Encapsulated fish oil enriched in α‐tocopherol alters plasma phospholipid and mononuclear cell fatty acid compositions but not mononuclear cell functions

Abstract

Background: Several studies have reported that dietary fish oil (FO) supplementation alters cytokine production and other functional activities of peripheral blood mononuclear cells (PBMC). However, few of these studies have been placebo controlled and few have related the functional changes to alterations in PBMC fatty acid composition Patients and methods: Healthy subjects supplemented their diets with 9 g day−1 of encapsulated placebo oil (3 : 1 mix of coconut and soybean oils), olive oil (OO), safflower oil (SO), evening primrose oil (EPO) or FO [providing 2.1 g eicosapentaenoic acid (EPA) plus 1.1 g docosahexaenoic acid (DHA) per day] for 12 weeks; the capsules also provided 205 mg α‐tocopherol per day. Blood was sampled at 4‐weekly intervals and plasma and PBMC prepared. Plasma phospholipid and PBMC fatty acid composition, plasma α‐tocopherol and thiobarbituric acid‐reactive substance concentrations, plasma total antioxidant capacity, the proportions of different PBMC subsets, the proportions of PBMC expressing the adhesion molecules CD2, CD11b and CD54, and PBMC functions (lymphocyte proliferation, natural killer cell activity, cytokine production) were measured. All measurements were repeated after a ‘washout’ period of 8 weeks. Results: The placebo, OO and SO capsules had no effect on plasma phospholipid or PBMC fatty acid composition. The proportion of dihomo‐γ‐linolenic acid in plasma phospholipids was elevated in subjects taking EPO and was decreased in subjects taking FO. There was no appearance of γ‐linolenic acid in the plasma phospholipids or PBMC in subjects taking EPO. There was a marked increase in the proportion of EPA in the plasma phospholipids (10‐fold) and PBMC (four‐fold) of subjects taking FO supplements; this increase was maximal after 4 weeks of supplementation. There was an increase in the proportion of DHA in plasma phospholipids and PBMC, and an approximately 20% decrease in the proportion of arachidonic acid in plasma phospholipids and PBMC, during FO supplementation. Plasma concentrations of α‐tocopherol were significantly elevated during supplementation in all subjects and returned to baseline values after the washout period. There were no effects of supplementation with any of the capsules on total plasma antioxidant activity or plasma thiobarbituric acid‐reactive substances or on the proportion of different PBMC subsets, on the proportion of PBMC expressing adhesion molecules, on natural killer cell activity, on the proliferation of mitogen‐stimulated whole blood cultures or PBMC, or on the ex vivo production of a range of cytokines by whole blood cultures or PBMC cultures stimulated by either concanavalin A or lipopolysaccharide. Conclusion: Supplementation of the diet with 3.2 g EPA plus DHA per day markedly alters plasma phospholipid and PBMC fatty acid compositions. The lack of effect of FO upon PBMC functions may relate to the level of α‐tocopherol included in the supplements.