THE EFFECT OF DIETARY COD LIVER OIL SUPPLEMENTATION ON LEUKOCYTE PHYSIOLOGY; A POSSIBLE MEDIATOR OF THE ANTIATHEROGENIC EFFECT OF MARINE OIL

Abstract

Leukocytes appear to be important in the pathophysiology of atherogenesis. Fish oil derived, omega-3 fatty acids suppress atherogenesis in experimental atherosclerosis models and select human populations. We assessed the effect of dietary cod liver oil (CLO) supplementation for 6 weeks on human monocyte and polymorphonuclear leukocyte (PMN) inflammatory potential in healthy controls and patients with a purported autoimmune disorder, multiple sclerosis (MS) in whom monocytes appear to be chronically activated. Baseline and 6 week venous blood samples were obtained from 6 stable MS patients and 6 healthy controls. . Monocyte hydrogen peroxide (HO) production (pMoles/minute/Ix10 monocytes) was measured in a spectrophotofluorometer after stimulation with latex particles. Baseline H2O2 production was 1.551.60 (mean 1 S.D.) in the MS patients and 1.19± .49 in the controls. Post-CLO the values were 1.021.24 and 1.091.27 respectively, representing a significant decline with CLO supplementation in the MS group (P< .01). PMN chemiluminescence (counts x10 /5min/PMN) levels was assessed by a liquid scintillation counter after stimulation with latex particles. Baseline levels were 17.416.1 in the MS group and 17.814.8 in the controls Post-CLO the levels were 12.812.3 and 12.313.3; both signifi-antly lower than baseline (P < .05). PMN superoxide (0 —) levels (nMoles/20min/lxl0 PMN) were measured by the reduction of cyto-chrome-c after stimulation with zymosan. Baseline O2- levels were 21.0±5.8 in the MS group and 22.115.9 in the controls. Post-CLO the O2- levels declined to 8.210.7 and 7.811.5, both significantly lower than baseline (P< .O2-). These data demonstrate that CLO supplementation reduces the intensity of PMN and monocyte reactions to a standard stimulus as measured by toxic oxygen metabolite production, although the monocyte effects were only observed in a population (MS) with increased baseline activity levels.It has previously been assumed that omega-3 fatty acids might exert antiatherogenic effects via their inhibitory effects on platelet reactions. If leukocytes are important mediators of endothelial damage and/or cholesterol deposition in arterial walls, then our data suggest another mechanism by which fish oil may confer benefit in reducing the risk of arterial disease.