bluuebunny/crossref_metadata_2025_split huggingface dataset:
The effect of 5,8,11,14‐eicosatetraynoic acid on lipid metabolism
Authors: Tobias L. D. , Hamilton J. G. 
Published: November 2006

AbstractThe purpose of this presentation is to review the current state of knowledge regarding 5,8,11,14‐eicosatetraynoic acid (ETYA, Ro 3‐1428) and its effects on lipid metabolism. Accordingly, the topics discussed include hypocholesterolemic and dermatological studies involving ETYA in both animals and man, as well as the effects of ETYA on desaturate enzymes. Metabolic studies involving ETYA are also noted. Primary interest is focused on the effects of ETYA on selected processes of arachidonate metabolism, and the effect of ETYA on inflammation, platelet aggregation and tumor growth are discussed, keeping in mind the relevance of arachidonate metabolism to these processes.
Stereospecificity of linoleic acid hydroperoxide isomerase from corn germ
Authors: Gardner H. W. 
Published: November 2006

AbstractLinoleic acid hydroperoxide isomerase from corn germ inverted the stereoconfiguration of its substrate. 9‐D(S)‐Hydroperoxy‐trans‐10,cis‐12‐octadecadienoic acid was converted to 10‐oxo‐9‐L(R)‐hydroxy‐cis‐12‐octadecenoic acid. Presumably, the H2O solvent of OH− acted as a nucleophile. In the presence of another nucleophile, linoleate, the 9‐D(S)‐hydroperoxide was transformed into 9‐L(R)‐linoleoyloxy‐10‐oxo‐cis‐12‐octadecenoic acid. The substitution of nucleophiles from the incubation solution and the inversion of stereoconfiguration at carbon‐9 are consistent with a bimolecular nucleophilic substitution (SN2) mechanism.
Oxidative activation of guanylate cyclase by prostaglandin endoperoxides and fatty acid hydroperoxides
Authors: Graff Gustav , Stephenson Janish H. , Winget Rodner R. , Goldberg Nelson D. 
Published: November 2006

AbstractPurified prostaglandin endoperoxides (PGG2 and PGH2) and hydroperoxides (15‐OOH‐PGE2) as well as fatty acid hydroperoxides (12‐OOH‐20∶4, 15‐OOH‐20∶4, and 13‐OOH‐18∶2) were examined as effectors of soluble splenic cell guanylate cyclase activity. The procedures employed for the preparation and purification of these components circumvented the use of diethyl ether which obscured effects of lipid effectors because of contaminants presumed to be ether peroxides which were stimulatory to the cyclase. Addition of prostaglandin endoperoxides or fatty acid hydroperoxides to the reaction mixture led to a time‐dependent activation of guanylate cyclase activity; 2.5‐to 5‐fold stimulation was seen during the first 6 min. The degree of stimulation and rate of activation were dependent on the concentration of the fatty acid effector; when initial velocities (6 min) were assessed, half maximal stimulation was achieved in the range of 2 to 3 μM. However, by extending the incubation time to 90 min, similar maximal increases in specific activity could be achieved with 3 or 10 μM PGG2 or PGH2. Activation of guanylate cyclase upon addition of prostaglandin endoperoxides or fatty acid hydroperoxides was prevented or reversed by the thiol reductants dithiothreitol (3 to 5 mM) or gluthathione (10 to 15 mM). Na2S2O4, not known as an effective reducing agent of disulfieds, prevented but was relatively ineffective in reversing activation after it had been induced by PGG2. Pretreatment of the enzyme preparation with increasing concentrations of N‐ethyl‐maleimide in the range of 0.01 to 1.0 mM prevented activation by PGG2 without effecting basal guanylate cyclase activity. These observations indicate that fatty acid hydroperoxides and prostaglandin endoperoxides promote activation of the cyclase by oxidation of enzyme‐related thiol functions. In contrast, PGE2, PGF2α, hydroxy fatty acids (13‐OH‐18∶2, 12‐OH‐20∶4) as well as saturated (18∶0), monoenoic (18∶1), dienoic (18∶2), and tetraenoic (20∶4) fatty acids were ineffective in promoting cyclase activation in the range of 1 to 10 μM. Studies to identify the species of the rapidly metabolized prostaglandin endoperoxides that serve as effectors of the cyclase indicated that PGG2 but not 15‐OOH‐PGE2 (the major buffer‐rearrangement product of PGG2) is most likely an activator. In the case of PGH2 a rapidly generated (30 sec) metabolite of PGH2 was found which contained a hydroperoxy or endoperoxy functional group and was equally as effective as PGH2 as an apparent activator of the enzyme. The combined effects of PGG2 and dehydroascorbic acid, another class of activator, exhibited additivity with respect to the rate at which the time‐dependent activation was induced. These results suggest that activation of soluble guanylate cyclase from splenic cells can be achieved by the oxidation of sulfhydryls that may be associated with specific hydrophobic sites of the enzyme or a related regulatory component.
Molecular species of sphingomyelin in sphingomyelinase‐sensitive and sphingomyelinase‐resistant pools of HL‐60 cells
Authors: Fitzgerald Veronica , Blank Merle L. , Snyder Fred 
Published: November 2006

AbstractThis study of sphingomyelin molecular species in undifferentiated and differentiated (granulocytic form) HL‐60 cells demonstrated only minor differences in the distribution of species between the sphingomyelinase‐sensitive and sphingomyelinase‐resistant pools of sphingomyelin in these cells. The two most prominent species of sphingosine present in both the undifferentiated and differentiated cells were those containing 16∶0 (slightly higher in the sphingomyelinase‐resistant membranes) and 24∶1N‐acyl moieties. Cell differentiation exerted little effect on the distribution of molecular species of sphingomyelin between the sphingomyelinase‐sensitive and sphingomyelinase‐resistant pools in HL‐60 cells, although the levels ofN‐palmitoyl sphinganine were significantly lower and theN‐nervonoyl sphingosine higher in both pools from the differentiated cells. Our results indicate the same species of sphingomyelin, available at both the outer layer of the plasma membrane and inner layer of the plasma membrane (plus intracellular membranes) of HL‐60 cells, serve as precursors for generation of the ceramides that participate in signal transduction processes initiated by cell activation.
Lipid changes in HL‐60 cells on differentiation into macrophages by treatment with a phorbol ester
Authors: Manning Ray , Fallani Anna , Ruggieri Salvatore 
Published: November 2006

AbstractWe studied changes in lipid composition of human promyelocytic leukemia cells (HL‐60) on differentiation to the macrophage/monocytic lineage by treatment with the phorbol ester, 12‐O‐tetradecanoyl‐phorbol‐13‐acetate. Differentiation was accompanied by: (i) a decrease in the level of phospholipids; (ii) a greater amount of triacylglycerols; (iii) an increase in 1‐alk‐1′‐enyl‐2‐acyl‐ and 1‐alkyl‐2‐acyl‐sn‐glycero‐3‐phosphoethanolamine and a decrease in 1‐alkyl‐2‐acyl‐sn‐glycero‐3‐phosphocholine; and (iv) an increase in the level of arachidonic acid in ethanolamine phospholipids. The increased levels of ether‐linked lipids and of arachidonic acid in ethanolamine phospholipids are consistent with an enhanced biosynthesis of platelet‐activating factor and eicosanoids, which are particularly important in the macrophage function.
Pathogenesis of oleic acid‐induced lung injury in the rat: Distribution of oleic acid during injury and early endothelial cell changes
Authors: Beilman Greg 
Published: November 2006

AbstractOleic acid‐induced lung injury, a well‐described laboratory model for acute pulmonary injury in the rat and other species, causes morphologic and cellular changes similar to human adult respiratory distress syndrome (ARDS). Experiments were performed to test the hypothesis that the initial event of oleic acid lung injury is damage of the pulmonary vascular endothelium by oleic acid, with subsequent pulmonary damage and inflammation. Oleic acid levels were followed in the lung and other tissues by measuring accumulation of14C‐oleic acid; the direct effects of oleic acid and other fatty acids on rat endothelial cells, alveolar type II cells, and hepatocytes in culture were determined. Lung tissue from treated rats was also examined by light and electron microscopy for evidence of endothelial cell damage. At 30 min after injury, oleic acid reached high concentrations in lung tissue as demonstrated by presence of radiolabel (3.24×10−6 moles per gram of tissue), with counts in the lung nearly an order of magnitude greater than in any other organ measured. Oleic acid was present in the lung mostly as free fatty acid (85%), and was also present in the alveolar fluid supernatans, rather than being cell‐associated (1.7×10−7 moles vs. 1.1×10−8 moles at 30 min). Oleic acid was toxic to endothelial cells after one minute of exposure at concentrations of 5×10−4M and above. Electron microscopy showed endothelial cell changes as early as 10 min after induction of injuryin vivo, including the presence of endothelial cell blebbing. The results of these studies suggest that the initial event in oleic acid lung injury is damage to the pulmonary vascular endothelial cell.
Thyroid hormone is required for dietary fish oil to induce hypersecretion of biliary cholesterol in the rat
Authors: Prigge William F. , Ketover Scott R. , Gebhard Roger L. 
Published: November 2006

AbstractIn the rat, both fish oil diet and thyroid hormone replacement are reported to augment bile cholesterol secretion out of proportion to bile flow or secretion of other bile lipids. We sought common mechanisms for these effects and evaluated the role of phospholipid fatty acid composition in the process. Methimazole‐treated hypothyroid rats were fed low‐fat chow or chow supplemented with 10% corn oil or fish oil, and were studied before and after thyroid hormone treatment. Serum, hepatic, and bile lipids were measured, phospholipid fatty acid composition determined, and hepatic 3‐hydroxy‐3‐methylglutaryl CoA reductase activity assayed. Fish oil diet stimulated cholesterol secretion into bile only after thyroid hormone was given, and this action was synergistic with that of thyroid hormone. Reduced serum cholesterol in fish oil‐treated rats was associated with increased biliary cholesterol secretion and diminished hepatic cholesterol content. This suggests that augmented biliary cholesterol secretion may contribute to the fish oil‐induced reduction of serum cholesterol. No definite relationship between hepatic or biliary phospholipid fatty acid composition and biliary secretion was apparent, although high bile cholesterol secretion was associated with a low percentage of hepatic and bile phospholipid linoleic acid.
Enteral absorption in man of eicosapentaenoic acid in different chemical forms
Authors: Boustani S. El , Colette C. , Monnier L. , Descomps B. , Crastes de Paulet A. , Mendy F. 
Published: November 2006

AbstractAfter administering the equivalent of 1 g of eicosapentaenoic acid (EPA) in four different chemical forms, the kinetics of EPA incorporation into plasma triglycerides (TG) were compared by gas liquid chromatography on a capillary column following separation of the lipid fraction by thin layer chromatography.EPA incorporation into plasma TG was markedly smaller and later when EPA was administered as an ethyl ester rather than as EPA free fatty acid, EPA arginine salt or 1,3‐dioctanoyl‐2‐eicosapentaenoyl glycerol (2‐EPA). Our results and the data in the literature are compatible with the hypothesis that 2‐EPA is absorbed with minimum hydrolysis and escapes random distribution between the other positions of the glycerol molecule during the absorption process.
Short‐term biological reproducibility of serum fatty acid composition in children
Authors: Moilanen Teemu 
Published: November 2006

AbstractTo assess the biological day‐to‐day reproducibility of the fatty acid composition in serum lipid fractions in children on their habitual diets, fasting serum specimens were collected from healthy 8‐ to 9‐year‐old boys at 2‐day (n=21) or 7‐day (n=19) intervals. Percentage compositions of fatty acids in serum cholesteryl esters (CE), triglycerides (TG), free fatty acids (FFA) and phospholipids (PL) were analyzed by gas chromatography. The reproducibility was estimated by calculating linear correlation coefficients between the values obtained at the two time‐points. Generally the correlations were higher in CE and PL than in TG and FFA. In CE the 7‐day correlations of major fatty acids were only slightly lower than the 2‐day ones. In PL the impairment of correlations was somewhat greater than in CE, but in TG and FFA there was a marked drop in reproducibility from 2‐ to 7‐day intervals. The 2‐day correlation coefficients of the percentages of linoleate, dihomo‐γ‐linolenate, arachidonate and eicosapentaenoate in CE were 0.95, 0.84, 0.91 and 0.92, respectively. In PL, the respective values were 0.86, 0.82, 0.95 and 0.90. The persent results indicate high short‐term biological reproducibility of fatty acid composition in serum CE and PL and clearly lower in those of TG and FFA.
Calmodulin antagonists suppress cholesterol synthesis by inhibiting sterol Δ24 reductasereductase
Authors: Filipovic Ivan , Buddecke Eckhart 
Published: November 2006

AbstractPreincubation of hepatoma cells and human skin fibroblasts in the presence of the calmodulin antagonists trifluoperazine and N‐(6‐aminohexyl)‐5‐chloro‐1‐naphthalene sulfonamide resulted in a dose‐dependent suppression of [14C] mevalonolactone incorporation into cholesterol. At a calmodulin antagonist concentration of 25 μmol, the incorporation of [14C] mevalonolactone into cellular cholesterol was suppressed to about 30% (hepatoma cells) and 10% (human skin fibroblasts) of control values. When the total nonsaponifiable [14C] lipids were separated and analyzed by two‐dimensional thin layer chromatography, an accumulation of [14C] desmosterol was observed along with reduced formation of [14C] cholesterol. However, when cells were preincubated in the presence of [14C] dihydrolanosterol, [14C] cholesterol formation was not inhibited by the calmodulin antagonists. About 25% of the cell‐associated dihydrolanosterol radioactivity was converted to cholesterol in both control and calmodulin antagonist‐pretreated cells. The data suggest that calmodulin antagonists prevent the conversion of desmosterol into cholesterol by inhibiting sterol Δ24 reductase and that the enzymes catalyzing sterol ring modifications are not affected by the inhibitors.
Effect of environmental temperature changes on liver Δ6 and Δ5 fatty acid desaturases depressed by hyperglycidic diet on male rats
Authors: Losada Ana Ves , Peluffo Raúl O. 
Published: November 2006

AbstractMale rats maintained on a control diet at 24 C and shifted to 12 C for five days showed no modification in Δ6 or Δ5 desaturase activity. When Δ6 and Δ5 desaturase activities were diminished by a hyperglycidic diet, shifting to cold increased both enzymatic activities. In general, modifications observed in liver microsomal fatty acid composition are consistent with those associated with the enzymatic desaturation activity.
Acyltransferases in subcellular fractions of developing seeds of rape (Brassica napus L.)
Authors: Murphy Denis J. , Mukherjee Kumar D. 
Published: November 2006

AbstractAcyltransferase activities responsible for the transfer of oleoyl moieties from oleoyl‐CoA to various lipids have been examined in subcellular fractions of developing seeds of rape,Brassica napus L. In the absence of exogenous acyl acceptors, the microsomal and oil body fractions transferred oleoyl moieties mostly to phosphatidylcholines and phosphatidic acids, although there was substantial incorporation of the oleoyl moieties into monoacylglycerols, diacylglycerols and triacylglycerols. The soluble (150,000‐g supernatant) fraction incorporated oleoyl moieties mainly into the neutral lipids (monoacylglycerols and diacylglycerols) and also exhibited a relatively high acyl‐CoA hydrolase activity. In the presence of the exogenous acyl acceptors, lysophosphatidylcholine and lysophosphatidic acid, both microsomal and oil body fractions transferred most of the oleoyl moieties to phosphatidylcholines and phosphatidic acids, respectively. Other lysophospholipids, such as lysophosphatidylethanolamine and lysophosphatidylonositol, were not very effective as acyl acceptors, nor were glycerol‐3‐phosphate, monoacylglycerols or diacylglycerols. In contrast, the soluble fraction showed little or no stimulation of acyltransfer in the presence of exogenous lysophospholipids but was able to utilize, to some extent, exogenous monoacylglycerols and diacylglycerols as acyl acceptors.
The kinetics of the autoxidation of polyunsaturated fatty acids
Authors: Cosgrove John P. , Church Daniel F. , Pryor William A. 
Published: November 2006

AbstractThe kinetics of the autoxidation of a series of polyunsaturated fatty acids (PUFA) with increasing degrees of unsaturation and the mono‐, di‐and triglycerides of linoleate have been studied in homogeneous chlorobenzene solution at 37 C under 760 torr of oxygen. The autoxidations were initiated by thermal decomposition of azo initiators and followed by measuring the rate of oxygen uptake. The rate of chain initiation was determined by the induction period method using α‐tocopherol as the chainbreaking antioxidant. The measured oxidizabilities of the PUFA are linearly dependent on the number of doubly allylic positions present in the molecule. Thus, the oxidizability of linoleate is 2.03×10−2 M−1/2 sec−1/2, and the value for docosahexaenoate is five times greater, 10.15×10−2 M−1/2 sec−1/2. The rate of autoxidation for all PUFA studied and for the mono‐ and diglyceride is proportional to the substrate concentration and to the square root of the rate of chain initiation, implying that the autoxidation of these compounds follows the usual kinetic rate law. The autoxidation of the triglyceride is more complex and does not appear to follow the same rate law at all substrate concentrations. This deviation from the usual kinetic rate expression may be due to lipid aggregation at low concentrations of the triglyceride.
Comparison of the clearances of serum chylomicron triglycerides enriched with eicosapentaenoic acid or oleic acid
Authors: Chen Isabel S. , Le Truc , Subramanian Satchithanandam , Cassidy Marie M. , Sheppard Alan J. , Vahouny George V. 
Published: November 2006

AbstractRat mesenteric lymph chylomicrons containing triglycerides enriched with either [14C]oleic acid (OA) or [14C]‐eicosapentaenoic acid (EPA) were prepared by ultracentrifugation of lymph samples collected for 6 hr after a single duodenal infusion of an emulsion containing either fatty acid. These chylomicrons were injected into the jugular vein of recipient rats and, at various time intervals, blood was drawn and serum was assayed for radioactivity. In separate animals, serum lipoprotein fractions were separated by ultracentrifugation, and the redistribution of labeled fatty acid among circulating lipoproteins was determined by liquid scintillation spectrometry. When the early disappearance rates (10 min) of either total serum radioactivity or specifically the chylomicron fraction were compared, there were no differences between the groups receiving OA‐or EPA‐enriched chylomicrons. However, disappearance rates of EPA‐enriched chylomicrons were slower than those of OA‐enriched chylomicrons from 25 to 90 min. The small but significant differences in the disappearance rates for the longer time periods cannot be ascertained without further studies. At 5 min after injection of either type of chylomicron, the d<1.006 g/ml lipoprotein fraction of serum chylomicrons and very low density lipoproteins contained almost 90% of the original radioactivity. By 240 min, when less than 2% of the radioactivity remained, this radioactivity in the d<1.006 g/ml fraction was 43–46%, with concomitant increases in the low and high density lipoprotein fractions and in the lipoprotein‐free serum.
Thermal and metal‐catalyzed decomposition of methyl linolenate hydroperoxides
Authors: Frankel E. N. , Neff W. E. , Selke E. , Brooks D. D. 
Published: November 2006

AbstractMuch work has been reported on the volatile oxidative products of fats and their impact on flavor deterioration, cellular damage and the decrease in safety of fatcontaining foods. However, relatively little information is available on the mechanism of hydroperoxide decomposition. Pure methyl linolenate hydroperoxides were decomposed thermally at 150 C and catalytically with ferric chloride‐ascorbic acid at room temperature. The volatile decomposition products were collected on porous polymer (Tenax) traps and concentrated by gel permeation chromatography. The total volatile products showed significant differences in composition by capillary gas chromatography‐mass spectrometry (GC‐MS). Thermal decomposition produced much more methyl octanoate (60.1%) and less 2,4‐heptadienal (0.5%) than catalytic decomposition (13.2 and 60.8%, respectively). The volatiles from the ferric chloride‐ascorbic acid system also contained unique products tentatively identified by GC‐MS as isomers of chloromethyl butene. These results may have important implications in evaluating precursors of flavor deterioration in vegetable oils containing linolenate and in understanding better the biological significance of lipid peroxidation.
Platelet‐activating factor modulates phospholipid acylation in human neutrophils
Authors: Tou Jen‐sie 
Published: November 2006

AbstractThe present study showed that platelet‐activating factor (1‐O‐hexadecyl‐2‐acetyl‐sn‐glycero‐3‐phosphocholine, PAF), but not lysoPAF (1‐O‐hexadecyl‐sn‐glycero‐3‐phosphocholine) rapidly (within 15 sec) stimulated the incorporation of both [1‐14C]arachidonate and [1‐14C]docosahexaenoate into phosphatidylinositol (PI) and phosphatidylcholine (PC) in human neutrophils. Concomitantly, it inhibited the formation of labeled phosphatidic acid from both fatty acids. The magnitude of stimulation (percentage of control) was greater in PI than in PC for the incorporation of arachidonate and vice versa for the incorporation of docosahexaenoate. It reached a maximum at 10−7 M and started to decline at 10−6 M. Extracellular Ca2+ was not essential for the action of PAF on phospholipid acylation. The distribution of labeled arachidonate in the molecular species of PC was not altered by PAF after 1 min incubation, suggesting that the increased formation of arachidonyl‐PC during the early stage of neutrophil‐PAF interaction was not originated from the added PAF. No measurable changes in the mass of each phospholipid were detected in neutrophils challenged by PAF from 15 sec to 2 min. The data suggest that the increased incorporated of extracellular fatty acids into PI and PC elicited by PAF may be secondary to increased deacylation of these phospholipids, and the magnitude of stimulation reflects the specificity of acyltransferase catalyzing the acylation of lysoPI and lysoPC by fatty acyl‐CoA.
High performance liquid chromatographic analysis of 1‐alkyl‐2‐acyl‐ and 1‐alkyl‐3‐acyl‐sn‐glycerols
Authors: Foglia Thomas A. , Vail P. D. , Iwama Takashi 
Published: November 2006

AbstractA high performance liquid chromatographic (HPLC) method is described for separation and quantitation of 1‐alkyl‐3‐acyl‐ and 1‐alkyl‐2‐acyl‐sn‐glycerol, products of the detritylation reaction of 1‐alkyl‐2‐acyl‐3‐trityl‐sn‐glycerol. The alkyl glycerides were separated on a 25 cm×4.6 mm ID column packed with ∼5–6 μm silica and eluted isocratically with isooctane/isopropanol (98∶2, v/v) as mobile phase. The good separation and linear refractive index (RI) detector responses using cholesterol as an internal standard indicated the applicability of the method not only for the quantitative determination of the alkylglycerols but also for their semipreparative isolation. This HPLC method shows excellent reproducibility and accuracy and is applicable to other types of glycerides such as mono‐ and diacylglycerols.