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Arachidonic acid peroxidation in inflammation and its inhibition as a mechanism for anti-inflammatory activity

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Part of the book series: Inflammation: Mechanisms and Treatment ((FTIN,volume 4))

Abstract

It is 10 years since arachidonic acid metabolism was first associated with the development of the inflammatory response. The detection of prostaglandin release in experimental inflammation1 and anaphylaxis2 initiated a series of experiments in which arachidonic acid peroxidation was demonstrated in numerous inflammatory conditions in animals and man. In parallel with these studies, prostaglandins were shown to have potent inflammatory properties. It is now generally accepted that prostaglandins, along with vasoactive amines and kinins are the most likely chemical mediators of vascular responses in acute and chronic inflammation3. An important stimulus to this area of research came with the discovery that aspirin and other non-steroid anti-inflammatory drugs selectively inhibit prostaglandin symthesis4–6. This led Vane to propose his now famous theory that inhibition of prostaglandin biosynthesis explains the therapeutic and toxic effects of aspirin-like drugs4. The other major group of anti-inflammatory drugs, the coricosteroids, do not have a direct effect on arachidonate metabolizing enzymes but they are thought to interfere with the release of fatty acids from phospholipids7-10. The role of prostaglandins in inflammation and the effects of prostaglandin synthetase inhibitors have been comprehensively reviewed by Ferreira and Vane11.

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Higgs, G., Eakins, K. (1980). Arachidonic acid peroxidation in inflammation and its inhibition as a mechanism for anti-inflammatory activity. In: Willoughby, D.A., Giroud, J.P. (eds) Inflammation: Mechanisms and Treatment. Inflammation: Mechanisms and Treatment, vol 4. Springer, Dordrecht. https://doi.org/10.1007/978-94-010-9423-8_11

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