High impact information on Ethyl arachidonate

• CONCLUSIONS: The mass of FAEEs in liver and adipose tissue and the presence of ethyl arachidonate can serve as postmortem markers of premortem ethanol intake when no blood sample can be obtained [1].
• Among the polyunsaturated, long-chain FAEEs, there was weak evidence that the incidence (21.5% vs 6.5%, p = 0.057) and concentration (p = 0.064) of ethyl arachidonate (AA) were significantly higher in the alcohol-exposed groups than the control groups [2].
• Esterification of the free carboxylic group (arachidonic acid ethyl ester) prevented most of the inhibitory activity, arguing against mere membrane lipid disruption [3].
• Nearly optimal PKC activation was obtained when non-activating ethyl oleate or ethyl arachidonate was added to sub-optimally activating concentrations of oleic or arachidonic acids [4].
• The threshold dose being as little as 9 mg of ethyl arachidonate/rat/day for reversal of PL fatty acid composition, collagen-induced platelet aggregation and TXA2 production, and 18 mg of ethyl arachidonate/rat/day for reversal of aortic PGI2 production [5].

Biological context of Ethyl arachidonate

• These changes in prostanoid production, platelet aggregation and PL fatty acid composition were dose-dependently reversed by the daily oral administration of ethyl arachidonate (9, 18, 36, or 72 mg) [5].

Associations of Ethyl arachidonate with other chemical compounds

• Male Sprague Dawley rats were fed a butter-enriched diet (50% fat) for 2 weeks and then supplemented orally with either 90 mg of ethyl arachidonate or ethyl linoleate daily for 2 weeks [6].

Gene context of Ethyl arachidonate

• In ethyl arachidonate (100 mg, IP) supplemented EFAD rats, plasma TxB2 rose to 873 +/- 204 pg/ml (N = 8), 30 min after endotoxin [7].

References