Effects of essential fatty acid-deficient diets on growth, mortality, tissue histopathology and fatty acid compositions in juvenile turbot (Scophthalmus maximus)

Abstract

Three diets in which the lipid component was supplied either as fish oil (FO), linseed oil (LO) or olive oil (OO) were fed to duplicate groups of juvenile turbot (Scophthalmus maximus) of initial weight 1.2 g for a period of up to 12 weeks. The latter two diets resulted in a significant reduction in specific growth rate and an increased mortality compared to the FO (control) fed fish. A liver histopathology was evident in around half of the fish fed the LO and OO diets but was absent in fish fed FO. The lesion showed indications of cellular alterations consisting of foci of densely basophilic cells but without evidence of inflammatory activity. The total lipid fatty acid composition of the carcass from fish fed LO had increased percentages of 18:2n-6 and 18:3n-3, but decreased percentages of all other polyunsaturated fatty acids (PUFA) including the physiologically important 20:4n-6, 20:5n-3 and 22:6n-3, compared to fish fed FO. Almost 2/3 of the total fatty acids in the carcass of OO-fed fish were monounsaturated while the percentages of total saturated fatty acids and all other PUFA, except 18:2n-6, were significantly reduced compared to fish fed FO. Broadly similar effects on total lipid fatty acid composition were observed in liver. In the liver glycerophospholipid classes of fish fed LO, percentages of 18:2n-6, 18:3n-3 and 20:3n-3 were significantly increased whereas all C20 and C22 PUFA, with the exception of 20:5n-3 in PI, were significantly reduced compared to fish fed FO. The liver glycerophospholipids of fish fed OO all showed significantly increased total monounsaturates, 18:2n-6, 20:2n-6, 18:2n-9 and 20:2n-9 as well as reduced percentages of 20:4n-6 and 22:6n-3, compared to fish fed FO. The brain glycerophospholipids showed broadly similar changes in response to dietary treatment although the magnitude of fatty acid alterations was less than those observed in liver. The greater mortalities in the OO-fed fish compared to the LO-fed fish suggests that incorporation of 18:3n-3 into tissue phospholipids can offset losses of long-chain PUFA more effectively than incorporation of 18:1n-9. However, levels of dietary long-chain PUFA must be optimised to allow normal growth and development. We conclude that the very low flux through the fatty acid desaturase/elongase pathways in turbot is not up-regulated by diets deficient in 20:5n-3 and 22:6n-3.