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Prostaglandins, Arachidonic Acid, and Inflammation

1980/11/28 by Frederick A. Kuehl, Robert W. Egan · 2 citations
Medicine · Biochemistry, Genetics and Molecular Biology · Chemistry · #Inflammatory mediators and NSAID effects #Eicosanoids and Hypertension Pharmacology #Estrogen and related hormone effects #Arachidonic acid #Inflammation #Chemistry #Internal medicine #Biochemistry #Medicine

paper · doi:10.1126/science.6254151

openalex publication_date 1980/11/28 · openalex created_date 2025/10/10 · openalex updated_date 2026/07/23

Abstract

The enzymatic oxidation of arachidonic acid has been shown to yield potent pathological agents by two major pathways. Those of the prostaglandin (PG) pathway, particularly PGE2, have been implicated as inflammatory mediators for many years. The discovery and biological activities of thromboxane A2 and prostacyclin as well as a destructive oxygen-centered radical as additional products of this biosynthetic pathway now require these to be considered as potential inflammatory mediators. Like PGE2, their biosynthesis is prevented by nonsteroidal anti-inflammatory agents. More recently, the alternative metabolic route, the lipoxygenase pathway, has been shown to yield a new class of arachidonic acid oxygenation products, called the leukotrienes, which also appear to be important inflammatory mediators. Unlike the prostaglandins, some of which play important roles as biological regulators, the actions of the lipoxygenase products appear to be exclusively of a pathological nature.

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