Interaction of (n−3) and (n−6) fatty acids in desaturation and chain elongation of essential fatty acids in cultured glioma cells

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Abstract
Recent research in various biological systems has revived interest in interactions between the (n−6) and (n−3) essential fatty acids. We have utilized cultured glioma cells to show that linolenic acid, 18∶3(n−3), is rapidly desaturated and chain elongated; 20∶5(n−3) is the major product and accumulates almost exclusively in phospholipids. We examined effects of various (n−6), (n−3), (n−9) and (n−7) fatty acids at 40 μM concentration on desaturation and chain elongation processes using [1-14C]18∶3(n−3) as substrate. In general, monoenoic fatty acids were without effect. The (n−6) fatty acids (18∶2, 18∶3, 20∶3, 20∶4 and 22∶4) had little effect on total product formed. There was a shift of labeled product to triacylglycerol, and in phospholipids, slightly enhanced conversion of 20∶5 to 22∶5 was evident. In contrast, 22∶6(n−3) was inhibitory, whereas 20∶3(n−3) and 20∶5(n−3) had much less effect. At concentrations <75 μM, all acids were inhibitory. Most products were esterified to phosphatidylcholine, but phosphatidylethanolamine also contained a major portion of 20∶5 and 22∶5. We provide a condensed overview of how the (n−6) and (n−3) fatty acids interact to modify relative rates of desaturation and chain elongation, depending on the essential fatty acid precursor. Thus, the balance between these dietary acids can markedly influence enzymes providing crucial membrane components and substrates for biologically active oxygenated derivatives.

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