Key Findings:
Oxidative stress resulting in lipid peroxidation is thought to be an important contributor to the atherosclerosis process. The levels of hydroperoxyoctadecanoic acids and F2-isoprostanes have been shown to be elevated in animal models and in humans with conditions associated with increased oxidative stress. Supplementation with ALA ( 9 g/d of flaxseed oil for 4 wk) led to significant increases in oxidation products of ALA (F1-phytoprostanes) in plasma compared with olive oil. The increase in plasma F1- phytoprostanes in the flaxseed oil group appears to be due to an increase in ALA and/or intake of F1-phytoprostanes present in the flaxseed oil. Flaxseed oil did not affect oxidation products of AA (F2-isoprostanes) in plasma or urine, indicating that flaxseed oil supplementation had no effect on plasma or whole-body lipid peroxidation. F1- phytoprostanes in the diet may make a substantial contribution to the concentration in plasma and urine. Flaxseed oil did not alter markers of AA-derived lipid peroxidation. Further research into the biological actions of F1- phytoprostanes is suggested. It is possible that ALA-induced F1-phytoprostane formation could beneficially affect inflammatory pathways and contribute to the reduced risk for myocardial infarction associated with ALA intake.
ABSTRACT:
Supplementation with eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) has been reported to reduce lipid peroxidation products formed from arachidonic acid (F2-isoprostanes) in healthy humans, as well as in those under oxidative stress. a-Linolenic acid (ALA) is a precursor to EPA and DHA; however, its conversion in humans is thought to be inefficient. ALA can also undergo free radical oxidation, forming compounds known as F1-phytoprostanes, which are found in all plants and are in high concentrations in plant pollens. In this study, we examined the effect of ALA supplementation on plasma and urine F1-phytoprostane and F2-isoprostane concentrations in men. Thirty-six nonsmoking men, aged 20–65 y, were recruited from the general population and randomly allocated to consume 9 g/d of either flaxseed oil (62% ALA, 5.4 g/d) or olive oil (placebo) for 4 wk in a parallel design. At baseline and after 4 wk of supplementation, blood samples and a 24-h urine sample were collected for measurement of plasma and urinary F1-phytoprostanes and F2-isoprostanes and plasma fatty acids. Compared with the olive oil group, plasma phospholipid ALA was greater (P<0.0001), as were F1-phytoprostanes in plasma (P = 0.049) and urine (P = 0.06) in the flaxseed oil group after 4 wk supplementation. Flaxseed oil did not affect plasma or urinary F2-isoprostanes. The greater plasma F1-phytoprostane concentration in the flaxseed oil group most likely resulted from the increased plasma concentration of the ALA substrate and/or the F1-phytoprostane content of the flaxseed oil. Future studies are needed to determine the physiological importance of increased plasma and urine F1-phytoprostanes and their relevance to heart disease prevention. (Authors abstract)
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