Echium oil is better than rapeseed oil in improving the response of barramundi to a disease challenge

Pathogen infection stimulates the fatty acid (FA) metabolism and the production of pro-inflammatory derivatives of FA. Barramundi, Lates calcarifer, was fed on a diet rich in preformed long-chain (?C₂₀) polyunsaturated fatty acids (LC-PUFA) from fish oil (FO), to compare with diets containing high levels of C₁₈ precursors for LC-PUFA – stearidonic (SDA) and γ-linolenic acid (GLA) – from Echium plantagineum (EO), or rapeseed oil (RO) rich in α-linolenic acid (ALA), but a poor source of LC-PUFA and their precursors. After 6 weeks, when growth rates were similar amongst the dietary treatments, a sub-lethal dose of Streptococcus iniae was administered to half of the fish, while the other half were maintained unchallenged and were pair-fed with the infected fish. Under a disease challenge situation, the tissue FA depots depleted at 3 days post-infection (DPI) and were then restored to their previous concentrations at 7 DPI. During the infection period, EO fish had a higher content of n3 and n6 PUFA in their tissues, higher n3:n6 PUFA ratio and reduced levels of the eicosanoids, TXB₂ and 6-keto-PGF_1α, in their plasma compared with RO fish. Fish fed on FO and EO had a longer lasting and enduring response in their FA and eicosanoid concentrations, following a week of bacterial infection, compared with those fed on RO. EO, containing SDA and GLA and with a comparatively higher n3:n6 PUFA ratio, proved more effective than RO in compensating for immunity stress.     

Signal Transduction of Barnacle Egg-Hatching Pheromone: Pharmacological Assays Indicate a Comparatively Simple Mechanism of Eicosanoid Action

Eicosanoids are generally regarded as autocoids that act via G-protein-linked receptors. There are exceptions to this model, however, both in terms of function and mechanism of action. The present paper concerns one such example, an hydroxy fatty acid that acts as a pheromone, not an autocoid, in inducing barnacle egg hatching. Preliminary findings of pharmacological assays on the mechanism of action of this eicosanoid pheromone do not support the involvement of G proteins, Ca²⁺, or protein kinase C in signal transduction. Instead it is concluded, tentatively, that barnacle egg hatching pheromone acts via a comparatively simple pathway involving the second messenger, cyclic AMP.     

Dietary Linseed Oil Reduces Growth While Differentially Impacting LC-PUFA Synthesis and Accretion into Tissues in Eurasian Perch (Perca fluviatilis)

The aim of this study was to evaluate the impact of replacing dietary fish oil (FO) with linseed oil (LO) on growth, fatty acid composition and regulation of lipid metabolism in Eurasian perch (Perca fluviatilis) juveniles. Fish (17.5 g initial body weight) were fed isoproteic and isoenergetic diets containing 116 g/kg of lipid for 10 weeks. Fish fed the LO diet displayed lower growth rates and lower levels of DHA in the liver and muscle than fish fed the FO diet, while mortality was not affected by dietary treatment. However, DHA content recorded in the liver and muscle of fish fed the LO diet remained relatively high, despite a weight gain of 134 % and a reduced dietary level of long‐chain polyunsaturated fatty acids (LC‐PUFA), suggesting endogenous LC‐PUFA biosynthesis. This was supported by the higher amounts of pathway intermediates, including 18:4n‐3, 20:3n‐3, 20:4n‐3, 18:3n‐6 and 20:3n‐6, recorded in the liver of fish fed the LO diet in comparison with those fed the FO diet. However, fads2 and elovl5 gene expression and FADS2 enzyme activity were comparable between the two groups. Similarly, the expression of genes involved in eicosanoid synthesis was not modulated by dietary LO. Thus, the present study demonstrated that in fish fed LO for 10 weeks, growth was reduced but DHA levels in tissues were largely maintained compared to fish fed FO, suggesting a physiologically relevant rate of endogenous LC‐PUFA biosynthesis capacity.     

Transformation of Prostaglandin D2 to 11-Dehydro Thromboxane B2 by Baeyer-Villiger Oxidation

Prostaglandin D₂ is one of five chief prostanoids formed in the cyclooxygenase pathway of arachidonic acid oxidation. Except for a single oxygen atom, PGD₂ is structurally identical to 11-dehydro thromboxane B₂ (11d-TxB₂), a urinary metabolite of the pro-aggregatory platelet activator, thromboxane A₂. The close structural relationship suggested that one might be transformed to the other. Accordingly, we tested whether the cyclopentanone of PGD₂ can be expanded to the δ-lactone of 11d-TxB₂ in a Baeyer-Villiger oxidation. Oxidation of PGD₂ with two standard oxidants showed that 11d-TxB₂ was formed only with H₂O₂ but not with peracetic acid. Byproducts of the H₂O₂-mediated oxidation were hydroperoxide derivatives and isomers of PGD₂. Chemical oxidation of PGD₂ to 11d-TxB₂ may be a model for an equivalent enzymatic transformation, suggesting a possible link in the metabolism of PGD₂ and thromboxane A₂.     

Renal Cyclooxygenase Products are Higher and Lipoxygenase Products are Lower in Early Disease in the pcy Mouse Model of Adolescent Nephronophthisis

Nephronophthisis (NPHP) is a pediatric form of hereditary polycystic kidney disease (PKD), and is the leading cause of end stage renal disease in children. The pcy mouse is an orthologous model of human NPHP, with a mutation in the Nphp3 gene. Renal phospholipase A₂, cyclooxygenase (COX) 1 and cyclic AMP are elevated in this model, suggesting that eicosanoid formation may be altered. In another type of PKD observed in the Han:SPRD-Cy rat, inhibition of eicosanoid production slows disease progression. If renal eicosanoids are similarly altered in NPHP, potential for pharmacologic intervention also may exist for this disorder. Therefore, renal fatty acids and eicosanoids were determined in pcy and normal mice at 15, 30 and 60 days of age by gas chromatography and HPLC–tandem mass spectrometry, respectively. Renal cysts in enlarged kidneys were observed in pcy mice by 15 days of age and increased over time. Renal phospholipid ARA levels were higher in pcy compared to normal mice at 15 and 30 days. Eicosanoid differences were observed starting at 30 days, when the COX products 6-keto-prostaglandin (PG) F_1α, thromboxane B₂ and PGE₂ were higher in pcy compared to normal kidneys. Overall, total COX products were elevated at 30 and 60 days. In contrast, the levels of the lipoxygenase (LOX) products were not altered until 60 days of age and these were lower in pcy kidneys compared to normal. These findings suggest that altered eicosanoids play a role in NPHP, and that manipulating these levels with pharmacologic agents may have therapeutic potential.