Formation of lipid mediators in farmed rainbow trout under stress conditions

Fish response to stress might resemble inflammatory process in which a series of derived oxidation metabolites from PUFAs seemed to play an important role. Recently, many authors focused on the connection between stress and eicosanoids production in different tissues of fish. C20 long chain fatty acids such as arachidonic (ARA, C20:4n6), eicosapentaenoic (EPA, C20:5n3), and dihomo-gamma-linolenic (DGLA, C20:3n6) are precursors of many lipid mediators: 4-series leukotrienes (LT), lipoxine (LX), 12-hydroxy-eicosatetraenoic acid (12-HETE), 12-hydroxy-eicosapentaenoic acid (12-HEPE), 2-series prostaglandins (PG), and tromboxanes (TX). As well, DHA is the precursor of 14S-hydroxy-docosanoids (14-HDoHE), 17S-hydroxy-docosanoids (17-HdOHE), neuroprotectin D1, resolvin D5, resolvin D1, and resolvin D2. The present work focused on the formation of lipid metabolites in plasma of farmed rainbow trout (Oncorhynchuss mykiss) subjected to stress conditions by means of a slaughtering under asphyxia. Control trout were a set of non stressed fish using percussion slaughter method. The lipid metabolites were studied through the determination of several eicosanoids and docosanoids, such as prostaglandins, leukotrienes, tromboxanes, isoprostanes, resolvins, hydroxides, hydroperoxides, coming from EPA, ARA, and DHA, using SPE extraction prior to LC-MS/MS analysis. The present trial revealed that stress during slaughter widely affected the formation of lipid oxygenated metabolites. Lipid mediators were found highly concentrated in stressed fish rather than in control. Metabolic biomarkers of stress were identified as well. The results suggest that suffering during slaughter affected the enzymatic oxidative response of fish shifted eicosanoid synthesis towards less inflammatory species derived from EPA. Additionally, the larger endogenous concentration of lipid oxygenated products formed can affect the stability of the final fish flesh leading a major susceptibility to oxidation.