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Phosphatidylcholine and Related Lipids



1.  Phosphatidylcholine - Structure and Occurrence

Phosphatidylcholine (once given the trivial name 'lecithin') is usually the most abundant phospholipid in animals and plants, often amounting to almost 50% of the total complex lipids, and as such it is obviously a key building block of membrane bilayers. In particular, it makes up a very high proportion of the outer leaflet of the plasma membrane. Phosphatidylcholine is also the principal phospholipid circulating in plasma, where it is an integral component of the lipoproteins, especially the HDL. On the other hand, it is less often found in bacterial membranes, perhaps 10% of species, but there is none in the 'model' organisms Escherichia coli and Bacillus subtilis.

Formulae for phosphatidylcholine

Phosphatidylcholine is a neutral or zwitterionic phospholipid over a pH range from strongly acid to strongly alkaline. In animal tissues, some of its membrane functions appear to be shared with the structurally related sphingolipid, sphingomyelin, although the latter has many unique properties of its own.

In animal tissues, phosphatidylcholine tends to exist in mainly in the diacyl form, but small proportions (in comparison to phosphatidylethanolamine and phosphatidylserine) of alkylacyl and alkenylacyl forms may also be present. Data for the compositions of these various forms from bovine heart muscle are listed in our web pages on ether lipids. As a generalization, animal phosphatidylcholine tends to contain lower proportions of arachidonic and docosahexaenoic acids and more of the C18 unsaturated fatty acids than the other zwitterionic phospholipid, phosphatidylethanolamine. Saturated fatty acids are most abundant in position sn-1, while polyunsaturated components are concentrated in position sn-2. Indeed, C20 and C22 polyenoic acids are exclusively in position sn-2, yet in brain and retina the unusual very-long-chain polyunsaturated fatty acids (C30 to C38) of the n-6 and n-3 families occur in position sn-1. Dietary factors obviously influence fatty acid compositions, but in comparing animal species, it would be expected that the structure of the phosphatidylcholine in the same metabolically active tissue would be somewhat similar in terms of the relative distributions of fatty acids between the two positions. Table 1 lists some representative data.

Table 1. Positional distribution of fatty acids in the phosphatidylcholine of some animal tissues.
Position Fatty acid
16:0 16:1 18:0 18:1 18:2 20:4 22:6
 
  Rat liver [1]
sn-1 23 1 65 7 1 trace
sn-2 6 1 4 13 23 39 7
 
  Rat heart [2]
sn-1 30 2 47 9 11 - -
sn-2 10 1 3 17 20 33 9
 
  Rat lung [3]
sn-1 72 4 15 7 3 - -
sn-2 54 7 2 12 11 10 1
 
  Human plasma [4]
sn-1 59 2 24 7 4 trace -
sn-2 3 1 1 26 32 18 5
 
  Human erythrocytes [4]
sn-1 66 1 22 7 2 - -
sn-2 5 1 1 35 30 16 4
 
  Bovine brain (gray matter) [5]
sn-1 38 5 32 21 1 - -
sn-2 33 4 trace 48 1 9 4
 
  Chicken egg [6]
sn-1 61 1 27 9 1 - -
sn-2 2 1 trace 52 33 7 4
1, Wood, R. and Harlow, R.D. Arch. Biochem. Biophys., 131, 495-501 (1969); 2, Kuksis, A. et al. J. Lipid Res., 10, 25-32 (1969); 3, Kuksis, A. et al. Can. J. Physiol. Pharm., 46, 511-524 (1968); 4, Marai, L. and Kuksis, A. J. Lipid Res., 10, 141-152 (1969); 5, Yabuuchi, H. and O'Brien, J.S. J. Lipid Res., 9, 65-67 (1968); 6, Kuksis, A. and Marai, L. Lipids, 2, 217-224 (1967).

There are some exceptions to the rule as the phosphatidylcholine in some tissues or organelles contains relatively high proportions of disaturated molecular species. For example, it is well known that lung phosphatidylcholine in most if not all animal species studied to date contains a high proportion (50% or more) of dipalmitoylphosphatidylcholine.

The positional distributions of fatty acids in phosphatidylcholine in representative plants and yeast are listed in Table 2. In the leaves of the model plant Arabidopsis thaliana, saturated fatty acids are concentrated in position sn-1, but monoenoic fatty acids are distributed approximately equally between the two positions, and there is a preponderance of di- and triunsaturated fatty acids in position sn-2; the same is true for soybean ‘lecithin’. In the yeast Lipomyces lipoferus, the pattern is somewhat similar except that much of the 16:1 is in position sn-1.

Table 2. Composition of fatty acids (mol %) in positions sn-1 and sn-2 in the phosphatidylcholine from plants and yeast.
Position Fatty acid
16:0 16:1 18:0 18:1 18:2 18:3
 
   Arabidopsis thaliana (leaves) [1]
sn-1 42   4 5 23 26
sn-2 1   trace 5 47 47
 
   Soybean 'lecithin' [2]
sn-1 24   9 14 47 4
sn-2 5   1 13 75 6
 
   Lipomyces lipoferus [3]
sn-1 24 18 trace 37 16 4
sn-2 4 5 trace 39 31 19
1, Browse, J., Warwick, N., Somerville, C.R. and Slack, C.R. Biochem. J., 235, 25-31 (1986).
2, Blank, M.L., Nutter, L.J. and Privett, O.S. Lipids, 1, 132-135 (1966).
3, Haley, J.E. and Jack, R.C. Lipids, 9, 679-681 (1974).


2.  Phosphatidylcholine – Biosynthesis

There are several mechanisms for the biosynthesis of phosphatidylcholine in animals, plants and micro-organisms. Choline itself is not synthesised as such by animal cells and is an essential nutrient. It must be obtained from dietary sources or by degradation of existing choline-containing lipids, for example those produced by the second pathway described below. Once taken up into cells by specific transporters, choline is immediately phosphorylated by a choline kinase (1) in the cytoplasm of the cell to produce phosphocholine, which is reacted with cytidine triphosphate (CTP) by the enzyme CTP:phosphocholine cytidylyltransferase (2) to form cytidine diphosphocholine (CDP-choline). The latter is usually the rate-limiting step, and the activity of the enzyme is regulated by signals from a sensor in the membrane that reports on the relative abundance of phosphatidylcholine. However, choline kinase (ChoKα) also has regulatory functions. The CDP-choline produced is acted upon in the endoplasmic reticulum by the membrane-bound enzyme CDP-choline:1,2-diacylglycerol choline-phosphotransferase, which catalyses the reaction with sn-1,2-diacylglycerols to form phosphatidylcholine. This is the main pathway for the synthesis of phosphatidylcholine in animals and plants, and it is analogous to that for a major route to phosphatidylethanolamine; it is also found in a few bacterial species (e.g. Sinorhizobium meliloti). Phosphatidylcholine in mitochondria is obtained by transfer from the endoplasmic reticulum.

Main pathway for the biosynthesis of phosphatidylcholine

The discovery of the importance of this pathway depended a little on serendipity in that in experiments in the laboratory of Professor Eugene Kennedy, samples of adenosine triphosphate (ATP) contained some cytidine triphosphate (CTP) as an impurity. However, luck is of little value without receptive minds, and Kennedy and co-workers demonstrated that the impurity was an important metabolite that was essential for the formation of phosphatidylcholine.

The above reaction, together with the biosynthetic mechanism for phosphatidylethanolamine, is significantly different from that for phosphatidylglycerol, phosphatidylinositol and cardiolipin. Both make use of nucleotides, but with the latter, the nucleotide is covalently linked directly to the lipid intermediate, i.e. cytidine diphosphate diacylglycerol. However, a comparable pathway to the latter for biosynthesis of phosphatidylcholine occurs in bacteria (see below).

The source of the sn-1,2-diacylglycerol precursor, which is also a key intermediate in the formation of phosphatidylethanolamine and phosphatidylserine, and of triacylglycerols, is phosphatidic acid. In this instance, the important enzyme is phosphatidic acid phosphatase (or ‘phosphatidate phosphatase’ or ‘lipid phosphate phosphatase’ or ‘phosphatidate phosphohydrolase’).

Conversion of phosphatidic acid to diacylglycerol

This enzyme is also important for the production of diacylglycerols as essential intermediates in the biosynthesis of triacylglycerols and of phosphatidylethanolamine. Yeasts contain two such enzymes, one of which is Mg2+-dependent (PAP1) and the other Mg2+-independent (PAP2). In mammals, much of the phosphatidic acid phosphatase activity resides in three related cytoplasmic proteins, termed lipins-1, -2, and -3 (see our web page on triacylglycerol biosynthesis). Lipin-1 is found mainly in adipose tissue, while lipin-2 is present mainly in liver.

The second pathway for biosynthesis of phosphatidylcholine involves sequential methylation of phosphatidylethanolamine, with S-adenosylmethionine as the source of methyl groups, with mono- and dimethylphosphatidylethanolamine as intermediates and catalysed by the enzyme phosphatidylethanolamine N-methyltransferase. A single enzyme (~20 Kda) in two isoforms catalyses all three reactions in hepatocytes; the main form is located in the endoplasmic reticulum (ER) where it spans the membrane, while the second is found in the mitochondria-associated ER membrane; at least two N-methyltransferases are present in yeasts. This is a major pathway in the liver, generating one third of the phosphatidylcholine in this organ, but not in other animal tissues or in general in higher organisms. It may be the main route to phosphatidylcholine in those bacterial species that produce this lipid and in yeasts, but it does not appear to operate in higher plants. When choline is deficient in the diet, this liver pathway is especially important.

Second biosynthetic route to phosphatidylcholine

Phosphatidylcholine biosynthesis by both pathways in the liver is necessary for normal secretion of the plasma lipoproteins (VLDL and HDL), and it is relevant to a number of human physiological conditions. A by-product of the biosynthesis of phosphatidylcholine from phosphatidylethanolamine is the conversion of S‑adenosylmethionine to S‑adenosylhomocysteine, which is hydrolysed in the liver to adenosine and homocysteine. An elevated level of the latter in plasma is a risk factor for cardiovascular disease and myocardial infarction.

It should be noted that all of these pathways for the biosynthesis of diacylphosphatidylcholine are very different and are separated spatially from that producing alkylacyl- and alkenylacyl-phosphatidylcholines de novo. Also, synthesis of phosphatidylcholine does not occur uniformly throughout the endoplasmic reticulum but is located at membrane interfaces or where it meets other organelles, and especially where the membrane is expanding dynamically.

A third pathway for phosphatidylcholine biosynthesis was found first in one bacterial species symbiotic with plants (Sinorhizobium meliloti), though it is now known to occur more widely. In this instance, the lipid is formed in one step via condensation of choline directly with CDP-diacylglycerol, with cytidine monophosphate (CMP) formed as a by-product; the choline comes from the host plant. In Agrobacterium species and some other bacteria, both this route and that via phosphatidylethanolamine operate.

Phosphatidylcholine biosynthesis via a bacterial pathway

The yeast Saccharomyces cerevisiae and some plant species are able to reacylate endogenously generated glycero-phosphocholine with acyl-CoA in the microsomal membranes by means of a glycerophosphocholine acyltransferase (GPCAT), first to lysophosphatidylcholine and then to phosphatidylcholine; the enzyme can also use lysophospholipids as acyl donors. While phosphatidylcholine is a major lipid in yeasts, recent work suggests that it is not essential if suitable alternative growth substrates are available, unlike higher organisms where perturbation of phosphatidylcholine synthesis can lead to inhibition of growth or even cell death.

Alternative route for phosphatidylcholine biosynthesis in yeasts and some plants species

In plant cells, phosphatidylcholine biosynthesis occurs mainly in the endoplasmic reticulum, and it is a major components of most membranes other than the internal membranes of plastids; it is absent from the thylakoids and the inner envelope membrane, but is the main glycerolipid of the outer monolayer of the outer envelope membrane. Further complications arise in plants in that turnover or partial synthesis via lysophosphatidylcholine occurs in different organelles from different fatty acid pools or with enzymes with differing specificities, and in addition fatty acids esterified to phosphatidylcholine serve as substrates for desaturases. The result is that an appreciable pool of the diacylglycerols for the biosynthesis of triacylglycerols, galactosyldiacylglycerols and other glycerolipids pass through phosphatidylcholine as an intermediate, so that the fatty acid compositions in different membranes change after the initial synthetic process. This mechanism has obvious differences from the remodelling of molecular species in animal tissues discussed next, although a comparable exchange of acyl groups does occur in part catalysed by the GPCAT enzyme.

Remodelling - the Lands' cycle: Whatever the mechanism of biosynthesis in animal tissues, it is apparent that the fatty acid compositions and positional distributions on the glycerol moiety are determined post synthesis by extensive re-modelling involving orchestrated reactions of hydrolysis (phospholipase A2 mainly) to lysophosphatidylcholine, acyl-CoA synthesis and re-acylation by lysophospholipid acyltransferases or transacylases, a process that is sometimes termed the 'Lands' Cycle' after its discoverer W.E.M. (Bill) Lands. There are at least fifteen different groups of enzymes in the phospholipase A2 super-family, which differ in calcium dependence, cellular location and structure. All hydrolyse the sn-2 ester bond of phospholipids specifically, generating a fatty acid and lysophospholipid, both of which have important functions in their own right in addition to their role in the Lands cycle. There is also a phospholipase A1, which is able to cleave the sn-1 ester bond.

The Lands' cycle and phosphatidylcholine

The re-acylation step is catalysed by membrane-bound coenzyme A-dependent lysophosphatidylcholine acyltransferases such as LPCAT3 (also designated ‘MBOAT5’), which has been located chiefly within the endoplasmic reticulum, though also in mitochondria and the plasma membrane, in organs such as the liver, adipose tissue and pancreas. This enzyme incorporates linoleoyl and arachidonoyl chains specifically into lysophosphatidylcholine as does a related enzyme LPCAT2. While LPCAT3 prefers 1-acyl lysophosphatidylcholine as an acyl acceptor, LPCAT2 utilizes both 1-acyl and 1-alkyl precursors. LPCAT2 is highly expressed in inflammatory cells such as macrophages and neutrophils, which contain ether-phospholipids, where it contributes to the production of eicosanoid lipid mediators. The highly saturated molecular species of phosphatidylcholine found in lung surfactant are formed from species with a more conventional composition by remodelling by an acyltransferase with a high specificity for palmitoyl-CoA acid (LPCAT1). These and further related enzymes are involved in remodelling of all other phospholipids.

Catabolism: Phosphatidylcholine in membranes can be metabolized by lipolytic enzymes, some isoforms of which are specific for this lipid in humans. For example, in addition to the action of phospholipase A (above),phospholipase C yields diacylglycerols and phosphocholine, while phospholipase D produces phosphatidic acid and choline (see the web pages on the lipid products for further discussion).

Hydrolysis of phosphatidylcholine by phospholipases C and D

On catabolism in this way, the lipid components are re-cycled or have signalling functions, while much of the choline is re-used for phosphatidylcholine biosynthesis, often after being returned to the liver (the CDP-choline cycle). Some choline is oxidized in the kidney and liver to betaine, which serves as a donor of methyl groups for S-adenosylmethionine production, and some is lost through excretion of phosphatidylcholine in bile. A proportion is used in nervous tissues for production of acetylcholine, a neurotransmitter of importance to learning, memory and sleep. Phosphatidylcholine in the high-density lipoproteins of plasma is taken up by the liver, and perhaps surprisingly a high proportion of this is eventually converted to triacylglycerols via diacylglycerol intermediates.


3.  Phosphatidylcholine – Biological Functions

Because of the generally cylindrical shape of the molecule, phosphatidylcholine organizes spontaneously into bilayers, so it is ideally suited to serve as the bulk structural element of biological membranes, and as outlined above it is makes up a high proportion of the lipids in the outer leaflet of the plasma membrane. The unsaturated acyl chains are kinked and confer fluidity on the membrane. Such properties are essential to act as a balance to those lipids that do not form bilayers or that form specific micro-domains such as rafts. While phosphatidylcholine does not induce curvature of membranes, as may be required for membrane transport and fusion processes, it can be metabolized to form lipids that do.

In contrast, dipalmitoyl phosphatidylcholine is the main surface-active component of human lung surfactant, although in other animals the lung surfactant can be enriched in some combination of short-chain disaturated and monounsaturated species, mainly palmitoylmyristoyl- and palmitoylpalmitoleoyl- in addition to the dipalmitoyl-lipid. This is believed to provide alveolar stability by decreasing the surface tension at the alveolar surface to a very low level. Also, the internal lipids of the animal cell nucleus (after the external membrane has been removed) contain a high proportion of disaturated phosphatidylcholine. This is synthesised entirely within the nucleus, unlike phosphatidylinositol for example, and in contrast to other cellular lipids its composition cannot be changed by extreme dietary manipulation; it has been suggested that it may have a role in stabilizing or regulating the structure of the chromatin, as well as being a source of diacylglycerols with a signalling function. A further unique molecular species, 1-oleoyl-2-palmitoyl-phosphatidylcholine, is located specifically at the protrusion tips of neuronal cells and appears to be essential for their function, while 1-palmitoyl-2-arachidonoyl-phosphatidylcholine is important in the regulation of the progression of the cell cycle and cell proliferation, and this is independent of eicosanoid production.

Phosphatidylcholine is present bound non-covalently in the crystal structures of a number of membrane proteins, including cytochrome c oxidase and yeast cytochrome bc1. The ADP/ATP carrier protein has two binding sites for phosphatidylcholine, one on each side. In addition, it is known that the enzyme 3-hydroxybutyrate dehydrogenase requires to be bound to phosphatidylcholine before it can function optimally. Both the head group and the acyl chains may be involved in the interactions depending on the protein.

Scottish thistleAs noted above, phosphatidylcholine is by far the most abundant phospholipid component in plasma and in all plasma lipoprotein classes. Although it is especially abundant in high density lipoproteins (HDL), it influences strongly the levels of all circulating lipoproteins and especially of the very-low-density lipoproteins (VLDL), which are surrounded by a phospholipid monolayer. Indeed, phosphatidylcholine with polyunsaturated fatty acids in position sn-2 is essential for the assembly and secretion of VLDLs and chylomicrons in liver and the intestines. Similarly, phosphatidylcholine synthesis is required to stabilize the surface of lipid droplets in tissues where triacylglycerols are stored.

Some of the phosphatidylcholine synthesised in the liver is secreted into bile by a specific flippase together with bile acids where it assists in the emulsification of dietary triacylglycerols in the intestinal lumen to facilitate their hydrolysis and uptake. Eventually, it is absorbed across the intestinal brush border membrane after hydrolysis to lysophosphatidylcholine, which may then be involved in the initiation of chylomicron formation in the endoplasmic reticulum of enterocytes by activation of a protein kinase. In addition, phosphatidylcholine produced in enterocytes is secreted into the intestinal lumen and forms part of the hydrophobic mucus layer that protects the intestinal surface.

Phosphatidic acid generated from phosphatidylcholine by the action of phospholipase D in plants has key signalling functions. Similarly, phosphatidic acid generated in this way from phosphatidylcholine in animals is involved in the metabolism and signalling function of phosphoinositides by activating phosphatidylinositol 4-phosphate 5-kinase, the main enzyme generating the lipid second messenger phosphatidylinositol-4,5-bisphosphate. The plasmalogen form of phosphatidylcholine may also have a signalling function, as thrombin treatment of endothelial cells activates a selective hydrolysis (phospholipase A2) of molecular species containing arachidonic acid in the sn-2 position, releasing this fatty acid for eicosanoid production, while the diacyl form of phosphatidylcholine may have a related function in signal transduction in other tissues. In addition, phosphatidylcholine may have a role in signalling via the generation of diacylglycerols by phospholipase C, especially in the nucleus. Although the pool of the precursor is so great in many tissues that turnover is not easily measured, the presence of phospholipases C and D specific for phosphatidylcholine that are activated by a number of agonists suggests such a function especially in the cell nucleus. Diacylglycerols formed in this way would be much more saturated than those derived from phosphatidylinositol, and would not be expected to be as active. Phosphatidylcholine is the biosynthetic precursor of sphingomyelin and as such must have some influence on the many metabolic pathways that constitute the sphingomyelin cycle. It is also a precursor for phosphatidic acid, lysophosphatidylcholine and platelet-activating factor, each with important signalling functions, and of phosphatidylserine.

Because of the increased demand for membrane constituents, there is enhanced synthesis of phosphatidylcholine in cancer cells and solid tumours; the various biosynthetic and catabolic enzymes are seen as potential targets for the development of new therapeutic agents. Impaired phosphatidylcholine biosynthesis has been observed in a number of pathological conditions in the liver in humans, including the development of non-alcoholic fatty liver disease, liver failure and impaired liver regeneration. Similarly, a deficiency in phosphatidylcholine or an imbalance in the ratio of phosphatidylcholine to phosphatidylethanolamine has negative effects upon insulin sensitivity and glucose homeostasis in skeletal muscle.

Diacylglycerols formed by the action of a family of enzymes of the phospholipase C type on phosphatidylcholine may be more important in plants, especially during phosphate deprivation, for the generation of precursors for galactolipid biosynthesis and perhaps for lipid re-modelling more generally. In prokaryotes, phosphatidylcholine is essential for certain symbiotic and pathogenic microbe-host interactions. For example, in human pathogens such as Brucella abortus and Legionella pneumophila, this lipid is necessary for full virulence, and the same is true for plant pathogens, such as Agrobacterium tumefaciens. Bacteria symbiotic with plants, e.g. the rhizobial bacterium Bradyrhizobium japonicum, require it to establish efficient symbiosis and root nodule formation.


4.  Lysophosphatidylcholine

Formula of lysophosphatidylcholineLysophosphatidylcholine, with one mole of fatty acid per mole of lipid in position sn-1, is found in trace amounts in most animal tissues (at greater concentrations, it disrupts membranes). It is produced by hydrolysis of dietary and biliary phosphatidylcholine and is absorbed as such in the intestines, but it is re-esterified before being exported in the lymph. In addition, it is formed in most tissues by hydrolysis of phosphatidylcholine by means of the superfamily of phospholipase A2 enzymes as part of the de-acylation/re-acylation cycle that controls the overall molecular species composition of the latter, as discussed above. In plasma of animal species, an appreciable amount of lysophosphatidylcholine is formed by the action of the enzyme lecithin:cholesterol acyltransferase (LCAT), which is secreted from the liver. This catalyses the transfer of fatty acids from position sn-2 of phosphatidylcholine to free cholesterol in plasma, with formation of cholesterol esters and of course of lysophosphatidylcholine, which consists of a mixture of molecular species with predominately saturated and mono- and dienoic fatty acid constituents (see also our web page on lipoproteins). In plasma, it is bound to albumin and lipoproteins so that its effective concentration is reduced to a safe level. Identification of a highly specific phospholipase A in peroxisomes that is unique in generating sn-2-arachidonoyl lysophosphatidylcholine suggests that this may be of relevance to eicosanoid generation and signalling.

Lysophosphatidylcholine has pro-inflammatory properties and it is known to be a pathological component of oxidized lipoproteins (LDL) in plasma and of atherosclerotic lesions; for example, there is reportedly a specific enrichment of 2-arachidonoyl-lysophosphatidylcholine in carotid atheroma plaque from type 2 diabetic patients. Recently, it has been found to have some functions in cell signalling, and specific receptors (coupled to G proteins) have been identified. It activates the specific phospholipase C that releases diacylglycerols and inositol triphosphate with resultant increases in intracellular Ca2+ and activation of protein kinase C. It also activates the mitogen-activated protein kinase in certain cell types, and it promotes demyelination in the nervous system. In vascular endothelial cells, it induces the important pro-inflammatory mediator cyclooxygenase-2 (COX-2), a key enzyme in prostaglandin synthesis. Some biological effects of lysophosphatidylcholine may be simply due to its ability to diffuse readily into membranes, altering their curvature and indirectly affecting the properties of membrane proteins.

In contrast, stearoyl lysophosphatidylcholine has an anti-inflammatory role in that it is protective against lethal sepsis in experimental animals by various mechanisms, including stimulation of neutrophils to eliminate invading pathogens through a peroxide-dependent reaction. Similarly, there are suggestions that lysophosphatidylcholine may have beneficial effects in rheumatoid arthritis.

Via the action of the enzyme autotaxin, lysophosphatidylcholine is the precursor of the key lipid mediator lysophosphatidic acid, which may be the true source of some of the effects described for the former, especially on cell migration and survival.

Amylose-rich starch granules of cereal grains contain lysophosphatidylcholine as virtually the only lipid in the form of inclusion complexes or lining channels in the macromolecules.


5.  Other Phosphatidylcholine Analogues

Phosphatidylarsenocholine is a minor component of the lipids of a number of marine organisms and is discussed in the web page dealing with arsenolipids. Similarly, phosphatidylsulfocholine is described on the web page dealing with sulfonolipids. Platelet-activating factor (PAF) or 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine is an ether analogue of phosphatidylcholine that has its own web page because of its unique biological properties.


6.  Analysis

Analysis of phosphatidylcholine presents no particular problems. It is readily isolated by thin-layer or high-performance liquid chromatography methods. Determination of the dipalmitoyl species in lung surfactant is more demanding, but specific methods have been published, and modern mass spectrometry methodology has greatly simplified the task. Phospholipase A2 from snake venom is used in methods to determine the position of fatty acids on the glycerol moiety. Lysophosphatidylcholine can be formed inadvertently and over-estimated as a consequence of careless extraction of lipids from tissues.


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Lipid listings Credits/disclaimer Updated: October 6th, 2017 Author: William W. Christie LipidWeb icon