levuglandin

From Wikipedia, the free encyclopedia

Levuglandin D2
IUPAC name	(5Z,8R,9R,10E,12S)-9-acetyl-8-formyl-12- hydroxyheptadeca-5,10-dienoic acid
Identifiers
CAS number
PubChem	9548876
KEGG	C13808
SMILES	CCCCCC(C=CC(C(CC=CCCCC(=O)O)C=O)C(=O)C)O
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 disclaimer and 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
PubChem	5771742
KEGG	C13807
SMILES	CCCCCC(C=CC(C=O)C(CC=CCCCC(=O)O)C(=O)C)O
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 disclaimer and 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.

[edit] 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.

[edit] 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. 
2. ^ Bautaud et al (1999). "PGH -derived levuglandin adducts increase the neurotoxicity of Amyloid Β_1–42" (pdf). Biochemistry 38: 9389–9396. doi:10.1021/bi990470+. 
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.