Dietary n-3 long-chain polyunsaturated fatty acid deprivation, tissue lipid composition, ex vivo prostaglandin production, and stress tolerance in juvenile Dover sole (Solea solea L.).

Larval Dover sole fed an Artemia diet supplemented with n-3 long-chain (C20 + C22) polyunsaturated fatty acids (PUFA) are known to be more resistant to low-temperature injury. Here we explore the relationship between tissue fatty acid composition and tolerance of stressful environmental conditions over the larval and early juvenile periods. Artemia nauplii supplemented with n-3 long-chain PUFA-deficient and PUFA-enriched oil emulsions were fed to two groups of larvae. Whole body tissue samples from the resulting PUFA-deficient and -enriched juveniles possessed 12.1 and 21.9% n-3 long-chain PUFA, respectively. These differences were at the expense of C18 PUFA, while proportions of saturated fatty acids, monounsaturated fatty acids, and total PUFA were unaffected. Brain and eye tissues from the PUFA-deficient fish contained lower levels of 22:6n-3, known to be important for optimal nervous system function, incorporating instead a range of fatty acids of lower unsaturation. PUFA-deprived juveniles showed substantially greater mortality when exposed to a combination of low temperature and low salinity, as well as to high temperature and to hypoxia. After adaptation to the different diets, both dietary groups were fed a common formulated feed high in n-3 long-chain PUFA. Tissue PUFA in both groups progressively increased to the same high value, with a consequent loss of the differences in cold-susceptibility. These correlated changes support a link between dietary manipulation of n-3 long-chain PUFA and development of a stress-sensitive phenotype. PUFA deprivation had no detectable effect upon static hydrocarbon order of purified brain membranes (as assessed by fluorescence polarization) but was associated with an increase in the whole-body content of prostaglandins. We conclude that susceptibility to environmental stress is responsive to dietary n-3 long-chain PUFA manipulation, possibly due to altered tissue development or the overproduction of eicosanoids.