I'm interested because there are several notions in the literature that they are not reesterified after production but I can't find any proof for this.
My understanding is that they have relatively short biological half-lives and are fairly unstable--which is one reason that so few assays for eicosanoids exist. Only a few have high enough stability that they can be detected by ELISA or similar types of assays. It was one of the problems I ran into when trying to design experimental systems that could address the nonspecific acute inflammatory response.
From my understanding eicosanoids are derivatives of lipids such as arachidonic acid or linoleic acid, etc, which include many signalling molecules. The parent lipid compound themselves are most likely derived from membrane bilayers (normally in the sn2 position, cleaved by some kind of phospholipase). Although most of the eicosanoids are short lived, some can also linger in vivo through interactions with protein albumine (for example). Eicosanoids are an entire class of molecules, so I don't know if a general statement such as "not reesterified after production" can apply in this case. The parent compounds, such as linoleic acid, might be esterified after it is cleaved from the membrane, although I can't say with absolute certainty.
For some help on eicosanoid isolation and identification (in vitro and in vivo) it might be worth checking out works by Dr. Robert C. Murphy (University of Colorado).
@ Christina: I know that most often the eicosanoids have a short half life. Nevertheless this is also due to enzymatic degradation. Even though I would speculate that having instable oxidized fatty acids in your lipid bilayer is something less desirable, there is no apparent reason why this would be impossible.
Concerning the ELISA I recall the conversation with one of our clinical chemists, who told me that the included antibodies are not specific enough for the small lipid molecules (especially the small differences in oxidation between PGs) and for proper discrimination chromatography or mass spectrometry would be better.
@ Dong: Thank you for the hint. I will look out for his work.
The statement that eicosanoids in general are not stored also surprised me. Anyway you can read this in many publications about these mediators. The reesterification of the educts has been proven.
You are absolutely right in that eicosanoids are not stored for future use in cell membranes. You are also correct that storage of significant quantities of oxidized lipids in membranes affect membrane structure and function. That is why eicosanoids are mainly synthesized on demand and then either secreted out of the cell, degraded, or a minority reacylated back into the phospholipid pool. However this reacylateion is not a means of storing eicosanoids. The reacylated pool of eicosanoids have been shown to be biologically acitve, and the activity is different from that of the unacylated eicosanoids.
There are numerous reports demonstrating eicosanoids in phospholipids and neutral lipids in multplie cell types as well as platelets and lipoproteins. There are reports of mid-chain alcohols primairly in neutral lipids while epoxides seem to be more commonly reported in phospholipid. The loading of epoxides into phospholipids potentiates vascular reactivity, however I am not sure the definitive experiment has been done on that yet... I could compile a rather large list of references, but its easier to refer you to this review:
PMID 19852880 (see p3 & 4)
One often overlooked potential function of reesterification is to clear signal in the same way clearance of neurotransmitter at the neuronal junction is the most important component of signaling life there.