FATTY-ACID COMPOSITION, EICOSANOID PRODUCTION AND PERMEABILITY IN SKIN TISSUES OF RAINBOW-TROUT (ONCORHYNCHUS-MYKISS) FED A CONTROL OR AN ESSENTIAL FATTY-ACID DEFICIENT DIET

Rainbow trout (Oncorhynchus mykiss) were fed either a control diet con taining fish oil or an essential fatty acid (EFA) deficient diet conta ining only hydrogenated coconut oil and palmitic acid as lipid source (93.4% saturated fatty acids) for 14 weeks and the fatty acid composit ions of individual phospholipid classes from skin and opercular membra ne (OM) determined. The permeability of skin and OM to water and the p roduction of eicosanoids in skin and gills challenged with the Ca2+ io nophore A23187 were also measured. Phospholipid (PL) fatty acid compos itions were substantially modified in EFA-deficient fish, with increas ed saturated fatty acids and decreased polyunsaturated fatty acids (PU FA), especially arachidonic acid (AA) and eicosapentaenoic acid (EPA), while docosahexaenoic acid (DHA) was largely retained. The onset of E FA deficiency was shown by the appearance of n-9 PUFA, particularly 20 .3n-9. The main effects of EFA deficiency on phosphatidylcholine (PC) and phosphatidylethanolamine (PE) were to increase saturated fatty aci ds and monoenes, especially 16:1 and 18:1, and to decrease EPA and DHA . The content of DHA in phosphatidylserine (PS) was high in control an imals (40% in skin and 35% in opercular membrane) and was mostly retai ned in EFA deficient animals. Arachidonic acid (AA) was the most abund ant PUFA esterified to phosphatidylinositol (PI) and was significantly reduced in EFA deficient animals (from 31% to 13% in skin), where a l arge amount of 20:3n-9 (9% in skin) was also present. Influxes and eff luxes of water through skin and opercular membrane were measured in vi tro. No differences were detected between rainbow trout fed the contro l or the EFA deficient diet. 12-Hydroxyeicosatetraenoic acid (12-HETE) , 12-hydroxyeicosapentaenoic acid (12-HEPE) and 14-hydroxydocosahexaen oic acid (14-HDHE) could not be detected in skin from control or EFA d eficient fish. There was no difference between control and EFA deficie nt trout in the levels of leukotriene C-4 (LTC4) and leukotriene C-5 ( LTC5) in skin cells challenged with the calcium ionophore A23187, and of prostaglandin F-2 alpha (PGF(2 alpha)) 12-HETE and 12-HEPE in gill cells challenged similarly. Prostaglandin F-3 alpha (PGF(3 alpha)) pro duction by ionophore stimulated gill cells was significantly reduced i n fish fed the EFA-deficient diet. 14-HDHE produced by gill cells was 3.3 fold higher in EFA deficient fish compared to controls.