These facts suggest that modification of eicosanoid synthesis could have beneficial effects. Three methods exist to modify the prostaglandin milieu: blockage of prostaglandin synthesis globally with nonsteroidal anti-inflammatory drugs; exogenous administration of prostacyclins or their analogues; and use of alternative lipid to alter the arachido-nate-derived metabolites.
The latter approach entails the use of lipids high in o>-3 PUFAs, either from plant oils containing a-linolenic acid (18:3o>3), such as linseed oil, or from marine fish oils containing eicosapentaenoic acid (20:5o>3) and docosahexae-noic (22:6<*)3) acid. The o>-3 PUFAs are known to inhibit the metabolism of the <0-6 PUFAs through their competition for desaturase, an early step in eicosanoid synthesis, thereby lowering the formation of the 2-series prostaglandins and the 4-series leukotrienes. At the same time, fish oil yields the alternative 3-series prostaglandins and 5-series leukotrienes, which exhibit a dramatically different spectrum of activity.’17 TXA3 has an attenuated vasodepressor effect and will not aggregate platelets,18 and LTBS is much less chem-otactic than LTB4.10 In contrast, PCI3 produced from fish oils has all the vasodilating and antiaggregatory effects of PGI,. Hence, the net effect of fish oil is to shift the balance of actions of the eicosanoids toward the vasodilated state.
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