Abstract
The biological transformation of arachidonic acid (AA) leads to a wide array of physiologically active products which are involved in several aspects of the inflammatory process. Depending upon various factors, including its anatomical location, arachidonic acid undergoes biotransformation by the membrane-bound enzyme cyclo-oxygenase and by cytoplasmic lipoxygenase enzymes. The capacities of the prostaglandins PGE2 and PGD2 and of prosta- cyclin (PGI2)--all derived via the cyclo-oxygenase pathway--to enhance the vascular-exudative com- ponent of inflammation have been most extensively studied. Furthermore, substances such as the hydroxy acid 12-HETE and particularly the recently discovered leukotrienes--all generated via the lipoxygenase pathways--are markedly chemotactic and contribute to cellular infiltration during inflam- mation. Thus, the majority of established concepts of inflammation emphasize these and other metabolites of AA as proinflammatory substances. The fact that inhibitors of cyclo-oxygenase are powerful anti- inflammatory agents is also telling evidence in favour of the above view, which has gained additional momentum from more recent observations, suggest- ing that similar anti-inflammatory drugs may also counteract the formation of at least some lipoxy- genase products (Atkinson & Collier, 1980). Never- theless, the view that the inflammatory process is exclusively promoted by metabolites of AA is over- simplified. Evidence is accumulating that, depending on the experimental situation that is studied, PGE2 displays either pro- or anti-inflammatory effects (Morley, 1979; Bonta & Parnham, 1978, 1980). While such a dual function has not been convincingly shown for other products of AA-bioconversion, the bis-homo-gamma-linoleic acid derived PGEI does share this property with PGE2 (Kunkel, Thrall, Kunkel, McCormick, Ward & Zurier, 1979; Bonta & Parnham, 1978, 1980). AA and bis-homo-gamma- linoleic acid are essential fatty acids (EFA) and EFAs
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