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PubMed1983

Alteration of rat heart sarcolemma lipid composition by dietary elaidic acid.

Male weanling rats were fed a semisynthetic diet containing 5% of either elaidic acid or oleic acid for 4 weeks. The heart sarcolemma were isolated and examined for purity by using marker enzymes. The sarcolemma preparations were enriched in phosphodiesterase I, 5'-nucleotidase and p-nitrophenyl phosphatase as compared with the heart homogenates. Succinic dehydrogenase activity was not detected in these preparations. The lipids of sarcolemma fractions from animals fed the trans fatty acids were enriched with the fatty acid fed. Most of this incorporation was found to be associated with the two major phospholipids, phosphatidylcholine and phosphatidylethanolamine. The incorporation of elaidic acid into the membranes resulted in an increase in membrane cholesterol without affecting either membrane phospholipid content or profile. The alterations induced in the lipid composition of heart sarcolemma by feeding this dietary trans fatty acid suggest some functional alterations in these membranes.

Animals↗
PubMed1988

Motility of the pyloric sphincter studied by the inductograph method in conscious dogs.

The aim of the study is to evaluate the motility of the pyloric sphincter in conscious dogs by means of extraluminal transducers. For this purpose induction coils were chronically implanted in 12 dogs. After a meal the pylorus opened and closed in relation to the gastric waves. The mean changes in pyloric diameter were 5.4 +/- 1.0 mm. During phase I of the interdigestive state, the mean degree of pyloric opening was 39 +/- 18%. Gastric contractions occurring during phase II or phase III were accompanied with a marked increase in pyloric diameter; the degree of pyloric opening was 93 +/- 12%. Duodenal instillations of hydrochloric acid or oleic acid significantly diminished the pyloric diameter. Nutrients added to a viscous meal also diminished the pyloric opening significantly in comparison with an acaloric meal. Results suggest that the pyloric sphincter is involved in the control of gastric emptying. The inductograph is a useful technique to study pyloric activity without impediment of luminal flow in animals.

Animals↗
PubMed1983

Pulmonary vasodilator effects of nitroglycerin and sodium nitroprusside in canine oleic acid-induced pulmonary hypertension.

The hemodynamic effects of nitroglycerin (TNG) and sodium nitroprusside (SNP) were studied in a canine model of pulmonary hypertension. Oleic acid administration resulted in pulmonary hypertension with a 133% increase in pulmonary vascular resistance (PVR), a 40% increase in mean pulmonary artery pressure (MPAP), and a 28% decrease in cardiac output (CO). In this model, subsequent TNG administration increased CO 40%, decreased PVR 43%, and decreased MPAP 12%; pulmonary hemodynamics during TNG administration were not significantly different from those prior to oleic acid administration. SNP produced systemic hypotension but did not alter either PVR or MPAP and increased CO only 14%. The efficacy of TNG in this model may relate to its ability to dilate preferentially the pulmonary vascular bed.

Animals↗
PubMed1999

Decrease and structural modifications of phosphatidylethanolamine plasmalogen in the brain with Alzheimer disease.

Several lipid modifications, some of which were attributed to oxidative stress, have been reported in the brains of patients with Alzheimer disease (AD). To evaluate this possibility, all phospholipids and their ether subclasses from the frontal cortex, hippocampus, and the white matter of AD brain were analyzed by high performance liquid chromatography and gas chromatography. The total phospholipid in the frontal cortex and hippocampus decreased on a DNA basis by about 20% and this change was essentially explained by a selective decrease in phosphatidylethanolamine and phosphatidylcholine. The lower content of phosphatidylethanolamine was due to a specific decrease in the plasmalogen subclass. Phosphatidylethanolamine plasmalogen was also the only lipid exhibiting major structural modifications: a significant decrease in polyunsaturated fatty acids and oleic acid as well as a shift of the aldehyde pattern from 18:1 to 18:0. The only modification observed in the other phospholipids was a decrease in oleic acid in diacyl-phosphatidylethanolamine and diacyl-phosphatidylcholine. None of these changes were observed in the white matter. Both the vinyl ether bond of phosphatidylethanolamine plasmalogen and polyunsaturated fatty acids are major targets in oxidative stress; thus, these specific lipid modifications strongly support the involvement of free radicals in the pathogenesis of AD.

Aged↗
PubMed1980

Characterization of an acyl-coenzyme a thioesterase associated with the envelope of spinach chloroplasts.

The enzymic hydrolysis of acyl-coenzyme A occurs in intact and purified chloroplasts. The different components of spinach chloroplasts were separated after a slight osmotic shock and the purified envelope membranes were shown to be the site of very active acyl-CoA thioesterase activity (EC 3.1.2.2.). The enzyme, which had a pH optimum of 9.0, was not affected by sulfhydryl reagents or by serine esterase inhibitors. However, the acyl-CoA thioesterase was strongly inhibited by unsaturated fatty acids, especially oleic acid, at concentrations above 100 micromolar. In marked contrast, saturated fatty acids had only a slight effect on the thioesterase activity. Substrate specificities showed that the velocity of the reaction increased with the chain length of the substrate from decanoyl-CoA to myristoyl-CoA and then decreased with the chain length from myristoyl-CoA to stearoyl-CoA. Interestingly, oleoyl-CoA was only slowly hydrolyzed. These results suggest that the envelope acyl-CoA thioesterase coupled with an envelope acyl-CoA synthetase may be involved in a switching system which indirectly allows acyl transfer from acyl carrier protein derivatives to unsaturated acyl-CoA derivatives and ensures the predominance of unsaturated 18 carbon fatty acids in plants. Furthermore, the position of both acyl-CoA thioesterase and synthetase in the envelope membranes suggest that these two enzymes may be involved in the transport of oleic acid from the stroma phase to the cytosol compartment of the leaf cell.

Journal Article↗
PubMed1986

Lesions to the corticostriatal pathways ameliorate hypoglycemia-induced arachidonic acid release.

The concentrations of free fatty acids (FFAs) in the neostriatum of control rats and rats subjected to unilateral cortical ablation were measured during and following severe insulin-induced hypoglycemia. The total FFA concentration in the caudate nucleus contralateral to the lesion increased to approximately 1.5 and 3 times the control level after 5 and 30 min of isoelectricity, respectively, and was similar to the control value following 1 h of recovery. After 5 min of isoelectricity, the total FFA pool was significantly smaller in the decorticated striatum. No difference between hemispheres was noted after 30 min of isoelectricity. After 5 min of isoelectricity the levels of stearic and arachidonic acid were selectively increased whereas palmitic acid and oleic acid remained at control levels. In the decorticated striatum of lesioned animals the arachidonic acid concentration was significantly lower, whereas the level of stearic acid was not significantly different from the control value. After 30 min of isoelectricity the levels of all four FFA species were increased. Apart from a significantly lower level of oleic acid on the decorticated side, there were no interhemispheric differences in the FFA levels. Since the early interhemispheric differences in the FFA levels. Since the early interhemispheric hemispheric differences in the levels of arachidonic and stearic acids coincide with a selective decrease in the levels of glutamate and a decreased energy utilization on the decorticated side, the results suggest that glutamate release during hypoglycemia induces an early receptor-mediated degradation of phospholipids, presumably via the phosphatidylinositol cycle.

Animals↗
PubMed1984

Microthrix parvicella, a filamentous bacterium from activated sludge: growth on Tween 80 as carbon and energy source.

Microthrix parvicella, cultivated in a medium with Tween 80 and Casamino acids, utilized only the oleic acid moiety of Tween 80 as carbon and energy source. The cell yield from Tween 80 was about 0.32 g dry weight of cells per g of Tween 80 consumed. As only the oleic acid moiety of Tween 80 was utilized, the cell yield from oleic acid was 1.3 g dry weight of cells per g oleic acid consumed. The amount of carbon produced as CO2 was less than 30% of the oleic acid-carbon and this low value was in agreement with the high cell yield. In batch culture M. parvicella stored large amounts of lipid material during the early growth phase. The fatty acids of the lipid globules were similar to the fatty acids supplied as carbon source. The percentage composition of the biomass changed to give C/N percentage ratios of about 15 during the early growth phase due to the high concentration of internal lipids and the low concentration of protein. The growth rate in batch culture was about 0.016 h-1 but was affected by the concentration of Casamino acids in the medium.

Amino Acids↗
PubMed1994

[Protective effect of interleukin-1 receptor antagonist on oleic acid-induced lung injury].

Thirty-six mice were divided into a control group, lung injury group by oleic acid and protected group with interleukin-1 receptor antagonist (IL-1ra). There were 12 mice in each group. Oleic acid was injected into the tail vein of the mouse with a dose of 0.2 ml/kg to produce a model of acute lung injury (ALI). The result indicates that preadministration of IL-1ra to the mouse with ALI can decrease the lung index, lung wet-to-dry weight ratio and leakage of protein from pulmonary capillary, elevate PaO2, and significantly attenuate lung histologic injury (alveoli edema, alveoli hemorrhage, lung necrosis, inflammatory cell invasion). It is suggested that IL-1ra has protective effect on oleic acid-induced lung injury and may be a potential tool for treatment of ARDS.

Animals↗
PubMed1992

Inhibition of Zn(2+)-dependent ATPase in prostasome membrane by nonsaturated, long-chain fatty acids.

Arachidonic and oleic acids, opposite to stearic and palmitic acids, at concentrations near 10(-5) mol/l markedly inhibited Zn(2+)-dependent ATPase in human prostasome membranes. Arachidonic acid was somewhat more potent as inhibitor than oleic acid and the involvement of the metabolites of arachidonic acid cascade was less probable. Deoxycholate, an anionic biological detergent, produced a similar inhibitory effect although at a much higher concentration. The restraining role of nonsaturated, long-chain fatty acids on sperm motility in human semen is discussed in terms of their established inhibitory action on prostasome ATPase systems.

Adenosine Triphosphatases↗
PubMed1991

The effect of prostaglandin E1 on acute pulmonary artery hypertension during oleic acid-induced respiratory dysfunction.

This study examined the general effect of intravenous PGE1 on RV Ees and effective PA elastance (EA) during acute pulmonary hypertension associated with oleic acid infusion. In eight pigs, RV end-systolic elastance was quantified with the Ees and Ea was defined with reference to the Windkessel model. Oleic acid infusion increased mean PAP and Ea. Prostaglandin E1 reduced PAP and decreased Ea. Ees did not change throughout the study. Mean arterial pressure was reduced and the pulmonary shunt was increased after PGE1 infusion. The PaO2 was reduced. Data from this study suggest that although PGE1 is effective in reducing PAP, it is not as effective in reducing RV afterload. Furthermore, PGE1 does have significant side effects such as reduction of systemic arterial pressure and an increase in pulmonary shunt.

Acute Disease↗
PubMed1988

Changes in fatty acid compositions of mitochondria during embryonic development.

1. A general trend among biomembranes of hepatocytes in the developing avian embryo is to display increasing percentages of unsaturated fatty acids, especially oleic acid (C18:1). 2. However, once increasing amounts of thyroxine appear in the plasma, mitochondria begin to exhibit increasing percentages of saturated fatty acids, primarily stearic acid (C18:0). 3. Increasing saturation of mitochondrial membrane lipids can be inhibited by exposure of embryonated eggs to 500 R of X-irradiation. 4. Injection of embryonated eggs with estrone increases the proportion of oleic acid (C18:1) in mitochondrial membranes but a balancing increase in palmitic acid (C16:0) enables their lipids to remain more saturated than unsaturated.

Animals↗
PubMed1985

Pulmonary artery wedge pressure may fail to reflect left ventricular end-diastolic pressure in dogs with oleic acid-induced pulmonary edema.

We investigated the accuracy with which pulmonary artery wedge pressure (WP) reflected left ventricular end-diastolic pressure (LVEDP) in dogs with oleic acid-induced pulmonary edema. We compared hemodynamic variables before and during edema, as measured from a pulmonary artery catheter placed before oleic acid (PA-1) and from a second catheter (PA-2) placed 2 h after oleic acid infusion. Oleic acid decreased arterial oxygen saturation and cardiac output and increased pulmonary vascular resistance and phasic pulmonary artery pressure. LVEDP did not change after oleic acid, although WP measured by both catheters was increased. In addition, WP measured by PA-2 (7.1 +/- 0.7 mm Hg) was greater than that measured by PA-1 (5.6 +/- 0.5 mm Hg) (p less than or equal to 0.037). Using PA-1, we found that WP increased in a linear manner with LVEDP both before and after pulmonary injury (r2 = 0.91, 0.68, respectively). There was no relationship between LVEDP and WP using PA-2 (r2 = 0.07). We conclude that oleic acid-induced pulmonary edema lessens the accuracy with which WP reflects LVEDP, and that WP from a catheter placed after edema less accurately reflects LVEDP than does WP from a catheter placed before edema.

Animals↗
PubMed1982

The effects of expiratory positive airway pressure on the resolution of oleic acid-induced lung injury in dogs.

It is not known whether positive end-expiratory pressure (PEEP) merely improves gas exchange in patients with the adult respiratory distress syndrome or also affects the resolution of their lung injury. We examined the effects of expiratory positive airway pressure (EPAP), a form of PEEP, on 13 pairs of spontaneously breathing mongrel dogs with permanent tracheostomies that were subjected to acute lung injury from oleic acid. One member of each pair was treated with 10 cm H2O EPAP by means of a special valve attached to its tracheostomy tube; the other member breathed through the tracheostomy tube alone. The EPAP was applied 3 h after an intravenous injection of 0.06 ml/kg oleic acid and continued for a total of 21 h. Functional residual capacity (FRC) was increased to preinjury values in the EPAP-treated dogs at 3, 12, and 24 h compared with that in the untreated dogs. The PaO2 was higher and the venous admixture (Qva/QT) was lower in the EPAP-treated dogs compared with that in the untreated dogs at 3 and at 12 h. However, over the 7 days after removal of EPAP no significant differences were noted between the 2 groups in FRC, PaO2, Qva/QT, inert gas elimination profiles, mortality, final lung compliance to initial lung compliance differences, lung water to dry lung weight ratios, or histologic features. We conclude that EPAP improves gas exchange during its administration but has no demonstrable effect on the resolution of lung injury induced by oleic acid in dogs.

Animals↗
PubMed1983

Release of neurotransmitter amino acids from synaptosomes: enhancement of calcium-independent efflux by oleic and arachidonic acids.

The release of preloaded [14C]neuroactive amino acids (glutamic acid, proline, gamma-aminobutyric acid) from rat brain synaptosomes can occur via a time-dependent, Ca2+-independent process. This Ca2+-independent efflux is increased by compounds that activate Na+ channels (veratridine, scorpion venoms), by the ionophore gramicidin D, and by low concentrations of unsaturated fatty acids (oleic acid and arachidonic acid). Saturated fatty acids have no effect on the efflux process. Neither saturated nor unsaturated fatty acids have an effect on the release of [14C]leucine, an amino acid not known to possess neurotransmitter properties. The increase in the efflux of neuroactive amino acids by oleic and arachidonic acids can also be demonstrated using synaptosomal membrane vesicles. Under conditions in which unsaturated free fatty acids enhance amino acid efflux, no effect on 22Na+ permeability is observed. Since Na+ permeability is not altered by fatty acids, the synaptosomes are not depolarized in their presence and, thus, the Na+ gradient can be assumed to be undisturbed. We conclude that unsaturated fatty acids represent a potentially important class of endogenous modulators of neuroactive amino acid transport in nerve endings and further postulate that their action is the result of an uncoupling of amino acid transport from the synaptosomal Na+ gradient.

Amino Acids↗
PubMedDate not supplied

The role of fatty acids in ischemic tissue injury: difference between oleic and palmitic acid.

Guinea pig hearts were subjected to low-flow perfusion (0.3 ml/g fresh weight/min) with an oxygen depleted perfusate. Fatty acids (palmitic or oleic acid), added to the perfusate, accelerated in a dose-dependent manner the anoxic decay of creatine phosphate and ATP, impaired lactate production and augmented enzyme release (lactate dehydrogenase, malate dehydrogenase). Palmitic and oleic acid, however, differed distinctly in their deleterious effect, this being greater for oleic acid. After 60 min anoxic low-flow perfusion with 11 mM glucose and 0.2 mM of either fatty acid, complexed in 5:1 molar relationship to albumin, the creatine phosphate content with palmitate is 39% greater than with oleate, the ATP content 23%, lactate production 15% greater, and release of malate dehydrogenase 24% lower, but the elevated contents of long-chain acyl CoA and acyl carnitine are not significantly different for the two fatty acids. These results accord with earlier experiences on subcellular systems showing that the physicochemical effects of the oleyl residue are more harmful than those of the palmityl residue.

Adenosine Triphosphate↗
PubMed2004

Linoleic acid increases monocyte deformation and adhesion to endothelium.

Fatty acids have been implicated in having both anti- or pro-inflammatory actions, which may contribute to the progression and severity of atherosclerosis. Linoleic acid has been shown by others to decrease CD18 expression and leukocyte adhesion under static conditions. We investigated the effect of steric acid (18:0), oleic acid (18:1), and linoleic acid (18:2) on the cortical tension (a measure of cell membrane deformability) and adhesion characteristics of the monocytic cell line Mono Mac 6 (MM6) cells to TNF-alpha activated HUVEC under fluid flow. Linoleic acid concentrations up to 23 microM decreased cortical tension and increased adhesion frequencies. Increased adhesion was not due to altered cell morphology or adhesion kinetics and occurred despite decreases in receptor expression (CD18 and CD11a). At higher levels of linoleic acid (> or = 46 microM), cell dissociation constants significantly increased. Results show that decreasing cortical tension increased the probability that contact between MM6 cells and endothelium would produce an adhesive interaction, possibly due to increased deformation of the microvilli and the cell membrane cortex. However, more deformable cells rolled more erratically at low shear rates. The different behavior during initial contact and rolling suggest that adhesion is influenced by two force-dependent mechanisms, deformation of microvilli and a steric barrier. Incubation of MM6 with 23 microM steric or oleic acid did not significantly affect cortical tension. However, cells incubated with steric acid greatly increased their adherence to HUVEC and cells incubated with oleic acid showed no significant effect, indicating factors other than deformability may dominate.

Annexin A5↗
PubMed1997

Inhibition of store-dependent capacitative Ca2+ influx by unsaturated fatty acids.

The effects of the unsaturated fatty acids, arachidonic and oleic acid, on the influx of Ca2+ activated by depletion of intracellular stores with thapsigargin were investigated in various cell types. By using a Ca2+ free/Ca2+ reintroduction protocol, we observed that arachidonic acid (2 to 5 microM) inhibited thapsigargin-induced rises in cytosolic free Ca2+ ([Ca2+]i) in Ehrlich tumor cells, Jurkat T lymphocytes, rat thymocytes, and Friend erythroleukemia and PC12 rat pheochromocytoma cells. This effect was attributed to the inhibition of Ca2+ entry, since arachidonate also inhibited thapsigargin-stimulated unidirectional entry of the Ca2+ surrogates Ba2+ and Mn2+. In Ehrlich cells, the IC50 for arachidonic and oleic acid was 1.2 and 1.8 microM, respectively. The inhibition appeared to depend on the ratio [fatty acid]/[cells] rather than on the absolute fatty acid concentration. Experiments with [3H]-oleic acid revealed that the inhibitory activity was not correlated with cell internalisation and metabolism of the fatty acid. The inhibition was reverted by removal of the fatty acid bound to cell membrane by fatty acid-free albumin treatment. The unsaturated fatty acids had no effect on ATP/ADP cell levels and plasma membrane potential. Pharmacological evidence indicated that cell phosphorylation/dephosphorylation events, and pertussis toxin-sensitive G proteins were not involved. Other amphipathic lipophilic compounds, i.e. 2-bromopalmitic acid, retinoic acid, sphingosine, and dihydrosphingosine, mimicked arachidonic/oleic acid as they inhibited thapsigargin-stimulated Ca2+ influx in an albumin-reversible fashion. These results suggest that physiologically relevant (unsaturated) fatty acids can inhibit capacitative Ca2+ influx possibly because they intercalate into the plasma membrane and directly affect the activity of the channels involved.

Animals↗
PubMed1986

Permeability behavior of liposomes prepared from fatty acids and fatty acid methyl esters.

The permeability properties of liposomes prepared at pH 8.7 from a fatty acid and either methyl oleate or methyl elaidate, with or without cholesterol, were investigated. The fatty acids used were oleic acid, elaidic acid, and the selenium-containing fatty acids 9-selenaheptadecanoic acid and 13-selenaheneicosanoic acid. The liposomes trapped sucrose and carboxyfluorescein. Their volume change resulting from osmotic shock was directly proportional to the change in absorbance (light scattering). Liposomes prepared from oleic acid and either methyl oleate or methyl elaidate underwent osmotic swelling much more slowly than liposomes prepared from elaidic acid and either methyl oleate or methyl elaidate. Incorporation of cholesterol decreased the initial rate of erythritol permeation, especially in liposomes containing methyl oleate. The swelling rates of liposomes prepared with the selenium-containing fatty acids indicated that incorporation of methyl elaidate gave more tightly packed bilayers than did incorporation of methyl oleate. The effect of cholesterol on the initial rate of erythritol influx was greater in oleic acid and elaidic acid liposomes than in selenium-containing fatty acid liposomes, indicating that the large bulk of the selenium heteroatom suppresses the ability of cholesterol to interact with the hydrocarbon chain.

Cholesterol↗