Search

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 6 $$\frac{1}{2}$$ months. The effects of these diets, both containing about 36% n-3 fatty acids, on the esterification, desaturation and elongation of [1-14C] 18:2n-6 and [1-14C] 18:3n-3 were investigated in isolated hepatocytes. The percentages of radioactivity which was esterified from [1-14C] 18:2n-6 or [1-14C]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 [1-14C] 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 [1-14C] 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.

The time of appearance in blood, and transport of astaxanthin, and catabolic transformation of astaxanthin to idoxanthin were investigated in Atlantic salmon (Salmo salar) that had been force-fed a single dose of 14C-astaxanthin. In addition to the LPs, a major protein, associated with radiolabeled astaxanthin was detected. The maximum level of radiolabeled carotenoids in blood was attained 30 h after administration of 14C-astaxanthin. Radioactive idoxanthin (combined 3′,4′-cisand 3′,4′- transglycolic isomers of idoxanthin) appeared after 6 h and a stable level was obtained after 18 h. LPDP and LP, separated by ultracentrifugation, contained on average 89 and 11% of the total radioactivity in plasma, respectively. During the 168 h experiment, maximum radioactivity in LP appeared after 22 h. Separation of plasma by ultracentrifugation on a discontinuous NaCl/KBr-gradient and an iodixanol-gradient confirmed that most of the radiolabeled carotenoids were present in the HDPF that did not contain LPs (58%), whereas HDL and LDL contained 36 and 6% of the radioactivity, respectively. Of the recovered radioactivity, astaxanthin in the HDPF comprised 82%, idoxanthin 5% and unidentified compounds 12%, whereas HDL contained 78% astaxanthin, 22% idoxanthin and no unidentified compounds. Proteins from the fractions with the high density and high radioactivity (iodixanol-gradient) were separated by PAGE under non-denaturing conditions and showed a radioactive band with parallel migration length to BSA and salmon albumin. These results show that astaxanthin is rapidly converted to idoxanthin and that the majority of astaxanthin in the plasma is associated with a protein other than LPs, presumably albumin. The identity of this protein requires verification.

The subcellular localization of dihydroxyacetone phosphate acyltransferase (DHAPAT) activity in rat small intestine was investigated by Nycodenz-gradient centrifugation. We found that DHAPAT had a predominant peroxisomal distribution, with a separate enzyme activity located in the microsomal fraction, the same distribution as found in rat liver. The effect of feeding rats on a diet with 20% (w/w) partially hydrogenated fish oil (PHFO) or 0.3% clofibrate on the activity of DHAPAT in rat small intestine and liver was studied. Both 20% PHFO and 0.3% clofibrate gave a 1.8-fold stimulation of the specific activities of DHAPAT in peroxisomes of the small intestine, whereas in the liver 20% PHFO gave a 1.4-fold stimulation and 0.3% clofibrate a 1.6-fold stimulation of the total DHAPAT activities in the postnuclear supernatant. The specific activities of DHAPAT in liver were not affected.