Enhanced incorporation of n-3 fatty acids from fish compared with fish oils.

This work was undertaken to study the impact of the source of n-3 FA on their incorporation in serum, on blood lipid composition, and on cellular activation. A clinical trial comprising 71 volunteers, divided into five groups, was performed. Three groups were given 400 g smoked salmon (n = 14), cooked salmon (n = 15), or cooked cod (n = 13) per week for 8 wk. A fourth group was given 15 mL/d of cod liver oil (CLO) (n = 15), and a fifth group served as control (n = 14) without supplementation. The serum content of EPA and DHA before and after intervention revealed a higher rise in EPA and DHA in the cooked salmon group (129% rise in EPA and 45% rise in DHA) as compared with CLO (106 and 25%, respectively) despite an intake of EPA and DHA in the CLO group of 3.0 g/d compared with 1.2 g/d in the cooked salmon group. No significant changes were observed in blood lipids, fibrinogen, fibrinolysis, or lipopolysaccharide (LPS)-induced tissue factor (TF) activity, tumor necrosis factor-alpha (TNFalpha), interleukin-8 (IL-8), leukotriene B4 (LTB4), and thromboxane B2 (TxB2) in whole blood. EPA and DHA were negatively correlated with LPS-induced TNFalpha, IL-8, LTB4, TxB2, and TF in whole blood. In conclusion, fish consumption is more effective in increasing serum EPA and DHA than supplementing the diet with fish oil. Since the n-3 FA are predominantly in TAG in fish as well as CLO, it is suggested that the larger uptake from fish than CLO is due to differences in physiochemical structure of the lipids.

Generation of tissue factor-rich microparticles in an ex vivo whole blood model.

The aim of this study was to investigate the role of blood cells in the expression of tissue factor (TF) and P-selectin in platelets and microparticles from blood stimulated with lipopolysaccharide (LPS), with or without the further addition of phorbol myristyl acetate (PMA). TF activity was found to be associated with platelets after 2 h incubation of whole blood with LPS or LPS + PMA, while no TF activity was detected in microparticles from blood subjected to such stimulation. In blood stimulated for 6 and 24 h, addition of PMA to the samples led to a substantial increase in TF activity associated with microparticles, compared with stimulation with LPS alone. Addition of PMA to blood samples also led to a three-fold increase in the amount of P-selectin found in the isolated microparticle fraction, and a 50% reduction in P-selectin measured in platelets, compared with LPS alone used for stimulation. In a different experiment, TF-rich microparticles were shown to be absorbed very efficiently by neutrophils in a calcium-independent reaction. Our results imply that LPS stimulation of whole blood is associated with a direct transfer of TF from monocytes to platelets in the absence of free TF-rich microparticles, which probably is accounted for by the fusion of TF-rich microparticles with activated platelets exposing P-selectin. Further addition of PMA to samples generates both free TF-rich microparticles as well as enhanced transfer of TF from monocytes to platelets.

Studies of biological functions in blood cells from individuals with large platelets.

The present study was performed to explore differences in the expression of P-selectin and IL-8 production of blood cells in healthy individuals with large size platelets (MI-families) as compared to people having normal size platelets. A positive correlation between LPS-induced IL-8 production per platelet in whole blood and mean platelet volume (MPV) was found in the large platelet group (R=0.74, P<0.05). When the large and normal groups were combined the correlation was nearly, but not quite significant (R=0.46, P<0.06). There was also a positive correlation between sP-selectin and MPV (R=0.42, P<0.05). Furthermore, IL-8 in serum was positively correlated to sP-selectin in serum (R=0.68, P<0.005). sP-selectin baseline values in citrated plasma correlated significantly with values found in serum (R=0.72, P<0.0005), indicating that sP-selectin in blood originates from the platelets rather than from endothelial cells. Significant correlations were also found in both groups between P-selectin and CD40L (R=0.44, P<0.05) and P-selectin and RANTES (R=0.44, P<0.05). A significant correlation was also found between PDGF and RANTES (R=0.44, P<0.05). Our results suggest that larger platelets enhance the production of IL-8 more than normally sized platelets. This phenomenon is probably mediated through P-selectin exposed on platelets.