15-lipoxygenase metabolites of -linolenic acid/eicosapentaenoic acid suppress growth and arachidonic acid metabolism in human prostatic adenocarcinoma cells: Possible implications of dietary fatty acids

2005 ◽  
Vol 72 (5) ◽  
pp. 363-372 ◽  
Author(s):  
Kao Vang ◽  
Vincent A. Ziboh
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Eicosapentaenoic Acid ◽  
Linolenic Acid ◽  
Acid Metabolism ◽  
Arachidonic Acid Metabolism ◽  
Prostatic Adenocarcinoma ◽  
Dietary Fatty Acids ◽  
Adenocarcinoma Cells

scholarly journals Polyunsaturated fatty acids and risk of Alzheimer’s disease: a Mendelian randomization study

2019 ◽  
Vol 59 (4) ◽  
pp. 1763-1766 ◽  
Author(s):  
Yasutake Tomata ◽  
Susanna C. Larsson ◽  
Sara Hägg
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Linoleic Acid ◽  
Docosahexaenoic Acid ◽  
Polyunsaturated Fatty Acids ◽  
Eicosapentaenoic Acid ◽  
Linolenic Acid ◽  
Mendelian Randomization ◽  
Docosapentaenoic Acid ◽  
Alpha Linolenic Acid

Abstract Purpose Observational studies have suggested that polyunsaturated fatty acids (PUFAs) may decrease Alzheimer’s disease (AD) risk. In the present study, we examined this hypothesis using a Mendelian randomization analysis. Methods We used summary statistics data for single-nucleotide polymorphisms associated with plasma levels of n-6 PUFAs (linoleic acid, arachidonic acid) and n-3 PUFAs (alpha-linolenic acid, eicosapentaenoic acid, docosapentaenoic acid, docosahexaenoic acid), and the corresponding data for AD from a genome-wide association meta-analysis of 63,926 individuals (21,982 diagnosed AD cases, 41,944 controls). Results None of the genetically predicted PUFAs was significantly associated with AD risk; odds ratios (95% confidence interval) per 1 SD increase in PUFA levels were 0.98 (0.93, 1.03) for linoleic acid, 1.01 (0.98, 1.05) for arachidonic acid, 0.96 (0.88, 1.06) for alpha-linolenic acid, 1.03 (0.93, 1.13) for eicosapentaenoic acid, 1.03 (0.97, 1.09) for docosapentaenoic acid, and 1.01 (0.81, 1.25) for docosahexaenoic acid. Conclusions This study did not support the hypothesis that PUFAs decrease AD risk.

THE EFFECT OF OMEGA 3 FATTY ACIDS ON MEGAKARYOCYTE ARACHIDONIC ACID METABOLISM

1987 ◽  
Author(s):  
Paul K Schick ◽  
Barbara P Schick ◽  
Pat Webster
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Polyunsaturated Fatty Acids ◽  
Linolenic Acid ◽  
Acid Metabolism ◽  
Striking Difference ◽  
Omega 3 Fatty Acids ◽  
Omega 3 ◽  
Marine Oils ◽  
Lipid Species

Dietary omega 3 polyunsaturated fatty acids are thought to prevent atherosclerosis. It has been proposed that omega 3 fatty acids modify platelet arachidonic acid (20:4) metabolism and platelet function and thereby reduce the incidence of thrombosis. We have previously shown that megakaryocytes (MK), like platelets, contain large amounts of esterified 20:4. The study addresses the following questions: 1) Do omega 3 fatty acids have a primary action on 20:4 metabolism in MK rather than in platelets. 2) Do omega 3 marine oils, docosahexaenoic acid (22:6) and eicosapentaenoic acid (20:5), have a different effect on megakaryocyte 20:4 metabolism than does alpha linolenic acid (18:3), the major omega-3 fatty acid present in normal diets? 3) How do omega-3 fatty acids modify megakaryocyte 20:4 acid metabolism? MK and platelets were isolated from guinea pigs. Isolated cells were incubated with radiolabeled 20:4 acid and unlabeled 18:3, 20:5 or 22:6. Incubations were terminated by lipid extraction, lipid classes were separated by thin-layer chromatography and the incorporation of radiolabeled 20:4 into lipid species was measured by scintillation spectrometry.MK (106) can incorporate about 4 times more 20:4 than 109 platelets. We have previously shown that 20:4 is incorporated into all endogenous pools of 20:4 in MK while platelets appear to have a limited capacity to incorporate 20:4 into phosphatidyl-ethanolamine (PE). Marine oils, 22:6 and 20:5, had similar effects on the incorporation of radiolabeled 20:4 in MK. Both marine oils reduced the total uptake of 20:4 in megakaryocytes but the reduction occured primarily in PE and phosphatidylserine (PS) rather than in phosphatidylcholine (PC) and phosphatidylinositol (PI). Both 20:5 and 22:6 caused a 50% reduction in the incorporation of radiolabeled 20:4 into megakaryocyte PE and PS while only a 20% reduction into PC and PI. There was a striking difference in the effect of 18:3. Even though the incubation of megakaryocytes with 18:3 reduced the uptake of 20:4, the distribution of the incorporated 20:4 in phospholipids of megakaryocytes incubated with 18:3 was similar to that in controls. Thus, 18:3 did not have a selective effect on the incorporation of 20:4 into PE or PS. Whereas megakaryocyte 20:4 metabolism was significantly affected by omega-3 fatty acids, the incubation of guinea pig or human platelets with 22:6, 20:5 or 18:3 did not result in any alteration of the incorporation of 20:4 into platelet phospholipids.20:4 may be initially incorporated into megakaryocyte PC and subsequently transfered to PE and other phospholipids. Omega 3 marine oils, 20:5 and 22:6, appear to have a selective action on the incorporation or transfer of 20:4 into PE and PS. One mechanism for these observations would be an effect of marine oils on megakaryocyte acyltransferase and/or transacylases. Omega 3 linolenic acid appears to reduce the uptake of 20:4 but does not affect the transfer of 20:4 into PE and PS since there was no selective inhibition of uptake into PE or other megakaryocyte phospholipids. The observation that marine oils did not have any effect on 20:4 metabolism in platelets indicated that omega 3 polyunsaturated fatty acids primarily affect megakaryocytes. This phenomenon may result in the production of platelets with abnormal content and compartmentalization of arachidonic acid. The localization of 20:4 in different pools in these platelets could influence the availability of esterified 20:4 for the production of thromboxanes and other eicosanoids. Another implication of the study is that omega 3 fatty acids may have a greater effect on precursor cells than on differentiated cells and tissues and influence cellular maturation.

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