Influence of dietary n-3 fatty acids on the desaturation and elongation of [1-14C] 18:2 n-6 and [1-14C] 18:3 n-3 in Atlantic salmon hepatocytes

Atlantic salmon (Salmo salar) were fed diets containing fish oil supplemented with 22:6n-3 (FO diet) or linseed oil supplemented with 20:5n-3 (LO diet) for 61/2 months. The effects of these diets, both containing about 36% n-3 fatty acids, on the esterification, desaturation and elongation of [1-C-14] 18:2n-6 and [1-C-14] 18:3n-3 were investigated in isolated hepatocytes. The percentages of radioactivity which was esterified from [1-C-14] 18:2n-6 or [1-C-14]18:3n-3 into total lipids, were approximately 20% lower in hepatocytes from fish fed the FO diet than in hepatocytes from fish fed the LO diet. The percentages of radioactivity esterified in both groups were further reduced when 0.1 mM unlabelled 22:6n-3 was added to the incubation. The percentage of desaturation and elongation products formed from [1-C-14] 18:2n-6 was twice as high in hepatocytes from salmon fed the FO diet as it was in hepatocytes from fish fed the LO diet. The ratio of 18:2n-6 to 18:3n-3 was five times higher in the FO diet, and this probably promoted the conversion of 18:2n-6 to longer chain n-6 fatty acids. When 0.1mM unlabelled 22:6n-3 was added to the incubation medium, the percentages of desaturation and elongation products formed were unchanged. Thus, a high level of 22:6n-3 in the diet is apparently not inhibiting the conversion of 18:2n-6 to 20:4n-6, as long as the amount of 18:2n-6 present is substantially higher than that of 18:3n-3. No desaturation and elongation products were recovered from the phospholipids of hepatocytes incubated with [1-C-14] 18:3n-3 in any of the groups. However, the `dead end' elongation product 20:3n-3 was found in the triacylglycerol fraction, and the percentage of this fatty acid increased when 22:6n-3 was added to the incubation medium.