[Effects of pretreatment with acetylsalicylic acid (ASA) on pulmonary ultrastructural alterations induced by oleic acid in sheep].
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Animals↗
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Oleic acid derived metabolites in mouse neuroblastoma N18TG2 cells.
Oleamide is an endogenous sleep-inducing lipid that has been isolated from the cerebrospinal fluid of sleep-deprived mammals. Oleamide is the best-understood member of the primary fatty acid amide family. One key unanswered question regarding oleamide and all other primary acid amides is the pathway by which these molecules are produced. One proposed pathway involves oleoyl-CoA and N-oleoylglycine as intermediates: oleic acid --> oleoyl-CoA --> N-oleoylglycine --> oleamide. The first and third reactions are known reactions, catalyzed by acyl-CoA synthetase and peptidylglycine alpha-amidating monooxygenase (PAM). Oleoyl-CoA formation from oleic acid has been demonstrated in vitro and in vivo while, to date, N-oleoylglycine cleavage to oleamide has been established only in vitro. PAM catalyzes the final step in alpha-amidated peptide biosynthesis, and its proposed role in primary fatty acid amide biosynthesis has been controversial. Mouse neuroblastoma N(18)TG(2) cells are an excellent model system for the study of oleamide biosynthesis because these cells convert [(14)C]-oleic acid to [(14)C]-oleamide and express PAM in a regulated fashion. We report herein that growth of the N(18)TG(2) cells in the presence of [(14)C]-oleic acid under conditions known to stimulate PAM expression generates an increase in [(14)C]-oleamide or in the presence of a PAM inhibitor generates [(14)C]-N-oleoylglycine. This represents the first identification of N-oleoylglycine from a biological source. In addition, N(18)TG(2) cell growth in the presence of N-oleoylglycine yields oleamide. These results strongly indicate that N-oleoylglycine is an intermediate in oleamide biosynthesis and provide further evidence that PAM does have a role in primary fatty acid amide production in vivo.
Animals↗
Comparative benzene-induced fatty acid changes in a Rhodococcus species and its benzene-sensitive mutant: possible role of myristic and oleic acids in tolerance.
A Gram positive bacterium of the genus Rhodococcus was isolated from a contaminated site in Sydney, Australia, for its ability to tolerate and degrade high concentrations of benzene. To identify fatty acids that may impart this Rhodococcus sp. with tolerance to toxic solvents, a benzene-sensitive strain, labeled M2b, was isolated using EMS mutagenesis. A comparative analysis of fatty acid profiles showed that strain M2b was unable to increase its saturated:unsaturated ratio of fatty acids to the level achieved by the w-t strain when both strains were challenged with benzene. This was due to M2b's increased abundance of myristic acid, and decreased abundance of oleic acid. In addition, by measuring the generalized polarization of the fluorescent membrane probe laurdan using fluorescence spectroscopy, we have shown for the first time the effects of an aromatic hydrocarbon on the membrane fluidity of a Rhodococcus sp. The fluidity of the membranes increased after only 0.5 hr of exposure to benzene, thus suggesting the partitioning of benzene within the lipid bilayer. The response of this Rhodococcus sp. to benzene may suggest a mechanism for how other microorganisms survive when toxic solvents are released within the vicinity of their environment.
Benzene↗
Yeast mitochondrial oxodicarboxylate transporters are important for growth on oleic acid.
The yeast genes ODC1 and ODC2 encode members of the Saccharomyces cerevisiae family of mitochondrial transport proteins that transport oxodicarboxylates. In these studies, the ODC1 gene was identified as able, in low-copy, to rescue a yeast strain that is unable to grow on oleic acid but can grow on other nonfermentable carbon sources. ODC2 was shown to be a high-copy suppressor of this mutant. Odc1delta odc2delta double mutants are unable to grow on oleic acid at 36 degrees C. ODC1 mRNA and protein expression is elevated in oleic acid medium as compared to glucose or glycerol. The ODC1 promoter contains sequences required for the oleic acid response. However, regulation of ODC1 does not require the transcription factors Oaf1p and Pip2p, known to mediate oleic acid induction of other genes. These studies provide the first link between these mitochondrial transporters and peroxisomal beta-oxidation.
Base Sequence↗
Dietary palmitic acid raises plasma LDL cholesterol relative to oleic acid only at a high intake of cholesterol.
Using a crossover design, the effects of exchanging up to 10% dietary energy (%en) between oleic (18:1) and palmitic acid (16:0) on plasma lipoprotein metabolism was investigated in 12 normocholesterolemic cebus monkeys, both in the absence and presence of dietary cholesterol (0.3%, w/w). In all the purified diets, which contained 33%en as fat blends, myristic acid (14:0) and linoleic acid (18:2) were held constant at 0.3%en and 3.7%en, respectively. Cholesterol-free diets containing either high 18:1 (19%en), roughly equivalent levels of 16:0 and 18:1 (12 and 15%en, respectively), or a high level of 16:0 (18%en), generated similar values for total plasma cholesterol (TC), HDL-C and LDL-C. Plasma triacylglycerol concentrations (TG) were significantly higher when monkeys were fed the 16: 0-rich diet than when fed the 18: 1-rich diet (75 +/- 6 vs. 52 +/- 8 mg/dl; P < 0.05). LDL and HDL kinetic parameters (assessed after simultaneous injection of homologous 131I-LDL and 125I-HDL) revealed no significant differences between the 18: 1-rich or 16: 0-rich diets. By contrast, with added dietary cholesterol (0.78 mg/kcal) the 16: 0-rich diet resulted in significantly higher TC (318 +/- 20 vs. 299 +/- 20 mg/dl; P < 0.05) and LDL-C (136 +/- 10 vs. 117 +/- 10 mg/dl; P < 0.05) in comparison to the 18: 1-rich diet. HDL-C was unaffected (159 +/- 8 vs. 156 +/- 5 mg/dl), but plasma TG concentrations also tended to be higher (70 +/- 8 vs. 60 +/- 6 mg/dl, P < 0.08). Kinetic studies revealed that the higher LDL-C concentration was associated with an elevated pool size of LDL apo B (40 +/- 2 vs. 34 +/- 2 mg/kg body weight; P < 0.005), the latter attributed to decreased FCR (1.06 +/- 0.07 vs. 1.27 +/- 0.12 pools/day; P < 0.04) with no effect on the transport rate of LDL apo B (41 +/- 2 vs. 42 +/- 3 mg/kg body weight per day). HDL kinetic parameters were comparable during the 16: 0 and 18: 1 dietary periods, but dietary cholesterol caused an increase in apo A-I pool size and transport rate without impacting FCR. In this study a palmitic acid-rich diet failed to alter plasma or LDL-C when compared to an oleic acid-rich diet, unless the diet also contained cholesterol. In the latter case, 16: 0 increased LDL-C, which reflected a decrease in the efficiency of LDL apo B removal.
Analysis of Variance↗
Turnover of plasma free arachidonic and oleic acids in men and women.
The turnover of plasma free arachidonic and oleic acids was determined in healthy men and women. The plasma pool of arachidonic acid in the men was 75 per cent higher than in the women. The fractional turnover of arachidonate was 0.80 +/- 0.04 min(-1) in the women and 0.47 +/- 0.04 min(-1) in the men. The turnover rate of arachidonic acid was similar in both sexes; calculated per kg body weight it was significantly higher in the women. No sex differences were observed in the concentration or turnover of plasma free oleic acid when corrected for differences in body size. The composition of the free fatty acid fraction differed between the sexes, the female subjects having a lower proportion of saturated fatty acids and higher proportions of oleic and eicosenoic acids. The results indicate that the metabolism of polyunsaturated fatty acids in man is influenced by gonadal steroid hormones.
Adult↗
High-frequency jet ventilation during oleic-acid induced pulmonary oedema.
In oleic acid-induced pulmonary oedema (OAPO) sequential intrapulmonary fluid accumulation occurs leading to different expiratory flow pattern in dependent lung regions. The potential effects on efficacy of high-frequency jet ventilation (HFJV, f = 3 Hz, I: E = 0.43, FiO2 = 0.4) were studied and compared with continuous positive pressure ventilation (CPPV, f = 12-18/min, I:E = 0.5, TV = 12 ml/kg, PEEP = 0.5 kPa, FiO2 = 0.4) in a dog model of OAPO. In the control state (lung-healthy dogs), 15 min after oleic acid lung injury (interstitial oedema, period I) and 60 min after onset of OAPO (alveolar oedema, period II), gas exchange, lung volumes, compliance, resistance and haemodynamics were measured. The course of lung oedema was determined indirectly by means of washout curves of helium (foreign gas bolus-test, FGB) and nitrogen (single breath-test for oxygen, SBO2). During control, there were no significant differences between the HFJV-group (n = 7) and the CPPV-group (n = 6) by virtue of gas exchange, lung volumes and haemodynamics. During period I, PaO2 decreased significantly both with HFJV (p less than 0.01) and CPPV (p less than 0.05), being lower in the HFJV-group (p less than 0.05). PaCO2, pulmonary and haemodynamic parameters were unchanged. Onset of phase IV of the alveolar plateau (closing volume CV) occurred significantly earlier (p less than 0.05) in all animals. Impaired ventilation of dependent lung regions, increased maldistribution of intrapulmonary gas and VA/Q-mismatching may be the underlying mechanisms for lower efficacy of HFJV during interstitial lung oedema. In period II, pulmonary and cardiocirculatory parameters had changed significantly in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Mathematical model of edema in the isolated rabbit lung perfused with oleic acid.
The development of edema by the isolated, perfused rabbit lung in response to oleic acid was analyzed with the equations of Kedem and Katchalsky (Biochim. Biophys. Acta 27: 229-246, 1958). A perfused cylinder and annulus surround was chosen as a model. Isolated lungs, perfused with an isosmotic solution containing dextran as an oncotic agent, received a bolus injection of oleic acid into the pulmonary artery, resulting in marked edema without a rise in mean pulmonary arterial pressure. Hydrostatic pressure was kept constant and in the model was converted to its equivalent concentration of osmotically active impermeant solute, with a reflection coefficient (sigma) of 1. Fluid changes could be analyzed with three principal components as follows: the capillary permeability to solute (Pk), the hydraulic coefficient (Lp), and sigma. The equations were solved using Euler's method for integration, and the values for the three coefficients were adjusted to fit the data. The analysis indicated that the edema measured experimentally could be simulated by a progressive increase in Lp at constant or increasing values of Pk and decreasing values for sigma but not after selective increases in Pk and/or decreases in sigma alone. The analysis suggests that an expanding hydraulic conductivity may be the rate-limiting factor in oleic acid-induced pulmonary edema in the isolated, perfused rabbit lung.
Animals↗
External 113Inm and 99Tcm radiation detection of lung edema induced by oleic acid in the guinea pig.
The establishment of a small animal model for studies of lung injury is in great demand. Therefore, a double radioisotope labeling method was applied to study the dynamics of lung injury with protein-rich edema in the anesthetized guinea pig. One external scintillation detector was placed over the lung and another over the heart, where they continuously sampled the energy spectrum of 113Inm labeled transferrin, a macromolecular marker, and 99Tcm labeled red blood cells (RBC), a blood pool marker. Lung injury was induced by i.v. oleic acid in doses of 0.03 and 0.06 ml/kg b.wt. infused for 10 min. We calculated the rate of increase of accumulated 113Inm-transferrin in the lung corrected for blood pool changes. Macromolecular leakage showed a graded response in regression line-slope (RLS) to oleic acid. Both oleic acid groups showed significantly different RLSs as compared to the saline control (mean +/- SD x 10(-3) min-1; 0.03 ml: 3.86 +/- 1.01 (n = 7); 0.06 ml: 10.75 +/- 4.06 (n = 6), and control 1.12 +/- 1.19 (n = 6]. Assays of changes of acid-base balance, cell dynamics, and lung wet-dry weight were in accordance with the occurrence of lung edema. The RLS was well correlated with the lung wet-dry weight (r = 0.98). We conclude that measurements of pulmonary edema in guinea pigs can be performed quantitatively with the aid of external detection of radiolabeled transferrin and RBC:s. Thus, the method could be useful in further studies on mechanisms and/or treatment of protein-rich lung edema.
Animals↗
Enhanced comedo formation in rabbit ear skin by squalene and oleic acid peroxides.
The comedogenicity of UVA-irradiated and non-irradiated substances (squalene, oleic acid, tetradecane, isopropyl myristate, squalane and liquid paraffin) was evaluated by surface microscopy and histological examination after treating the ventral skin of rabbit ears with these substances. The lipid peroxide levels of these substances were also measured. Squalene itself was scarcely comedogenic but squalene peroxides were highly comedogenic. Both oleic acid and its peroxides were able to induce fairly large comedones and there was a good correlation between the lipid peroxide levels and the size of the comedones. The specimens biopsied from these comedones showed marked hyperplasia and hyperkeratosis of the epithelium in the follicular infundibulum and marked proliferation of the sebaceous glands. Although free fatty acids might play a role in the pathogenesis of acne, it is proposed that squalene and free fatty acids in sebum may be less comedogenic than their peroxides.
Acne Vulgaris↗
Antioxidant responses to oleic acid in two-liquid-phase suspension cultures of Taxus cuspidata.
Two-liquid-phase plant cell cultures employ the use of a partitioning system to redirect extracellular product into a second phase. After the addition of organic solvent, in order to understand the defense system of Taxus cuspidata cells to organic solvent in two-liquid-phase suspension cultures, we investigated cells' antioxidant metabolism. The results showed that T. cuspidata cells responded to oleic acid with oxidative bursts in both intracellular H2O2 and extracellular O2-* production. Inhibition studies with diphenylene iodonium suggested that the key enzyme responsible for oxidative bursts was primarily NADPH oxidase. Investigation of the relationship between reactive oxygen species (ROS) and defense responses induced by oleic acid indicated that 4% (v/v) oleic acid increased the levels of antioxidant enzymes of superoxide dismutase, ascorbate peroxidase, and catalase and the antioxidant capacity of reduced ascorbate and glutathione. However, when oleic acid content reached a critical value (6% [v/v]), no further increase in antioxidant enzymes and antioxidant capacity was observed, indicating that the defense responses played a role in a certain range of oleic acid content, beyond which the overall ROS scavenging machinery was not induced and the peroxidation of membrane lipids emerged.
Antioxidants↗
Enhanced nasal delivery of luteinizing hormone releasing hormone agonist buserelin by oleic acid solubilized and stabilized in hydroxypropyl-beta-cyclodextrin.
The potential use of three 2-hydroxypropyl ether derivatives of cyclodextrins (HP-alpha-, HP-beta- and HP-gamma-CyDs) as biocompatible solubilizers and stabilizers for oleic acid, a lipophilic absorption enhancer, was assessed in the nasal absorption of buserelin, an agonist of luteinizing hormone-releasing hormone, in rats. HP-CyDs increased the aqueous solubility of oleic acid and protected it against oxidation through the formation of inclusion complexes with the efficacy increasing in the order: HP-gamma-CyD << HP-alpha-CyD < HP-beta- CyD. The bend structure due to a cis-double bond halfway along the acyl chain of oleic acid provided a better fit into the cavity of HP-beta-CyD, in which the double bond appears to be buried, and hence becomes less susceptible to oxidation. The rate and extent of nasal bioavailability of buserelin were remarkably increased by coadministration of oleic acid and HP-beta-CyD, compared with the sole use of the enhancer. This enhancement was ascribable to the lowering of both the enzymatic and physical barriers of the nasal epithelium to the peptide, probably through the facilitated transmucosal penetration of oleic acid solubilized in HP-beta-CyD.
2-Hydroxypropyl-beta-cyclodextrin↗
The effect of oleic acid on the human ileal brake and its implications for small intestinal transit of tablet formulations.
PURPOSE: A human volunteer study was carried out to investigate whether activation of the ileal brake mechanism affects the transit of tablets through the small intestine. METHODS: Oleic acid, which has previously been shown to activate the brake, was delivered to the small intestine in a modified release capsule at doses of 300 mg, 600 mg and 1200 mg. The effect of the oleic acid was determined by measuring the transit of two sets of radiolabelled tablets by gamma scintigraphy. One set of tablets was dosed with the capsule and the other one hour later. RESULTS: The results show that in the majority of the volunteers small intestinal residence time was greater with the oleic acid than control. The effect was most pronounced in the tablets given concomitantly with the capsule and with the higher doses of oleic acid. CONCLUSIONS: The ileal brake, activated by oleic acid, can slow the transit of tablets through the small intestine.
Feedback↗
Determining molecular binding sites on human serum albumin by displacement of oleic acid.
An NMR method was developed for determining binding sites of small molecules on human serum albumin (HSA) by competitive displacement of (13)C-labeled oleic acid. This method is based on the observation that in the crystal structure of HSA complexed with oleic acid, two principal drug-binding sites, Sudlow's sites I (warfarin) and II (ibuprofen), are also occupied by fatty acids. In two-dimensional [(1)H,(13)C]heteronuclear single quantum coherence NMR spectra, seven distinct resonances were observed for the (13)C-methyl-labeled oleic acid as a result of its binding to HSA. Resonances corresponding to the major drug-binding sites were identified through competitive displacement of molecules that bind specifically to each site. Thus, binding of molecules to these sites can be followed by their displacement of oleic acids. Furthermore, the amount of bound ligand at each site can be determined from changes in resonance intensities. For molecules containing fluorine, binding results were further validated by direct observations of the bound ligands using (19)F NMR. Identifying the binding sites for drug molecules on HSA can aid in determining the structure-activity relationship of albumin binding and assist in the design of molecules with altered albumin binding.
Binding Sites↗
[The effect of nifedipine on pulmonary hemodynamics after injection of oleic acid in rabbits].
Twelve rabbits were divided into two groups, A: control group; B: nifedipine group. Oleic acid (0.1 ml/kg) was injected into pulmonary arteries of 12 rabbits. Nifedipine (1 mg/kg) was given sublingually before oleic acid injected in B group. The results showed that the pulmonary vascular resistance (PVR), pulmonary artery pressure (PAP) were obviously increased and cardiac output (CO) heart rate (HR) decreased in two groups (P less than 0.05, P less than 0.01, P less than 0.001). The degree of increase of PVR, and the degree of decrease of CO were obviously less in B group than that of A group (P less than 0.05, P less than 0.01, P less than 0.001 in different periods). The results showed that nifedipine improved pulmonary hemodynamics of pulmonary damage by oleic acid.
Animals↗
Use of electroporation to accelerate the skin permeability enhancing action of oleic acid.
Rat skin permeability after treatment by electroporation (newly developed frog type electrode, 100V, 10 pulses), oleic acid/propylene glycol (PG) and a combination of both were investigated using Fourier transformed infrared attenuated total reflectance (FT-IR/ATR) analysis. Electroporation immediately disordered the stratum corneum lipid structure up to a certain threshold level. This action lasted throughout the experiment. This may be attributed to the formation of long lifetime of metastable lipid structures, which may allow molecules to pass to the inside of the stratum corneum due to the electroporation-induced fluidized lipid membranes. Electroporation also altered the protein structure of the stratum corneum. When electroporation was combined with 0.05 M oleic acid/PG, uptake of oleic acid and PG into the stratum corneum was remarkably accelerated compared to the application of only 0.05 M oleic acid/PG to the skin. This indicates that electroporation enables oleic acid and PG to penetrate the stratum corneum easily by disrupting the structure of the latter. PG transfer into the dermis from the epidermis was accelerated, not because of the direct action of electroporation on the dermis, but because electroporation induced the rapidly disordering action of oleic acid on the stratum corneum. Lipid-soluble indomethacin permeated the skin more rapidly when the skin was treated with electroporation plus oleic acid/PG than with 0.05 M oleic acid/PG in vitro.
Animals↗
Physiologic and histologic determinants of gas exchange during induction of oleic acid pulmonary edema.
Five anesthetized mongrel dogs were studied during the induction of acute oleic acid pulmonary edema to determine the influence of cardiac output (Qt), extravascular lung water (ETV), and the degree of alveolar flooding on pulmonary gas exchange. Ot and ETV were measured by thermal dye dilution techniques, alveolar flooding was assesed by histologic studies, and gas exchange was quantitated by the multiple inert gas elimination technique (MIGET). Estimates of the inert gas venous admixture [(Qva/ Qt) IG%] were obtained at different experimental stages from the MIGET data to provide an index of overall gas exchange impairment. Pulmonary edema was produced by the intravenous (IV) infusion of oleic acid (0.08 mL/kg). Measurements of Qt, ETV and (Qva/Qt) IG% were made prior to lung injury and at 40, 80, and 120 minutes after injury. After death the lungs were inflated and frozen. Thirty cores of lung parenchyma (2 mL each) were obtained for histologic assessment of alveolar flooding. In the early phase of edema formation (0 to 80 minutes), (Ova/Qt) IG% increased as ETV increased. After 80 minutes, ETV stabilized and further changes in (Qva/ Qt) IG% were then primarily determined by changes in Qt (r = .94). The histologically assessed degree of alveolar flooding correlated well with ETV at the 120-minutes stage (r = .85). However, by use of multivariate analysis, the addition of the histologic information did not appreciably improve the prediction of gas exchange in acute oleic acid pulmonary edema.
Animals↗
Alternatives to the isomerase-dependent pathway for the beta-oxidation of oleic acid are dispensable in Saccharomyces cerevisiae. Identification of YOR180c/DCI1 encoding peroxisomal delta(3,5)-delta(2,4)-dienoyl-CoA isomerase.
Fatty acids with double bonds at odd-numbered positions such as oleic acid can enter beta-oxidation via a pathway relying solely on the auxiliary enzyme Delta(3)-Delta(2)-enoyl-CoA isomerase, termed the isomerase-dependent pathway. Two novel alternative pathways have recently been postulated to exist in mammals, and these additionally depend on Delta(3,5)-Delta(2,4)-dienoyl-CoA isomerase (di-isomerase-dependent) or on Delta(3,5)-Delta(2,4)-dienoyl-CoA isomerase and 2,4-dienoyl-CoA reductase (reductase-dependent). We report the identification of the Saccharomyces cerevisiae oleic acid-inducible DCI1 (YOR180c) gene encoding peroxisomal di-isomerase. Enzyme assays conducted on soluble extracts derived from yeast cells overproducing Dci1p using 3,5,8,11,14-eicosapentenoyl-CoA as substrate demonstrated a specific di-isomerase activity of 6 nmol x min(-1) per mg of protein. Similarly enriched extracts from eci1Delta cells lacking peroxisomal 3,2-isomerase additionally contained an intrinsic 3,2-isomerase activity that could generate 3, 5,8,11,14-eicosapentenoyl-CoA from 2,5,8,11,14-eicosapentenoyl-CoA but not metabolize trans-3-hexenoyl-CoA. Amplification of this intrinsic activity replaced Eci1p since it restored growth of the eci1Delta strain on petroselinic acid for which di-isomerase is not required whereas Eci1p is. Heterologous expression in yeast of rat di-isomerase resulted in a peroxisomal protein that was enzymatically active but did not re-establish growth of the eci1Delta mutant on oleic acid. A strain devoid of Dci1p grew on oleic acid to wild-type levels, whereas one lacking both Eci1p and Dci1p grew as poorly as the eci1Delta mutant. Hence, we reasoned that yeast di-isomerase does not additionally represent a physiological 3,2-isomerase and that Dci1p and the postulated alternative pathways in which it is entrained are dispensable for degrading oleic acid.
Acyl Coenzyme A↗