A novel arachidonic acid-selective cytosolic PLA2 contains a Ca2+-dependent translocation domain with homology to PKC and GAP

The modification of mammalian membrane polyunsaturated fatty acid composition in relation to membrane fluidity and function

Over the last 25 years a considerable research effort has concentrated on the eicosanoids, and great progress has been made in the elucidation of the chemical structure of these compounds, of their physiological roles, and of the ways in which their synthesis is controlled. It is on the last of these that this Review will concentrate, for it is now established that in most tissues the synthesis of eicosanoids is limited by the availability of their common precursor, free arachidonic acid, which must be liberated from esterified stores in complex lipids (van Dorp et al., 1964; Bergstrom et al., 1964; Vogt et al., 1966; Lands & Samuelsson, 1968; Vonkeman & van Dorp, 1968). Control of the subsequent metabolism of the free acid will not be discussed here, nor will the original derivation of arachidonate from dietary sources (reviewed by Willis, 1981). The purposes of this Review are twofold: firstly, it is useful to summarize briefly the present state of knowledge in order to help newcomers in the field; secondly, and more importantly, in order to move forward both conceptually and experimentally it is necessary to take a critical look at the complexities and problems associated with studying arachidonate liberation. Liberation of arachidonate, as defined here, must involve hydrolysis of an ester bond i.e. lipase activity. The three essential questions concerning the control of arachidonate availability are therefore: (1) Which lipases are involved? (2) How are they controlled? (3) Which substrates are hydrolysed?

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How is the level of free arachidonic acid controlled in mammalian cells

Fatty acid composition of adipose tissue and blood in humans and its use as a biomarker of dietary intake.

Nano-electrospray tandem mass spectrometry allows qualitative and quantitative analysis of complex membrane lipid mixtures at the subpicomole level. We have exploited this technique to selectively detect individual classes of phospholipids from unprocessed total cellular lipid extracts by either precursor ion or neutral loss scanning. This way phosphatidylcholine, sphingomyelin, phosphatidylinositol and -phosphates, phosphatidylethanolamine, phosphatidylserine, phosphatidylglycerol, phosphatidic acid, and their plasmalogen analogues can be detected. The optimized ionization and fragmentation conditions described together with the principle of internal standardization by nonnatural analogues allow the rapid and quantitative determination of membrane lipid compositions down to sample amounts of 1000 cells.

https://www.pnas.org/content/pnas/94/6/2339.full.pdf

Merle L. Blank

Papers

Antihypertensive activity of an alkyl ether analog of phosphatidylcholine.

A specific acetylhydrolase for 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine (a hypotensive and platelet-activating lipid).

Novel quantitative method for determination of molecular species of phospholipids and diglycerides.

Inactivation of 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine by a plasma acetylhydrolase: higher activities in hypertensive rats.

The enzymic synthesis of ethanolamine plasmalogens.