Decreased formation of porstaglandins derived from arachidonic acid by dietary linolenate in rats.

Accumulated evidence now suggests that availability of precursor acid is an important factor controlling the biosynthesis of prostaglandins (PG's). Since linolenic acid inhibits the conversion of linoleic acid to arachidonic acid (PGE2, PGF2 alpha, and thromboxane A2 precursor), rats receiving more linolenic acid are expected to have less arachidonic acid and thus less PG's synthesized from arachidonic acid than those receiving linoleic acid alone. Essential fatty acid-deficient rats, induced by feeding hydrogenated coconut oil diet for 15 weeks, were divided into six groups and fed graded amounts of purified methyl linolenate for 6 weeks. Each group of rats except essential fatty acid-deficient group received the same amount of linoleate. The results showed that the level of arachidonic acid in serum lipids and serum concentrations of PG's synthesized from arachidonic acid by platelets decreased as the amount of dietary linolenate increased. This indicated that biosynthesis of PG's in platelets can be influenced by the availability of precursors, and thus it can be modified by the manipulation of dietary fatty acids.