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

摘要

Three diets in which the lipid component was supplied as fish oil (FO), linseed oil (LO) or olive oil (OO) were fed to duplicate groups of juvenile turbot, S. maximus, initial weight 1.2 g, for 12 weeks. Six tanks containing 60 fish each were used.The latter two diets resulted in a significant reduction in specific growth rate and increased mortality compared with the FO- (control) fed fish. Cellular alterations consisting of foci of densely basophilic cells without evidence of inflammatory activity were observed in a number of liver samples from fish fed on LO and OO diets but were absent in fish fed FO. 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 percentagesof all other polyunsaturated fatty acids (PUFA) including the physiologically important 20:4n-6, 20:5n-3 and 22:6n-3, compared with fish fed FO. Almost 2/3 of the total fatty acids in the carcass of OO-fed fish were monounsaturated while the percentagesof total saturated fatty acids and all other PUFA, except 18:2n-6, were significantly reduced compared with fish fed FO. Broadly similar effects on total lipid fatty acid composition were observed in the liver. In the liver glycerophospholipid classes offish 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 with fish fed FO. The liver glycerophospholipids of fish fed OOall 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 with fish fed FO. The brain glycerophospholipids showed broadly similar changes in response todietary treatment although the magnitude of fatty acid alterations was less than those observed in liver. The greater mortality in the OO-fed fish compared with 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. It is concluded 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.