To study whether Atlantic salmon beta-oxidation was affected by dietary FA composition, an in vitro study with primary hepatocytes was undertaken. Isolated hepatocyte cultures were stimulated with either 16:0, 18:1n-9, 18:2n-6, 18:3n-3, 20:5n-3, or 22:6n-3 in triplicate for 24 h. In addition, a control was included where no FA stimulation was performed, also in triplicate. After stimulation, radiolabeled [1-14C] 18:3n-3 was added and the cells were incubated for 2 h at 20 degrees C. The cells were then harvested, and radioactivity was determined in the acid-soluble part of the cells and medium, i.e., the end products of the beta-oxidation pathway. Specific beta-oxidation activity was significantly higher in hepatocytes stimulated with 18:3n-3. Further, when taking into account the amount of radiolabeled [1-14C]18:3n-3 taken up by the cells--the relative amount of beta-oxidized [1-14C]18:3n-3 of the total FA taken up by the hepatocytes-no significant differences were found. Thus, the regulation of beta-oxidation activity in the primary Atlantic salmon hepatocytes seems to be at the level of FA uptake and transport into the cell. This in vitro study shows that the catabolism processes in salmon hepatocytes are affected by the FA available and probably already regulated at the level of FA uptake.