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'''Levuglandins''' are reactive ]s formed by the spontaneous rearrangement of ] (PGH). Enantiomerically pure levuglandin (LG) E<sub>2</sub> can also be formed through the cyclooxygenase (COX) pathway by a rearrangement of the prostaglandin (PG) endoperoxide PGH <sub>2</sub>.<ref name="pmid16037255">{{cite journal |author=Salomon RG |title=Isolevuglandins, oxidatively truncated phospholipids, and atherosclerosis |journal=Ann. N. Y. Acad. Sci. |volume=1043 |pages=327–42 |year=2005 |pmid=16037255 |doi=10.1196/annals.1333.040|bibcode=2005NYASA1043..327S |s2cid=12782911 }}</ref> They are ]s. One species, levuglandin E<sub>2</sub>, (LGE<sub>2</sub>), forms neurotoxic ]s with |
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'''Levuglandins''' are reactive ]s formed by the spontaneous rearrangement of ] (PGH). Enantiomerically pure levuglandin (LG) E<sub>2</sub> can also be formed through the cyclooxygenase (COX) pathway by a rearrangement of the prostaglandin (PG) endoperoxide PGH <sub>2</sub>.<ref name="pmid16037255">{{cite journal |author=Salomon RG |title=Isolevuglandins, oxidatively truncated phospholipids, and atherosclerosis |journal=Ann. N. Y. Acad. Sci. |volume=1043 |pages=327–42 |year=2005 |issue=1 |pmid=16037255 |doi=10.1196/annals.1333.040|bibcode=2005NYASA1043..327S |s2cid=12782911 }}</ref> They are ]s. One species, levuglandin E<sub>2</sub>, (LGE<sub>2</sub>), forms neurotoxic ]s with |
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|doi = 10.1111/j.1471-4159.2005.03586.x|title = PGH2-derived levuglandin adducts increase the neurotoxicity of amyloid beta1-42|year = 2006|last1 = Boutaud|first1 = Olivier|last2 = Montine|first2 = Thomas J.|last3 = Chang|first3 = Lei|last4 = Klein|first4 = William L.|last5 = Oates|first5 = John A.|journal = Journal of Neurochemistry|volume = 96|issue = 4|pages = 917–923|pmid = 16412101|pmc = 1621054}}</ref><ref>{{cite journal|doi=10.1021/bi990470+|pmid=10413514|year=1999|last1=Boutaud|first1=O.|last2=Brame|first2=C. J.|last3=Salomon|first3=R. G.|last4=Roberts Lj|first4=2nd|last5=Oates|first5=J. A.|title=Characterization of the lysyl adducts formed from prostaglandin H2 via the levuglandin pathway|journal=Biochemistry|volume=38|issue=29|pages=9389–96}}</ref> |
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|doi = 10.1111/j.1471-4159.2005.03586.x|title = PGH2-derived levuglandin adducts increase the neurotoxicity of amyloid beta1-42|year = 2006|last1 = Boutaud|first1 = Olivier|last2 = Montine|first2 = Thomas J.|last3 = Chang|first3 = Lei|last4 = Klein|first4 = William L.|last5 = Oates|first5 = John A.|journal = Journal of Neurochemistry|volume = 96|issue = 4|pages = 917–923|pmid = 16412101|pmc = 1621054}}</ref><ref>{{cite journal|doi=10.1021/bi990470+|pmid=10413514|year=1999|last1=Boutaud|first1=O.|last2=Brame|first2=C. J.|last3=Salomon|first3=R. G.|last4=Roberts Lj|first4=2nd|last5=Oates|first5=J. A.|title=Characterization of the lysyl adducts formed from prostaglandin H2 via the levuglandin pathway|journal=Biochemistry|volume=38|issue=29|pages=9389–96}}</ref> |
Though spontaneous rearrangements of PGH2 are known to generate prostaglandins (PG) PGD2 and PGE2. Prof. Robert Salomon at Case Western Reserve University discovered that a novel alternative rearrangement also occurs that producing two γ-ketoaldehydes and named them levuglandins LGD2 and LGE2 as they are derivatives of levulinaldehyde with prostanoid side chains.
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