Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: CAS:22276-27-3 (hexadecyl)
 2,701 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Platelet activating factor was isolated from scales of psoriatic patients by the procedure of Bligh and Dyer and purified by silica gel thin layer chromatography. The purified PAF was digested with phospholipase C and the resulting diglyceride was derivatized into PFB ethers. The PAF-PFB ethers were analyzed using fused silica capillary chromatography-negative ion chemical ionization mass spectrometry. Different molecular species of PAF were identified by their negative ion mass spectra and by their elution time from the capillary column. All the molecular species had high abdundance (greater than 90%) of the molecular anion. 1-0-Hexadecyl-2-acetyl-GPC (16:0) was the major PAF species representing 51% of the total PAF. 17:0 and 18:1 were the next abundant species representing 15 and 16%, respectively. Several minor PAF molecular species were also present. The amount of each PAF molecular species was quantitated from 1-0-hexadecyl-2-2H3 acetyl-GPC used as the internal standard. Nanogram quantities of PAF were recovered from 100 mg of psoriatic scales. Significant amounts of lysoPAF were also present in these scales. The alkyl chain of the lysoPAF was compared with that of PAF.
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PMID:Identification and quantitation of PAF from psoriatic scales. 368 90

Acetyl-CoA: lyso platelet activating factor (1-O-alkyl-2-lyso-sn-glycero-3-phosphorylcholine) acetyltransferase was solubilized from rat spleen microsomes with ultrasonic irradiation in the presence of 25% glycerol and partially purified by Sepharose 6B column chromatography. The overall yield of this procedures was approximately 26% and its specific activity was 1.7 times compared with that of original microsomes. The solubilized enzyme was extremely labile, but did not lose the activity for several weeks at -70 degrees C. The solubilized enzyme was remarkably susceptible to various kinds of metal ions. Furthermore, sulfhydryl reagents such as N-ethylmaleimide and p-chloromercuribenzoate profoundly inhibited the enzyme reaction, suggesting that the enzyme was -SH enzyme. The acetyltransferase activity was remarkably decreased by tryptic digestion of spleen microsomes, which indicated that the enzyme was located in the cytoplasmic surface of microsomal membranes. On the substrate specificity, the enzyme preferentially acetylated 1-O-hexadecyl-2-lyso-sn-glycero-3-phosphorylcholine and 1-O-octadecenyl-2-lyso-sn-glycero-3-phosphorylcholine as compared with other chain length at sn-1 position of lyso platelet activating factor, which may suggest that biologically potent molecular species of PAF are selectively synthesized. On the other hand, the enzyme also acetylated an acyl analog of lyso platelet activating factor. Some experimental results have shown that these two acetylation reaction presumably would be performed by the same enzyme.
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PMID:[Studies on acetyl-CoA:lyso platelet activating factor acetyltransferase of rat spleen microsomes--solubilization and substrate specificity]. 378 69

A combination of CN- and 2-deoxy-D-glucose decreases the binding of fibrinogen to platelets stimulated with PAF-acether (1-O-hexadecyl/octadecyl-2-acetyl-sn-glycero-3-phosphocholine). Decreased binding is found after pretreatment with metabolic inhibitors, thereby lowering the energy content before stimulation as well as at various stages after stimulation of undisturbed cells. Binding and ATP hydrolysis occur in parallel, suggesting tight coupling between both phenomena. Energy appears to be predominantly required for exposure and maintenance of accessible binding sites, whereas the interaction between fibrinogen and the exposed sites does not depend on metabolic energy.
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PMID:PAF-acether (1-O-hexadecyl/octadecyl-2-acetyl-sn-glycero-3-phosphocholine)-induced fibrinogen binding to platelets depends on metabolic energy. 380 Sep 68

Platelet-activating factor (1-0-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine, PAF) promotes the incorporation of [1-14C]arachidonic acid most significantly into phosphatidylinositol (PI) and phosphatidylcholine (PC) during the early stages of guinea pig neutrophil-PAF interaction. The stimulation reached a maximum at 10(-7) M and started to decline at 10(-6) M. No changes in the mass of each phospholipid were detected in neutrophils challenged by PAF for 1 to 5 minutes. The stimulation by PAF on the formation of [14C]arachidonoyl-PC but not [14C]arachidonoyl-PI was dependent on the presence of external Ca2+. These results suggest that the increased acylation of PI and PC elicited by PAF is secondary to an increased deacylation of these phospholipids and the mechanisms by which PAF stimulates the deacylation of PI and PC may be different.
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PMID:Platelet-activating factor promotes arachidonate incorporation into phosphatidylinositol and phosphatidylcholine in neutrophils. 392 Oct 17

1-Alkylglycerophosphatide analogs which are known to activate macrophages to enhanced tumor cytotoxicity are structurally closely related to 1-acyl-sn-glycero-3-phosphocholine. In this study we have examined the influence of some of these compounds and of platelet-activating factor (PAF-acether, 1-0-alkyl-2-0-acetyl-sn-glycero-3-phosphocholine) on the arachidonoyl-CoA: 1-acyl-sn-glycero-3-phosphocholine acyltransferase (EC 2.3.1.23) in homogenate of bone-marrow-derived murine macrophages. This enzyme is suggested to be involved in the control of the availability of the icosanoid precursor, arachidonic acid. Kinetic experiments revealed apparent Km and V values for 1-palmitoyl-sn-glycero-3-phosphocholine of 6.0 microM and 16.10 nmol/mg protein per min, respectively. When the 1-palmitoyl-sn-glycero-3-phosphocholine concentration was equal to Km, the enzyme was dose-dependently inhibited by 1-O-octadecyl-2-O-methyl-rac-glycero-3-phosphocholine with a 50% inhibition at 30 microM. The kinetic parameters in the presence of 1-O-octadecyl-2-O-methyl-rac-glycero-3-phosphocholine (K'm = 10.0 microM, V' = 11.40 nmol X mg-1 X min-1) suggest that this alkyl phospholipid is a mixed-type inhibitor. All other alkyl analogs tested (1-O-methyl-2-O-octadecyl-rac-glycerol-3-phosphocholine, racemic PAF-acether, L-PAF-acether, D-1-O-hexadecyl-sn-glycero-3-phosphocholine, 1-O-octadecyl-rac-glycero-3-phosphocholine) inhibited the enzyme to various degrees. Arachidonic acid transfer to the 1-alkylglycerophosphatide analogs themselves could be ruled out under the assay conditions used. Therefore, we conclude that the arachidonoyl-CoA: 1-acyl-sn-glycero-3-phosphocholine acyltransferase can be inhibited by synthetic and naturally occurring ether phospholipids in homogenate of bone-marrow-derived murine macrophages.
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PMID:Ether phospholipids as inhibitors of the arachidonoyl-CoA: 1-acyl-sn-glycero-3-phosphocholine acyltransferase in macrophages. 394 67

Platelet-activating factor, 1 (PAF, 1-O-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine), and octadecyl-PAF were synthesized chemically as the racemates. The sn-1-O-alkyl isomers were isolated after treatment of the racemates with phospholipase A2 and subsequent reacetylation of the 1-O-alkyl-2-lyso-sn-glycero-3-phosphocholines released. Analogues of PAF containing unsaturated alkyl moieties at the sn-1 position (2, 4, 5) were synthesized by utilizing the methoxyethoxymethyl protecting group as a novel method for preparing unsaturated alkyl lipids. This procedure provides a facile means for preparing unsaturated either phospholipids of defined structure that may be tritiated to high radiospecific activity for metabolic studies. Unsaturation in the alkyl chain had minimal effect on the bioactivities examined in this study.
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PMID:Facile synthesis of platelet-activating factor and racemic analogues containing unsaturation in the sn-1-alkyl chain. 403 18

1-Alkyl-2-lyso-sn-glycero-3-phosphocholine:acetyl-CoA acetyltransferase catalyzes the conversion of biologically inactive lysophospholipid to bioactive platelet-activating factor (1-alkyl-2-acetyl-sn-glycero-3-phosphocholine, PAF) by an acetylation reaction. The activity of this enzyme in eosinophils isolated from patients with eosinophilia is stimulated (up to 4-fold) in a dose-, time-, and Ca2+/Mg2+-dependent manner after exposure to the eosinophil chemotactic factor of anaphylaxis (ECF-A), C5a, formyl-methionylleucylphenylalanine (fMLP), or ionophore A23187. The three naturally occurring chemotactic factors (ECF-A, C5a, and fMLP) cause a rapid and transient increase of enzyme activity, with a maximum at 1 or 3 min, whereas ionophore A23187 maintains an elevated level for up to 15 min. The activity of 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine acetylhydrolase, an enzyme that catalyzes the breakdown of PAF to lyso-PAF, is not affected by C5a, fMLP, or ionophore A23187. The presence of PAF in eosinophils was established by demonstrating the lipid nature of the compound, the RF value being identical with that of synthetic 1-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine on thin layer chromatograms, and by its ability to induce serotonin release from rabbit platelets. Furthermore, ECF-A, C5a, fMLP, and ionophore A23187 all induce the secretion of PAF from eosinophils. These findings suggest that the generation and release of PAF could be a consequence of eosinophil chemotactic activation and may thus function in inflammatory and allergic reactions in which eosinophils participate.
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PMID:Increased biosynthesis of platelet-activating factor in activated human eosinophils. 642 92

1-O-hexadecyl-2-acetyl-sn-3-glycerophosphorylcholine (PAF) was examined as a potential mediator of aggregation induced by thrombin or high concentrations of collagen in indomethacin treated platelet rich plasma by investigating the response to collagen and thrombin of platelets previously desensitized to PAF. No reduction in the response to collagen or thrombin was observed and it was concluded that PAF was not a mediator of non-prostanoid dependent aggregation in platelets exposed to thrombin or collagen.
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PMID:1-O-hexadecyl-2-acetyl-sn-3-glycerophosphorylcholine (PAF): some effects on the aggregation of human platelets by thrombin or collagen. 663 35

We have compared for rabbit platelet aggregating and desensitizing activity two different preparations of platelet-activating factor (PAF-acether) (1-O-alkyl-2-O-acetyl-sn-glycero-3-phosphocholine) and of its enantiomer (3-O-alkyl-2-O-acetyl-sn-glycero-1-phosphocholine). After phospholipase A2 treatment, the unnatural enantiomers appeared about 3000-fold less active than PAF-acether, a result which definitively establishes the stereospecificity of the mode of action of this mediator. A new structural analog of PAF-acether, 1-O-hexadecyl-3-O-acetyl-sn-glycero-2-phosphocholine, was isolated and characterized. It was a weak platelet agonist, stressing further the importance for PAF-acether activity of the acetyl group at position 2 of the glycerol.
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PMID:The enantiomer and the positional isomer of platelet-activating factor. 682 44

The beta 2-adrenergic agonist formoterol has been shown to inhibit plasma extravasation in the respiratory mucosa associated with neurogenic inflammation as well as that caused by histamine or bradykinin. It is unknown whether these effects of formoterol are mediated through an action of sensory nerves or through a direct effect on the leaky blood vessels. In the present study we sought to determine whether capsaicin-sensitive sensory nerves are essential for the anti-edema effect of formoterol in the rat trachea. Substance P (5 micrograms/kg), PAF (hexadecyl-PAF, 5 micrograms/kg), or bradykinin (10 mg/kg) was injected intravenously to increase vascular permeability. The amount of plasma extravasation was measured with two tracers, Evans blue dye and Monastral blue pigment. The effectiveness of formoterol's anti-edema action was assessed in two groups of rats. One was pretreated with capsaicin to eliminate tachykinin-containing sensory nerves and another, the control group, was not pretreated. We found that in control rats formoterol inhibited to a similar extent the extravasation of Evans blue and Monastral blue caused by all three mediators. The highest intravenous dose of formoterol (10 micrograms/kg) reduced substance P-induced extravasation of Monastral blue by 59%, reduced PAF-induced extravasation by 74%, and reduced bradykinin-induced extravasation by 58%. Pretreatment of rats with a dose of capsaicin that eliminated at least 94% of the substance P-immunoreactive nerve fibers did not significantly reduce the effectiveness of formoterol against any of the mediators.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Anti-edema action of formoterol in rat trachea does not depend on capsaicin-sensitive sensory nerves. 750 46


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