Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2001 Jun;107(12):1481-9.
doi: 10.1172/JCI13375.

Unorthodox routes to prostanoid formation: new twists in cyclooxygenase-initiated pathways

C N Serhan  1 , E Oliw
Affiliations
Review

Unorthodox routes to prostanoid formation: new twists in cyclooxygenase-initiated pathways

C N Serhan et al. J Clin Invest. 2001 Jun.
No abstract available

PubMed Disclaimer

Figures

Figure 1
Figure 1
Cyclooxygenase reactions and products: prostaglandins and the impact of aspirin. Conversion of arachidonic acid to bioactive products involves stereoselective insertion of oxygen governed by COX (see text for details). Aspirin blocks formation of PGs from COX-1 and -2. In addition, with COX-2, aspirin triggers the formation of bioactive aspirin-triggered lipid mediators.
Figure 2
Figure 2
Biosynthesis of 19R-hydroxy-PGE from PGH2 by CYP4F8 and PGE synthases. 19R-hydroxy-PGE is a major eicosanoid in humans. This novel biosynthesis route indicates that the 19 position R alcohol is in place before the PGE2 ring is made (see text).
Figure 3
Figure 3
Aspirin-triggered lipid mediators: biosynthesis of 15-epi-LXs. Irreversible acetylation of COX-2 by aspirin changes the enzyme’s product from PGs intermediate to precursors of ATLMs. The acetylated COX-2 remains catalytically active (see text).
Figure 4
Figure 4
Functional arrays of lipid signals generated via transcellular processing ω-3 PUFA: endogenous inhibitors of microinflammation. At sites where COX-2 is expressed and treated with NSAIDs, although PG formation is blocked, systemic ω-3 PUFA can be converted via a COX-2-NSAID–dependent LO-type mechanism (stereospecific hydrogen abstraction at C16 or C13 in C20:5 to give R insertions of molecular O2) to yield 15R-H(p)EPE or 18R-H(p)EPE. These compounds are reduced to alcohols and converted to epoxide intermediates. Elucidation of the complete stereochemistry of the trihydroxy-compounds is in progress, and they are depicted in their likely configuration. The products interact with cells in the local microenvironment, inhibiting PMN recruitment. See text and suggested reading list (http://www.jci.org/cgi/content/full/107/12/1481/DC1) for details.
See this image and copyright information in PMC

References

    1. von Euler US. On the specific vaso-dilating and plain muscle stimulating substances from accessory genital glands in man and certain animals (prostaglandin and vesiglandin) J Physiol. 1936;88:213–234. - PMC - PubMed
    1. Clària J, Serhan CN. Aspirin triggers previously undescribed bioactive eicosanoids by human endothelial cell-leukocyte interactions. Proc Natl Acad Sci USA. 1995;92:9475–9479. - PMC - PubMed
    1. Serhan CN, et al. Novel functional arrays of lipid-derived mediators with antiinflammatory actions generated from omega-3 fatty acids via cyclooxygenase 2-nonsteroidal antiinflammatory drugs and transcellular processing. J Exp Med. 2000;192:1197–1204. - PMC - PubMed
    1. Bylund J, Hidestrand M, Ingelman-Sundberg M, Oliw EH. Identification of CYP4F8 in human seminal vesicles as a prominent 19- hydroxylase of prostaglandin endoperoxides. J Biol Chem. 2000;275:21844–21849. - PubMed
    1. Bergström, S. 1982. The prostaglandins: from the laboratory to the clinic. In Les prix nobel: Nobel prizes, presentations, biographies and lectures. Edited by The Nobel Foundation. Almqvist & Wiksell. Stockholm, Sweden. 129–148.

Publication types

MeSH terms