[The effect of corticosteroids on experimental respiratory distress syndrome using oleic acid].
Explore the source record for details and available documents.
Adrenal Cortex Hormones↗
SEARCH · Search PubMed
Results for “OLEIC ACID”
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Group V phospholipase A(2)-mediated oleic acid mobilization in lipopolysaccharide-stimulated P388D(1) macrophages.
P388D(1) macrophages prelabeled with [(3)H]arachidonic acid (AA) respond to bacterial lipopolysaccharide (LPS) by mobilizing AA in a process that takes several hours and is mediated by the concerted actions of the group IV cytosolic phospholipase A(2) and the group V secretory phospholipase A(2) (sPLA(2)). Here we show that when the LPS-activated cells are prelabeled with [(3)H]oleic acid (OA), they also mobilize and release OA to the extracellular medium. The time and concentration dependence of the LPS effect on OA release fully resemble those of the AA release. Experiments in which both AA and OA release are measured simultaneously indicate that AA is released 3 times more efficiently than OA. Importantly, LPS-stimulated OA release is strongly inhibited by the selective sPLA(2) inhibitors 3-(3-acetamide-1-benzyl-2-ethylindolyl-5-oxy)propane sulfonic acid and carboxymethylcellulose-linked phosphatidylethanolamine. The addition of exogenous recombinant sPLA(2) to the cells also triggers OA release. These data implicate a functionally active sPLA(2) as being essential for the cells to release OA upon stimulation with LPS. OA release is also inhibited by methyl arachidonyl fluorophosphonate but not by bromoenol lactone, indicating that the group IV cytosolic phospholipase A(2) is also involved in the process. Together, these data reveal that OA release occurs during stimulation of the P388D(1) macrophages by LPS and that the regulatory features of the OA release are strikingly similar to those previously found for the AA release.
Animals↗
Comparison between extra virgin olive oil and oleic acid rich sunflower oil: effects on postprandial lipemia and LDL susceptibility to oxidation.
The aim of our study was to determine whether the minor polar components of virgin olive oil could have favorable effects (1) on fasting and postprandial lipid profile and (2) on low-density lipoprotein (LDL) composition and susceptibility to oxidation in vitro. Ten normolipidic subjects were included in a crossover study (two diet periods of 3 weeks) and received either virgin olive oil (OO diet) or oleic acid rich sunflower oil. An oral fat load was performed at the end of each period. The plasma lipid levels were not significantly different after both diets in the fasting and postprandial states. A few minor variations of the LDL composition were observed only in the postprandial lipemia, and they were different after both diets. The LDL oxidation susceptibility was evaluated by the formation of conjugated dienes. With LDL isolated in the fasting state, the diene production decreased (p = 0.0573) only after the OO diet. The dienes determined at time 0 and the maximal dienes obtained during the oxidation reaction decreased (p = 0.0145 and p = 0.0184, respectively) only after the OO fat load. Nevertheless, the diene production decrease was not significant (p = 0.0848). Our results suggest a mild effect of minor components of virgin olive oil related to a decrease of LDL susceptibility to oxidation; further analyses are necessary to give clear conclusions about their role.
Adult↗
Spontaneous breathing with airway pressure release ventilation favors ventilation in dependent lung regions and counters cyclic alveolar collapse in oleic-acid-induced lung injury: a randomized controlled computed tomography trial.
INTRODUCTION: Experimental and clinical studies have shown a reduction in intrapulmonary shunt with spontaneous breathing during airway pressure release ventilation (APRV) in acute lung injury. This reduction was related to reduced atelectasis and increased aeration. We hypothesized that spontaneous breathing will result in better ventilation and aeration of dependent lung areas and in less cyclic collapse during the tidal breath. METHODS: In this randomized controlled experimental trial, 22 pigs with oleic-acid-induced lung injury were randomly assigned to receive APRV with or without spontaneous breathing at comparable airway pressures. Four hours after randomization, dynamic computed tomography scans of the lung were obtained in an apical slice and in a juxtadiaphragmatic transverse slice. Analyses of regional attenuation were performed separately in nondependent and dependent halves of the lungs on end-expiratory scans and end-inspiratory scans. Tidal changes were assessed as differences between inspiration and expiration of the mechanical breaths. RESULTS: Whereas no differences were observed in the apical slices, spontaneous breathing resulted in improved tidal ventilation of dependent lung regions (P < 0.05) and less cyclic collapse (P < 0.05) in the juxtadiaphragmatic slices. In addition, with spontaneous breathing, the end-expiratory aeration increased and nonaerated tissue decreased in dependent lung regions close to the diaphragm (P < 0.05 for the interaction ventilator mode and lung region). CONCLUSION: Spontaneous breathing during APRV redistributes ventilation and aeration to dependent, usually well-perfused, lung regions close to the diaphragm, and may thereby contribute to improved arterial oxygenation. Spontaneous breathing also counters cyclic collapse, which is a risk factor for ventilation-associated lung injury.
Animals↗
Inhibition of pentagastrin stimulated gastric acid secretion and rise in the plasma concentration of neurotensin-like immunoreactivity (NTLI) by intraduodenal oleic acid in man.
Explore the source record for details and available documents.
Duodenal Ulcer↗
Effect of wheat bran and wheat germ on the intestinal uptake of oleic acid, monoolein, and cholesterol in the rat.
The effects of fiber-rich wheat bran and wheat germ on the intestinal absorption of dietary cholesterol, free fatty acids, and monoglycerides were studied. Rats were given a test meal containing [(14)C]oleic acid, [(14)C]monoolein, and [(3)H]cholesterol. After a 1-hour digestion period, wheat bran or wheat germ (10% of meal solids) did not significantly modify the gastric emptying of lipids. No effect of wheat bran was evidenced on the amounts of lipids and cholesterol in the intestinal content or the mucosal segments, whereas wheat germ significantly increased the cholesterol in the small intestine content, decreasing its intestinal absorption. Both fractions only slightly influenced the levels of absorbed lipids and cholesterol in the plasma and liver. In vitro binding measurements showed that the wheat fractions bind only 7% to 15% of both lipids and cholesterol. Results indicate that wheat bran has no direct effect on the mucosal uptake process, whereas wheat germ might decrease the uptake of dietary cholesterol by an as yet unknown mechanism.
Journal Article↗
Modulation of CTP:phosphocholine cytidylyltransferase translocation by oleic acid and the antitumoral alkylphospholipid in HL-60 cells.
Short time effect of oleate and 1-O-alkyl-2-O-methyl-rac-glycero-3-phosphocholine (AMGPC) on choline incorporation into phosphatidylcholines were studied in HL-60 cells. The non lytic concentration of 50 microM oleate induced a three-fold increase in [3H]choline incorporation into phosphatidylcholine. This stimulation was accompanied by a translocation of the CTP:phosphocholine cytidylyltransferase (EC 2.7.7.15) from cytosol to membranes. By contrast, the ether-lipid AMGPC inhibited [3H]choline incorporation into phosphatidylcholine by 60% at 10 microM. AMGPC had no effect on choline kinase or choline phosphotransferase activities. When AMGPC was added separately to an homogenate, a particulate or a cytosolic fraction, cytidylyltransferase inhibition was observed only in the homogenate. However on particulates recovered from homogenates treated with increasing concentrations of AMGPC, membranous cytidylyltransferase activity decreased dose-dependently. Thus AMGPC had no effect on cytidylyltransferase activity itself but inhibited its translocation from cytosol to membrane. At variance with the well-established positive effect on cytidylyltransferase translocation induced by fatty acids, this is the first demonstration that AMGPC can inhibit cytidylyltransferase translocation in cell-free system.
Antineoplastic Agents↗
Effect of volume and dose on the pulmonary distribution of exogenous surfactant administered to normal rabbits or to rabbits with oleic acid lung injury.
Administration of exogenous lung surfactant to infants with or at risk for respiratory distress syndrome has been demonstrated to improve gas exchange and survival; administration of surfactant to patients with the adult respiratory distress syndrome is currently undergoing clinical evaluation. Although it is currently assumed the optimal effect will occur when administered surfactant is distributed homogeneously throughout the lung, little is known of the influence of variables inherent in the administration procedure on subsequent distribution. To address this question, we studied the effect of the volume size in which the surfactant is suspended for instillation, and demonstrated a marked relationship in the normal rabbit lung between this volume and the subsequent homogeneity of surfactant distribution. In the rabbit lung that was acutely injured by oleic acid, this relationship was not evident. Concentration of administered surfactant was not demonstrated to be of major influence on its distribution after administration. Our results focus attention on the importance of parameters of the administration procedure, and also demonstrate the usefulness of the techniques used for determination of surfactant distribution.
Animals↗
Stimulation by oleic acid of incorporation of L-[4,5-3H]leucine into very low density lipoprotein apoprotein by the isolated perfused rat liver.
Livers from normal fed or fasted (24h) rats were perfused in vitro to determine whether fatty acid affects the biosynthesis of very low density lipoprotein (VLDL) apoprotein. Oleate stimulated VLDL triacylglycerol output and increased incorporation of L-[4,5-3H]leucine into VLDL apoprotein in both the fed and fasted groups. The increased incorporation of [3H]leucine was mainly into VLDL-apoprotein E. The total mass of VLDL apoprotein secreted was also stimulated by oleate proportionately. These data suggest that fatty acids may stimulate hepatic synthesis and/or secretion of the VLDL apoproteins and that apo E, may be required for the formation and secretion of triacyl-glycerol in the VLDL.
Animals↗
The conversion of apoB100 low density lipoprotein/high density lipoprotein particles to apoB100 very low density lipoproteins in response to oleic acid occurs in the endoplasmic reticulum and not in the Golgi in McA RH7777 cells.
The site where bulk lipid is added to apoB100 low density lipoproteins (LDL)/high density lipoproteins (HDL) particles to form triglyceride-enriched very low density lipoproteins (VLDL) has not been identified definitively. We employed several strategies to address this question. First, McA RH7777 cells were pulse-labeled for 20 min with [35S]methionine/cysteine and chased for 1 h (Chase I) to allow study of newly synthesized apoB100 LDL/HDL remaining in the endoplasmic reticulum (ER). After Chase I, cells were incubated for another hour (C2) with/without brefeldin A (BFA) and nocodazole (Noc) (to block ER to Golgi trafficking) and with/without oleic acid (OA). OA treatment alone during C2 increased VLDL secretion. This was prevented by the addition of BFA/Noc in C2. When C2 media were replaced by control media for another 1-h chase (C3), VLDL formed during OA treatment in C2 were secreted into C3 medium. Thus, OA-induced conversion of apoB100 LDL/HDL to VLDL during C2 occurred in the ER. Next, newly synthesized apoB100 lipoproteins were trapped in the Golgi by treatment with Noc and monensin during Chase I (C1), and C2 was carried out in the presence of BFA/Noc with/without OA and without monensin. Under these conditions, OA treatment during C2 did not stimulate VLDL secretion. The same pulse/chase protocols were followed by iodixanol subcellular fractionation, extraction of lipoproteins from ER and Golgi, and sucrose gradient separation of extracted lipoproteins. Cells treated with BFA/Noc and OA in C2 had VLDL in the ER. In the absence of OA, only LDL/HDL were present in the ER. The density of Golgi lipoproteins in these cells was not affected by OA. Similar results were obtained when ER were immuno-isolated with anti-calnexin antibodies. In conclusion, apoB100 bulk lipidation, resulting in conversion of LDL/HDL to VLDL, can occur in the ER, but not in the Golgi, in McA RH7777 cells.
Animals↗
Oleic acid interacts with GPR40 to induce Ca2+ signaling in rat islet beta-cells: mediation by PLC and L-type Ca2+ channel and link to insulin release.
It has long been thought that long-chain free fatty acids (FFAs) stimulate insulin secretion via mechanisms involving their metabolism in pancreatic beta-cells. Recently, it was reported that FFAs function as endogenous ligands for GPR40, a G protein-coupled receptor, to amplify glucose-stimulated insulin secretion in an insulinoma cell line and rat islets. However, signal transduction mechanisms for GPR40 in beta-cells are little known. The present study was aimed at elucidating GPR40-linked Ca(2+) signaling mechanisms in rat pancreatic beta-cells. We employed oleic acid (OA), an FFA that has a high affinity for the rat GPR40, and examined its effect on cytosolic Ca(2+) concentration ([Ca(2+)](i)) in single beta-cells by fura 2 fluorescence imaging. OA at 1-10 microM concentration-dependently increased [Ca(2+)](i) in the presence of 5.6, 8.3, and 11.2 mM, but not 2.8 mM, glucose. OA-induced [Ca(2+)](i) increases at 11.2 mM glucose were inhibited in beta-cells transfected with small interfering RNA targeted to rat GPR40 mRNA. OA-induced [Ca(2+)](i) increases were also inhibited by phospholipase C (PLC) inhibitors, U73122 and neomycin, Ca(2+)-free conditions, and an L-type Ca(2+) channel blocker, nitrendipine. Furthermore, OA increased insulin release from isolated islets at 8.3 mM glucose, and it was markedly attenuated by PLC and L-type Ca(2+) channel inhibitors. These results demonstrate that OA interacts with GPR40 to increase [Ca(2+)](i) via PLC- and L-type Ca(2+) channel-mediated pathway in rat islet beta-cells, which may be link to insulin release.
Animals↗
Uptake capacity in vitro for glucose and methionine and in situ for oleic acid in the proximal small intestine of posthatch chicks.
The uptake capacity of the duodenum and jejunum was determined in vitro for glucose and methionine using 14C-inulin as an unabsorbed reference substance in posthatch chicks. Fatty acid uptake in situ was also determined in the duodenum. Methionine uptake capacity increased in both duodenum and jejunum between hatch and 7 d and was constant between 7 and 14 d. Calculation of apparent Michaelis constant (Kt) for both substrates indicated little change with age and thus the amount of carrier in the intestine may be increasing. Uptake capacity of the duodenum for glucose increased between hatch and 7 d of age but no changes were found between 7 and 14 d. In the jejunum, uptake capacity was constant from hatch to 14 d of age. In situ uptake of oleic acid in the duodenum did not change between hatch and 14 d of age. These results suggest that intestinal uptake capacity changes little after 7 d of age, and thus feed intake may be the major factor controlling nutrient uptake in chicks.
Aging↗
Reaction of oleic acid particles with NO3 radicals: Products, mechanism, and implications for radical-initiated organic aerosol oxidation.
The heterogeneous reaction of liquid oleic acid aerosol particles with NO3 radicals in the presence of NO2, N2O5, and O2 was investigated in an environmental chamber using a combination of on-line and off-line mass spectrometric techniques. The results indicate that the major reaction products, which are all carboxylic acids, consist of hydroxy nitrates, carbonyl nitrates, dinitrates, hydroxydinitrates, and possibly more highly nitrated products. The key intermediate in the reaction is the nitrooxyalkylperoxy radical, which is formed by the addition of NO3 to the carbon-carbon double bond and subsequent addition of O2. The nitrooxyalkylperoxy radicals undergo self-reactions to form hydroxy nitrates and carbonyl nitrates, and may also react with NO2 to form nitrooxy peroxynitrates. The latter compounds are unstable and decompose to carbonyl nitrates and dinitrates. It is noteworthy that in this reaction nitrooxyalkoxy radicals appear not to be formed, as indicated by the absence of the expected products of decomposition or isomerization of these species. This is different from gas-phase alkene-NO3 reactions, in which a large fraction of the products are formed through these pathways. The results may indicate that, for liquid organic aerosol particles in low NOx environments, the major products of the radical-initiated oxidation (including by OH radicals) of unsaturated and saturated organic compounds will be substituted forms of the parent compound rather than smaller decomposition products. These compounds will remain in the particle and can potentially enhance particle hygroscopicity and the ability of particles to act as cloud condensation nuclei.
Journal Article↗
Stability of HAMLET--a kinetically trapped alpha-lactalbumin oleic acid complex.
The stability toward thermal and urea denaturation was measured for HAMLET (human alpha-lactalbumin made lethal to tumor cells) and alpha-lactalbumin, using circular dichroism and fluorescence spectroscopy as well as differential scanning calorimetry. Under all conditions examined, HAMLET appears to have the same or lower stability than alpha-lactalbumin. The largest difference is seen for thermal denaturation of the calcium free (apo) forms, where the temperature at the transition midpoint is 15 degrees C lower for apo HAMLET than for apo alpha-lactalbumin. The difference becomes progressively smaller as the calcium concentration increases. Denaturation of HAMLET was found to be irreversible. Samples of HAMLET that have been renatured after denaturation have lost the specific biological activity toward tumor cells. Three lines of evidence indicate that HAMLET is a kinetic trap: (1) It has lower stability than alpha-lactalbumin, although it is a complex of alpha-lactalbumin and oleic acid; (2) its denaturation is irreversible and HAMLET is lost after denaturation; (3) formation of HAMLET requires a specific conversion protocol.
Ammonium Sulfate↗
Erythrocyte membrane stearic and oleic acid ratios in breast cancer.
A case control study has been conducted to determine the value of stearic/oleic acid ratios in the erythrocyte membranes of women at the time of presentation with breast cancer. No difference was found between the stearic/oleic acid ratio of cases and that of controls with benign breast condition or normal volunteers. Furthermore, within clinical stages of breast cancer, no differences were detected. This ratio does not appear to be of value as a marker of malignancy, or of tumour burden.
Breast Neoplasms↗
Superoxide anion, the main species of ROS in the development of ARDS induced by oleic acid.
It is believed that reactive oxygen species (ROS) play a very important role in the pathogenesis of acute respiratory distress syndrome (ARDS), but the mechanism has not been so clear, owing to the absence of direct measurable (experimental) data. In majority of the medical studies on free radicals, the analysis of ROS has generally been done by the way of measuring their secondary and breakdown products. In our study, we used electron spin resonance (ESR), a sensitive and accurate technique to detect ROS directly and also used some other sensitive techniques including ultra-weak luminescence and chemical luminescence to identify the species and relative amount of ROS. Furthermore, superoxide dismutase (SOD) was pre-administrated in ARDS rats to verify the results from the above studies and explore the possibility of the clinical application of SOD in ARDS. The spectra of ESR showed that the concentration of ROS increased at 10 min and reached a summit at 30 min after injection of oleic acid (OA), then dropped gradually. The scavenging effects of different scavenging agents on ROS by the analysis of ultra-weak luminescence proved that superoxide anion was the main species of ROS in the development of OA-induced ARDS. Moreover, the results of quantified measure of superoxide anion by chemical luminescence also showed the accordant tendency exhibited in ESR measurement. The pre-treatment of SOD might distinctly inhibit the production of superoxide anion, obviously improve the blood gas status, lung wet/dry ratio and lung/body ratio in ARDS rats. It is suggested that ROS may play a key role in the initiation phase of ARDS, while superoxide anion may be a leading actor in this process and SOD could effectively protect rats from ARDS. These results may provide helpful information for the treatment and prevention of ARDS.
Animals↗
Influence of Poly(ethylenimine) on the Monolayer of Oleic Acid at the Air/Water Interface.
The effect of poly(ethylenimine) (PEI) dissolved in water on the surface pressure-area isotherm of oleic acid (OA) at the air/water interface was investigated. On a concentrated PEI solution, the isotherm of the OA monolayers exhibited a noticeable difference as a function of subphase pH. PEI caused the collapse pressure of the OA monolayer to increase up to 45 mN/m, due to a stronger acid-base-type interaction occurring between the amine group of the PEI and the carboxyl group of OA; on a pure water subphase, the collapse pressure was;28 mN/m. On the other hand, owing to a stronger OA-PEI interaction, the OA monolayers favored a liquid-expanded state more on the PEI-containing water subphase than on the pure water. From the QCM measurement, each OA molecule appeared to interact, on average, with 4.3-5.8 ethylenimine repeating units at basic pHs. We also found that OA multilayers could be assembled on a hydrophilic substrate by a Z-type Langmuir-Blodgett (LB) deposition in a PEI-containing subphase at basic pHs. The ATR-IR spectral data revealed that, in a Z-type LB film, the headgroup of OA was mostly present as carboxylate, interacting in an ionic state with the protonated amine groups of PEI. In acidic conditions, neither a Y-type nor a Z-type deposition was really accomplished. Nonetheless, the ATR-IR spectral data suggested that OA molecules should exist in a monomeric state in a LB film assembled at acidic pHs without PEI while they would form intermolecular hydrogen bridges and/or dimers in the presence of PEI. Copyright 2000 Academic Press.
Journal Article↗
Oleic acid promotes changes in the subcellular distribution of protein kinase C in isolated hepatocytes.
The effect of oleate on the subcellular distribution of protein kinase C (PKC) was studied in isolated hepatocytes and in perfused rat liver in the presence of physiological concentrations of serum albumin. A time- and dose-dependent translocation of PKC from the cytosol towards the membranes was observed at oleate concentrations that fell within the range of concentrations reached under several physiological conditions. Analysis of the membrane-bound isoenzymes of PKC by hydroxylapatite chromatography revealed that the beta isoenzyme was preferentially translocated to this compartment in hepatocytes incubated with oleate. Activation of PKC after incubation of hepatocytes with oleate involved at least three different effectors of the enzyme: the fatty acid itself, the diacylglycerol synthesized from oleate, and the rise in the cytosolic calcium concentration elicited by oleate. As a result of PKC activation, protein phosphorylation of intact hepatocytes in response to oleate exhibited an enhancement in the phosphate content of a protein of 82 kDa, similar to that phosphorylated in the presence of phorbol dibutyrate.
Animals↗