thromboxane-b2 and docosapentaenoic-acid

The primary endpoint was to determine the plasma concentration of alpha-linolenic acid (ALA), and its metabolites, following milled flaxseed consumption at four doses. Secondary outcomes focused on plasma enterolignan concentrations and the effects on tolerability, platelet aggregation, plasma lipids and urinary thromboxane levels.. Healthy, younger adults (n = 34; 18-49 years old) were randomized into four groups consuming one muffin daily for 30 days fortified with 10, 20, 30 or 40 g of milled flaxseed. Blood and urine were collected at baseline and 4 weeks.. Plasma ALA concentrations increased with all flaxseed doses (P < 0.01), except the 20 g/day dose (P = 0.10), yet there was no significant dose-dependent response (P = 0.81). Only with the 30 g/day diet were n-3 polyunsaturated fatty acids (P = 0.007), and eicosapentaenoic acid (EPA) (P = 0.047) increased from baseline values. Docosapentaenoic acid and docosahexaenoic acid were not detected at any dose. Plasma total enterolignan concentrations significantly increased over time in all treatment groups, yet despite a dose-dependent tendency, no between-group differences were detected (P = 0.22). Flaxseed was well tolerated, even at the highest dose, as there were no reported adverse events, changes in cholesterol, platelet aggregation or urinary 11-dehydro-thromboxane B2.. In healthy, younger adults, 10 g/day of milled flaxseed consumption is sufficient to significantly increase circulating ALA and total enterolignan concentrations; however, 30 g/day is required to convert ALA to EPA. Although all doses were well tolerated, 40 g/day is too low to attenuate cholesterol in this population.

Topics: Adolescent; Adult; alpha-Linolenic Acid; Butylene Glycols; Cholesterol; Cholesterol, HDL; Cholesterol, LDL; Diet; Docosahexaenoic Acids; Eicosapentaenoic Acid; Fatty Acids, Omega-3; Fatty Acids, Unsaturated; Female; Flax; Glucosides; Humans; Male; Middle Aged; Plant Preparations; Platelet Aggregation; Seeds; Thromboxane B2; Triglycerides; Young Adult

Little is known about the effects of dietary supplementation on platelet survival with low doses of n-3 and n-6 fatty acids in patients with hypercholesterolemia. The effects of a 6-week intervention with fish oil capsules (daily intake: 216 mg eicosapentaenoic acid, 140 mg docosahexaenoic acid, 390 mg gamma-linolenic acid, and 3480 mg linoleic acid) on in vivo platelet survival (111 In-oxine labeled platelets) and on ex vivo markers of platelet activation were investigated in a placebo-controlled, double-blind study with 26 hypercholesterolemic patients. In vivo platelet survival increased in the fish oil group (T) from a mean of 159+/-14 hours to a mean of 164+/-12 hours (p=0.025), whereas it remained unchanged in the placebo (P) group (T vs. P; p=0.055). Ex vivo, thromboxane B2 decreased from a mean of 225+/-16 to 212+/-21 ng/mL (p=0.003) in T but did not change in P (T vs. P: p=0.002). Malondialdehyde formation was lowered significantly by fish oil supplementation from a mean of 5.49+/-1.3 to 5.12+/-1.05 nM/10(9) platelets, p=0.005, as compared with P (T vs. P; p=0.018). The trendwise decrease in 11-DH-thromboxane B2 plasma levels was not significant nor was the increase in platelet sensitivity to prostaglandin I2 by fish oil. Baseline platelet survival in patients with hyperlipoproteinemia type IIa was not different from those with hyperlipoproteinemia IIb and response to treatment in terms of platelet activation markers was not either. The changes in platelet activation parameters in T were associated with significant reductions in cholesterol (-2.9%), low density lipoprotein cholesterol (-3.5%), and triglycerides (-12.4%). Both ex vivo and in vivo platelet activation parameters exhibited signs of decreased activation by a 6-week diet supplemented with n-3 and n-6 fatty acids, which might be beneficial in reducing atherothrombotic risk, in patients with hyperlipoproteinemia type IIa and IIb.

Topics: Blood Platelets; Cell Survival; Combined Modality Therapy; Diet; Diet Records; Diet, Fat-Restricted; Double-Blind Method; Eicosapentaenoic Acid; Epoprostenol; Fatty Acids, Essential; Fatty Acids, Unsaturated; Female; Fish Oils; gamma-Linolenic Acid; Humans; Hyperlipoproteinemia Type II; Linoleic Acid; Linoleic Acids; Lipid Peroxidation; Lipoproteins; Male; Malondialdehyde; Oenothera biennis; Plant Oils; Platelet Activation; Thromboxane B2

Diurnal mechanisms are central to regulating host responses. Recent studies uncovered a novel family of mediators termed as specialized proresolving mediators that terminate inflammation without interfering with the immune response.. Herein, we investigated the diurnal regulation of specialized proresolving mediators in humans and their role in controlling peripheral blood leukocyte and platelet activation.. Using lipid mediator profiling and healthy volunteers, we found that plasma concentrations of n-3 docosapentaenoic acid-derived D-series resolvins (RvD. These results demonstrate that peripheral blood RvD

Topics: Adenosine; Animals; Blood Platelets; Circadian Rhythm; Fatty Acids, Unsaturated; Humans; Inflammation; Leukocytes; Lipoxygenase; Mice; Myocardial Infarction; Thromboxane B2

The effects of docosapentaenoic acid (DPA) on platelet aggregation and arachidonic acid metabolism were studied in comparison to those of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Collagen- or arachidonic acid-stimulated platelet aggregation was inhibited dose-dependently by n-3 fatty acids, among which DPA was the most potent inhibitor. These fatty acids inhibited U46619-induced aggregation but to almost the same extent. No effect of the acids on thrombin-induced aggregation was observed. Furthermore, these fatty acids suppressed thromboxane A2 formation by platelets which were exposed to collagen or thrombin, or by platelets to which arachidonic acid was added. In these experiments also, DPA was the most potent inhibitor, whereas DHA was the most effective inhibitor of cyclooxygenase-1 activity. DPA enhanced formation of 12-hydroxyeicosatetraenoic acid in response to collagen or from arachidonic acid by intact platelets, while the other two acids had less of an effect. These results suggest that DPA possesses potent activity for interfering with the cyclooxygenase pathway and accelerating the lipoxygenase pathway, thus inhibiting platelet aggregation most effectively.

Topics: 12-Hydroxy-5,8,10,14-eicosatetraenoic Acid; Animals; Collagen; Cyclooxygenase 1; Eicosapentaenoic Acid; Fatty Acids, Unsaturated; In Vitro Techniques; Isoenzymes; Lipoxygenase; Platelet Aggregation; Platelet Aggregation Inhibitors; Prostaglandin-Endoperoxide Synthases; Rabbits; Thromboxane B2