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Biomedical subjects

F Snyder

Publications and source records attributed to F Snyder.

286 records · Page 16Linked to original sources
PubMed1967

Characterization and identification of glyceryl ether diesters present in tumor cells.

The previously unidentified neutral lipid present in tumor tissues has been isolated from Ehrlich ascites cells and unequivocally identified as a lipid class of glyceryl ether diesters containing various degrees of unsaturation, and ranging in approximate molecular weight from 760 to 990. The glyceryl ether diester fraction was shown to be free from neutral plasmalogens (glyceryl diacyl alk-1'-enyl ethers). The tumor lipid was subjected to saponification, transesterification, and lithium aluminum hydride reduction. The glyceryl monoethers that resulted from deacylation were the 1-isomers ranging in hydrocarbon chain length from C(12) to C(24). The predominant glyceryl ethers were the hexadecyl (49%), octadecyl (21%), and octadecenyl (14%) derivatives. Saturated and mono- and polyunsaturated fatty acids ranging in chain length from C(12) to C(24) carbon atoms were esterified to the glyceryl monoether. Gas-liquid chromatography, thin-layer chromatography, and nuclear magnetic resonance and infrared spectroscopy were used to characterize and identify the intact tumor lipid and its derived products.

Animals↗
PubMedDate not supplied

Thyrotropin-releasing hormone blocks the hypotensive effects of platelet-activating factor in the unanesthetized guinea pig.

Platelet-activating factor (PAF) and leukotrienes, newly described classes of vasoactive lipids, may play a role in anaphylaxis. It has recently been suggested that the vasoconstrictor effects of PAF in isolated rat lung are related to release of leukotrienes C4 and D4. Thyrotropin-releasing hormone (TRH), a tripeptide, has potent antihypotensive activity in experimental shock, including that resulting from either leukotriene D4 administration or antigen-induced anaphylaxis. We utilized an unanesthetized guinea pig model to study the relationships among PAF, leukotrienes, and TRH and their potential interactions on the cardiovascular system. PAF (1 nmol/600 g body weight i.v.) produced profound hypotension which was completely blocked by TRH (2 mg/kg i.v.). Nafazatrom or FPL 55712, a presumed receptor antagonist of leukotrienes, was ineffective, whereas U-60257, a leukotriene synthesis inhibitor, displayed incomplete blockade. Moreover, leukotriene-like immunoreactivity in plasma did not increase following PAF administration. Thus, hypotension produced by PAF does not appear to result secondarily from release of cysteinyl leukotrienes. Moreover, the ability of TRH to block the hypotensive effects of PAF may partially account for its beneficial effects in experimental anaphylaxis and provides further rationale for the therapeutic evaluation of this peptide in anaphylactic shock.

Animals↗
PubMedDate not supplied

Intracellular location of acetyltransferase in the remodeling pathway of PAF biosynthesis in undifferentiated human leukemic cells (HL-60).

In order to determine the site of PAF synthesis via the remodeling pathway in undifferentiated HL-60 cells, a subcellular fractionation procedure (Ribbes et al., 1985) was adapted to separate various membrane fractions and cellular organelles of HL-60 cells across a Percoll gradient. The profile of alkyllyso-GPC:acetyl-CoA acetyltransferase activity closely paralleled the subcellular distribution of the endoplasmic reticulum marker, NADH dehydrogenase. These data indicate the acetyltransferase in the remodeling pathway of PAF synthesis is located at the same cellular site as the acyltransferase(s) that catalyze the transfer of long-chain acyl moieties from acyl-CoAs to lyso-phospholipids. Also the acetyltransferase in undifferentiated HL-60 cells appears to have a similar intracellular distribution as reported for human neutrophils.

Acetyltransferases↗
PubMedDate not supplied

Metabolism of platelet activating factor (PAF) and related ether lipids by neonatal rat myocytes.

Suspensions of neonatal rat myocytes were used to investigate the metabolism of [3H]PAF (1-alkyl-2-acetyl-(sn-glycero-3-phosphocholine) (GPC] and [3H]alkyllyso-GPC. [3H]Alkylacyl-GPC consisting of molecular species with four or more double bonds (87%) was the major metabolite formed when either [3H]PAF (4 x 10(-6) - 4 x 10(-9) M) or [3H]alkyllyso-GPC (2 x 10(-7) M) was the precursor. However, substantial amounts of [3H]alkyllyso-GPC (mostly in the media) were also generated from [3H]PAF during the early periods of the incubations. At 2 x 10(-7) M or higher concentrations of either [3H]PAF or [3H]alkyllyso-GPC, [3H]alkylglycerols were also formed (4-12% of the total radioactivity). The [3H]alkylglycerols appear to be produced from [3H]alkyllyso-GPC through the combined actions of lysophospholipase D and a phosphatase. Pretreatment of neonatal rat myocytes with phenylmethylsulfonyl fluoride partially blocked the deacetylation of [3H]PAF and decreased both the formation and subsequent acylation of [3H]alkyllyso-GPC in intact cells. Phenylmethylsulfonyl fluoride also significantly inhibited the activity of cytosolic acetylhydrolase, but it had no direct effect on the microsomal transacylase in vitro. Our data demonstrate that the metabolism of PAF and alkyllyso-GPC by neonatal rat myocytes is qualitatively, but not quantitatively, similar to what occurs in other cell types. In addition, when [3H]alkylacetylglycerol was the precursor, 75% of the label appeared as alkylglycerols in the neonatal rat myocytes, but [3H]PAF was not detected. Therefore, it appears that the de novo pathway via the dithiothreitol-insensitive cholinephosphotransferase step does not contribute to the biosynthesis of PAF in neonatal rat myocytes.

Animals↗