Disease relevance of Eicosapentaenoic acid

• Increased concentrations of cellular eicosapentaenoic acid (EPA) have been shown to be beneficial in coronary heart disease, hypertension, and inflammatory disorders [1].
• A wealth of evidence indicates that consumption of fish or dietary fish oils containing long-chain (n-3) PUFA such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) is associated with cardiovascular benefit, including a reduction in circulating triacylglycerol concentrations and reduced mortality from coronary heart disease [2].
• The purpose of this double-blind study was to investigate the influence of dietary supplementation with an algae source of docosahexaenoic acid [DHA; 22:6(n-3)], devoid of any eicosapentaenoic acid [EPA; 20:5(n-3)], on serum/platelet DHA status, the estimated retroconversion of DHA to EPA, and risk factors for heart disease in vegetarian subjects [3].
• As an application of the method, prostaglandins formed by EPA in human lung cancer A549 cells were determined [4].
• In conclusion, EPA inhibited EVLW accumulation and may be useful for ameliorating one of the ischemia-reperfusion-induced complications, pulmonary edema [5].

Psychiatry related information on Eicosapentaenoic acid

• The evidence base supports a dietary recommendation of approximately 500 mg/d of EPA and DHA for cardiovascular disease risk reduction [6].

High impact information on Eicosapentaenoic acid

• LTB4-stimulated neutrophil chemotaxis and IP3 formation correlated significantly (P < 0.0001); each response correlated closely and negatively with the EPA content of the neutrophil phosphatidylinositol (PI) pool (P = 0.0003 and P = 0.0005, respectively) [7].
• We show that oxidized, but not native unoxidized, EPA significantly inhibited human neutrophil and monocyte adhesion to endothelial cells in vitro by inhibiting endothelial adhesion receptor expression [8].
• In vivo, oxidized, but not native, EPA markedly reduced leukocyte rolling and adhesion to venular endothelium of lipopolysaccharide (LPS)-treated mice [8].
• Therefore, the beneficial effects of omega-3 fatty acids may be explained by a PPAR alpha-mediated anti-inflammatory effect of oxidized EPA [8].
• This occurred via a PPAR alpha-dependent mechanism because oxidized EPA had no such effect in LPS-treated PPAR alpha-deficient mice [8].

Chemical compound and disease context of Eicosapentaenoic acid

• Wistar rats received by gavage oleic acid, EPA, or DHA (360 mg/kg body weight/day) for a period of 1 or 4 wk [9].

Biological context of Eicosapentaenoic acid

• EPA and HMB also attenuated phosphorylation of p42/44 mitogen-activated protein kinase by PIF, thought to be important in PIF-induced proteasome expression [10].
• Conversely, DHA supplementation induced a doubling of the number of cells undergoing apoptosis (labeled by TUNEL), whereas EPA treatment was much less effective [11].
• It is concluded from the results of the present study that the anti-tumoral effect of EPA is related mainly to its inhibition of cell proliferation, whereas that of DHA corresponds with its induction of apoptosis [11].
• Platelet (co-)incubation with EPA, but not DCHA, provoked dose-dependent synthesis of n-3-lipid-derived thromboxane: kinetics of formation and absolute quantities of TxA3 approximated 20% of the respective TxA2 data upon stimulation with AA [12].
• We investigated the influence of free EPA and DCHA on platelet thromboxane (Tx) A2 and A3 formation by using a recently developed high performance liquid chromatography-ELISA technique for separate quantification of the stable hydrolysis products TxB2 and TxB3 [12].

Anatomical context of Eicosapentaenoic acid

• The inhibition of the summed formation of LTB4 plus LTB5 in calcium ionophore-stimulated neutrophils and in zymosan-stimulated neutrophils did not correlate significantly with the EPA content of the PI pool [7].
• RESULTS: Dietary SDA increased EPA and docosapentaenoic acid concentrations but not DHA concentrations in erythrocyte and in plasma phospholipids [13].
• Adipose tissue fatty acid profiles analyzed in three samples taken from each subject at 1-y intervals showed no within-subject differences for EPA and DHA [14].
• CONCLUSIONS: Consumption of < or = 600 mg DHA and 140 mg EPA/d for 4 wk increased n-3 PUFA concentrations in relevant tissues but did not cause perturbations in cytokine concentrations in human milk [15].
• Analysis of changes in phospholipid fatty acids in tumor-cell membranes after both treatments with EPA and DHA showed a significant reduction in arachidonic-acid levels [11].

Associations of Eicosapentaenoic acid with other chemical compounds

• We hypothesized that a smoker's risk of developing COPD is inversely related to physiologic levels of two fatty acids that have antiinflammatory properties: eicosapentaenoic acid (EPA, C20:5) and docosahexaenoic acid (DHA, C22:6) [16].
• Foods enriched with EPA and DHA or fish oil supplements are a suitable alternate to achieve recommended intakes and may be necessary to achieve intakes of 1 g/d [6].
• The influence of exogenously supplied free arachidonic acid (AA) and eicosapentaenoic acid (EPA) on the 5-lipoxygenase metabolism in human neutrophils (PMN) was investigated [17].
• A significant decrease in plasma triacylglycerol, plasma apolipoprotein B-48, and platelet phospholipid arachidonic acid concentrations and a significant increase in plasma HDL concentrations and platelet phospholipid EPA and DHA levels were observed after fish-oil supplementation [18].
• There was a significant inverse exponential relation between TNF alpha or IL-1 beta synthesis and mononuclear cell content of eicosapentaenoic acid (EPA), an n--3 fatty acid derived from ingested EPA (fish oil) or metabolism of ingested alpha-linolenic acid (flaxseed oil) [19].

Gene context of Eicosapentaenoic acid

• Oral/enteral supplementation of EPA ethyl ester (1.8 g/d) significantly reduced the postoperative IL-6 production (P < 0.05 at 1, 2, and 6 h after operation), and improved cell-mediated immune function 3 wk after operation (P = 0.05) [20].
• After adjustment for smoking exposure and other possible confounders, the prevalence odds of COPD were inversely related to the DHA (but not to the EPA) content of plasma lipid components in most of the models [16].
• Of the omega-3 PUFAs tested, alpha-linolenic acid (ALA) dramatically reduced FAS activity in a dose-dependent manner (up to 61%). omega-3 PUFA docosahexaenoic acid (DHA) demonstrated less marked but still significant inhibitory effects on FAS activity (up to 37%), whereas eicosapentaenoic acid (EPA) was not effective [21].
• Here the authors present data which suggests that PGs including thromboxane B2 (TXB2) and their precursors such as dihomo-gamma linolenic acid (DGLA), arachidonic acid (AA) and eicosapentaenoic acid (EPA) can inhibit T-cell proliferation and influence their ability to secrete IL-2, IL-4, IL-6 and TNF in vitro [22].
• In addition, both ALA and EPA enhanced the formation of superoxide anion, hydrogen peroxide and lipid peroxides, and caused a reduction in the levels of antioxidant enzymes: SOD, catalase and glutathione peroxidase and induced significant damage to DNA in SP 2/0 cells [23].

Analytical, diagnostic and therapeutic context of Eicosapentaenoic acid

• Both EPA and DHA inhibited growth of the hepatocarcinoma (50% reduction of tumor weight or volume at the 19th day after transplantation for both of the n-3 PUFA groups) [11].
• There were no changes in the plasma DHA or EPA levels in the control group [24].
• EVLW significantly increased up to two times of baseline during coronary ligation in the control group (P < 0.05) and more during reperfusion (P < 0.01), whereas EVLW did not increase in the EPA group [5].
• The maximum biomass and EPA volumetric yields obtained in this work are comparable with those reported for commercial photoautotrophic monoculture of large quantities of P. tricornutum in closed continuous-run tubular loop bioreactors with tubes that are typically less than 0.08 m in diameter [25].
• The contents of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), as well as arachidonic acid (AA), in phospholipid fractions in plasma and in erythrocytes were analyzed preoperatively, on postoperative days 1, 6, and 10 using liquid gas chromatography [26].

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