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At least 649 records · Page 36Linked to original sources
PubMed1991

Differential effects of oleic acid, sodium dodecyl sulfate, and protease inhibitors on the endopeptidase activities of the lobster multicatalytic proteinase.

1. Lobster muscles contain a latent multicatalytic proteinase; heating at 60 degrees C for 1-2 min converts the latent form to a heat-activated form with enhanced proteolytic activity. Both forms have three endopeptidase activities, which are classified as the trypsin-like, chymotrypsin-like, and peptidylglutamylpeptide bond hydrolyzing activities. 2. Sulfhydryl reagents (mersalyl acid, N-ethylmaleimide, hemin, iodoacetamide, and p-chloromercurisulfonic acid), benzamidine, and chloromethyl ketones inhibited all three activities of the heat-activated form. Leupeptin and antipain inhibited only the trypsin-like activity, while the chymotrypsin-like activity was the most sensitive to diisopropyl fluorophosphate, phenylmethanesulfonyl fluoride, aprotinin, and soybean trypsin inhibitor. Pepstatin and L-trans-epoxysuccinylpeptides had little effect on the peptidase activities. 3. Sodium dodecyl sulfate and oleic acid preferentially activated the peptidylglutamyl-peptide hydrolyzing activity of the latent form, whereas N-ethylmaleimide stimulated both the trypsin-like and peptidylglutamyl-peptide hydrolases. These results suggest that the lobster enzyme is an atypical serine proteinase.

Amino Acid Sequence↗
PubMed1991

Balance between fatty acid degradation and lipid accumulation in cultured smooth muscle cells and IC-21 macrophages exposed to oleic acid.

1. The effect of changes in fatty acid beta-oxidation activity on triglyceride and cholesteryl ester synthesis were studied in cultured smooth muscle cells (SMC) and in a macrophage cell line IC-21 in the presence of oleic acid (100 microM). 2. Etomoxir, an inhibitor of carnitine palmitoyltransferase I, stimulated the incorporation of [2-3H]glycerol into triglycerides in SMC and in macrophages 6.2- and 8.2-fold, respectively, and the incorporation of [4-14C]cholesterol into cholesteryl esters in macrophages 3.5-fold. 3. L-Carnitine, a cofactor of fatty acid beta-oxidation, decreased the incorporation of [2-3H]glycerol into triglycerides in smooth muscle cells by 69% and the incorporation of [4-14C]cholesterol into cholesteryl esters by 52%. L-Carnitine had no effect on the macrophages.

Animals↗
PubMed2006

Reproduction of MIGET retention and excretion data using a simple mathematical model of gas exchange in lung damage caused by oleic acid infusion.

The multiple inert-gas elimination technique (MIGET) is a complex mathematical model and experimental technique for understanding pulmonary gas exchange. Simpler mathematical models have been proposed that have a limited view compared with MIGET but may be applicable for use in clinical practice. This study examined the use of a simple model of gas exchange to describe MIGET retention and excretion data in seven pigs before and following lung damage caused by oleic acid infusion and subsequently at different levels of positive end-expiratory pressure. The simple model was found to give, on average, a good description of MIGET data, as evaluated by a chi(2) test on the weighted residual sum of squares resulting from the model fit (P > 0.2). Values of the simple model's parameters (dead-space volume, shunt, and the fraction of alveolar ventilation going to compartment 2) compared well with the similar MIGET parameters (dead-space volume, shunt, log of the standard deviation of the perfusion, log of the standard deveation of the ventilation), giving values of bias and standard deviation on the differences between dead-space volume and shunt of 0.002 +/- 0.002 liter and 7.3 +/- 2.1% (% of shunt value), respectively. Values of the fraction of alveolar ventilation going to compartment 2 correlated well with log of the standard deviation of the perfusion (r(2) = 0.86) and log of the standard deviation of the ventilation (r(2) = 0.92). These results indicate that this simple model provides a good description of lung pathology following oleic acid infusion. It remains to be seen whether physiologically valid values of the simple model parameters can be obtained from clinical experiments varying inspired oxygen fraction. If so, this may indicate a role for simple models in the clinical interpretation of gas exchange.

Animals↗
PubMed2002

Regulation of the uncoupling protein-2 gene in INS-1 beta-cells by oleic acid.

Current evidence suggests that uncoupling protein-2 (UCP2) is a regulator of insulin secretion. It is also known that chronic exposure of pancreatic islets to free fatty acids (FFAs) blunts glucose-stimulated insulin secretion and is accompanied by elevated levels of UCP2. However, the mechanisms regulating expression of UCP2 in beta-cells are unknown. Here, we show that UCP2 mRNA and protein levels were increased after a 48-h exposure of INS-1(832/13) beta-cells to oleic acid (0.5 mm) by activation of the UCP2 promoter. Furthermore, progressive deletions of the mouse UCP2 promoter (from -7.3 kb to +12 bp) indicated that an enhancer region (-86/-44) was responsible for both basal and FFA-stimulated UCP2 gene transcription. This enhancer contains tightly clustered Sp1, sterol regulatory element (SRE), and double E-Box elements. While all three sequence motifs were required for basal activity of the UCP2 promoter, the mutations in either the SRE or the E-Box elements eliminated the response to FFAs. The SRE and sterol regulatory element binding protein-1 (SREBP1) appear to be crucial for the response of the UCP2 gene to FFAs, since overexpression of the nuclear forms of the SREBPs increased UCP2 promoter activity by 7-10-fold and restored the ability of E-Box mutants to respond to oleic acid. These data support a model in which SREBP is the major modulator of UCP2 gene transcription by FFA, while E-Box binding factors play a supportive role.

Animals↗
PubMed1990

Local and global function of the right ventricle in a canine model of pulmonary microembolism and oleic acid edema: influence of ventilation with PEEP.

Right ventricular (RV) dysfunction may occur due to increased RV afterload and, hence, might also contribute to the decrease in cardiac output following institution of PEEP in patients with adult respiratory distress syndrome (ARDS). To test this hypothesis, the authors examined the influence of PEEP on local and global RV function in 12 anesthetized dogs with experimental ARDS (eARDS) induced by pulmonary microembolization with glass beads and oleic acid. Local RV function was analyzed in the RV inflow tract (RVIT) and RV outflow tract (RVOT) by assessing both diastolic segment length, systolic segment shortening, and segment work (sonomicrometry). Global RV contractility was quantified by measuring maximum rate of pressure rise (dRVP/dtmax) and maximum velocity of contractile element shortening (Vmax). In eARDS, despite a fivefold increase in pulmonary vascular resistance, there was no change in cardiac index (CI), global RV contractility, RVIT and RVOT work, and RVIT shortening, whereas RVOT shortening decreased from 12.4 to 7.4% (P less than 0.01). Diastolic segment length increased in RVIT (P less than 0.05) but not in RVOT. PEEP of 10 cmH2O did not alter global RV contractility, RVIT and RVOT shortening, and RVIT work but reduced RVOT work (-35%; P less than 0.01) and CI (-11%; P less than 0.001). Cardiac index further decreased during PEEP of 20 cmH2O (-38%; P less than 0.001), while global RV contractility remained intact despite decreased RVIT and RVOT shortening (-32% and -69%; P less than 0.05) and work (-26% and -59%; P less than 0.01) in the presence of reduced fiber preload in both regions. From these findings, it was concluded that 1) the decreased CI during mechanical ventilation with PEEP at constant right ventricular end-diastolic pressure (RVEDP) is not caused by depressed global RV contractility in dogs with eARDS and a normal myocardium prior to insult. Decreased diastolic segment length and segment shortening during PEEP suggest that 2) PEEP reduces stroke volume by the Starling mechanism rather than by ischemia of the RV free wall. Finally, regionally incongruent changes of fiber preload indicate that 3) local differences in RV wall compliance are likely to occur subsequent to eARDS and PEEP.

Animals↗
PubMed1985

Effect of vasodilator treatment on the resolution of oleic acid injury in dogs.

Diffuse pulmonary injury is accompanied by reduction of blood flow to injured areas because of local pulmonary vasoconstriction, vascular thrombosis, and vascular obliteration. To assess whether reduced pulmonary arterial blood flow might produce relative ischemia in injured areas and consequent potentiation of the injury, we studied the effects of vasodilator treatment in a dog model of diffuse alveolar damage. Twenty-five awake dogs with arterial and pulmonary arterial catheters in place were given 0.08 ml/kg oleic acid, a dose that produces a diffuse lung injury that largely resolves over a 1-wk period. Ten of the animals were treated with minoxidil, a potent vasodilator and inhibitor of hypoxic pulmonary vasoconstriction. Observations were made for a total of 96 h. At 24 h, treated animals had lower pulmonary vascular resistance (207 +/- 85 versus 348 +/- 136 dyne X s X cm-5, p less than 0.01) but higher venous admixture (30 +/- 10% versus 18 +/- 12%, p less than 0.05) and thermodilution-measured lung water (17 +/- 8 ml/kg versus 9 +/- 2 ml/kg, p less than 0.05). However, by 96 h, there were no differences between the 2 groups in any measured parameters of hemodynamic status, gas exchange, or histologic examination. We conclude that pulmonary vasodilation increased blood flow to injured areas but did not affect eventual resolution of the injury.

Animals↗
PubMed1984

Effect of soy protein and casein intake on intestinal absorption and lymphatic transport of cholesterol and oleic acid.

Rats were fed for 4 wk on defined diets containing either casein or soy as the protein source, or diets in which the lysine/arginine ratios were modified by addition of arginine to casein, and lysine to the soy diet. During this period, weight gains and food intakes were comparable in the four dietary groups. Animals were subjected to cannulation of the left thoracic lymphatic duct, and after an overnight fast, were given a single intragastric dose of a lipid emulsion containing oleic acid and cholesterol. The overall 24-h recoveries of cholesterol and fatty acid in lymph were similar in the four groups, as were the distribution of lipids among the major lipid fractions and lipoprotein classes of thoracic duct lymph. However, analysis of timed lymph collections indicated that absorption of lipids was more rapid in casein-fed rats than in those fed soy protein. Furthermore, addition of arginine to the casein diet resulted in a slowed rate of lipid absorption, and addition of lysine to the soy diet markedly increased the rate of lipid absorption.

Animals↗
PubMed1985

Reduction in the stearic to oleic acid ratio in leukaemic cells--a possible chemical marker of malignancy.

Total lipid extracts of peripheral blood cells from patients with chronic leukaemias were analysed for relative values of saturation of the eighteen carbon chain length fatty acids (C 18 FA). The results are expressed as saturation index (C 18 S:C 18 U) of the saturated C 18 FA (stearic acid) over the unsaturated C 18 FA (oleic, linoleic and linolenic acids). The saturation indices of the white blood cells (WBC) and the red blood cells (RBC) in specimens from 14 patients with chronic granulocytic leukaemia (CGL) and 17 patients with chronic lymphocytic leukaemias (CLL) were significantly and consistently lower than control specimens. It is proposed that the relative increase in the unsaturated oleic acid could prove to be a chemical marker of malignancy reflecting a deficient cellular control of the process of stearic acid desaturation. The theoretical implications of the implied increase in membrane fluidity for the cells are discussed.

Chromatography, Gas↗
PubMed1997

The changes of stratum corneum interstices and calcium distribution of follicular epithelium of experimentally induced comedones (EIC) by oleic acid.

Abnormal follicular keratinization is important for comedo formation in acne, but the precise mechanism is not known. A recent report about acne vulgaris suggested that an impaired water barrier function may be responsible for comedo formation, since the barrier dysfunction is accompanied by hyperkeratosis of the follicular epithelium. Furthermore, the integrity of the water barrier is crucial for the maintenance of the epidermal calcium gradient. Yet stratum corneum intercellular lipid structures, a major factor of the skin barrier function, and calcium distribution in the follicular epithelium of comedones, were not reported. To see SC intercellular lipid and calcium distribution of the follicular epithelium of comedo by electron microscopy, we applied oleic acid on the inner surface of the ear of New Zealand white rabbits to induce comedones, and then we obtained specimens and performed osmium and ruthenium tetroxide postfixation and calcium ion-capture cytochemical procedure. We found incomplete lipid bilayer structures, prominent dilatation of lacunar domains and the loss of follicular epidermal calcium gradient in experimentally induced comedones. From our results, we suggest that the permeability barrier disruption in oleic-acid-applied follicular epithelium can be induced by the changes of SC intercellular membrane structures and lacunar dilatation, and the calcium gradient is lost, so follicular epithelial proliferation and hyperkeratosis can be induced and then comedo formation occurs.

Acne Vulgaris↗
PubMed1989

Oleic acid lung injury increases plasma prostaglandin levels.

To determine whether lung injury causes increased plasma prostaglandin (PG) levels, 35 rabbits received oleic acid and 35 served as controls. Half of each group also received 4 ml/kg of Intralipid over one hour and at least five in each subgroup received indomethacin 7.5 mg/kg. Arterial and venous plasma concentrations of PGE2, 6-keto-PGF1 alpha, and PGF2 alpha-M were measured. Venous PGE2 was significantly higher in the oleic acid-injured than in the normal lung group, 1560 +/- 270 (Mean +/- SEM) versus 880 +/- 140 pg/ml (p less than .05). Plasma levels were reduced by 50% with indomethacin, but PGE2 levels remained significantly higher than in the normal lung group, 850 +/- 180 versus 480 +/- 60 for arterial (p less than .05) and 820 +/- 140 versus 480 +/- 80 for venous (p less than .05), respectively. PGF2 alpha-M levels were significantly higher in the lung injury group, 240 +/- 50 versus 50 +/- 40 pg/ml for arterial (p less than .05) and 220 +/- 50 versus 95 +/- 40 for venous (p less than .05), respectively. These lung injury-related increases in PGE2 and PGF2 alpha-M appear related both to increased pulmonary production and to decreased pulmonary clearance. With Intralipid infusion, however, arterial PGE2 increased by 500 +/- 260 pg/ml compared to baseline (p less than .05) with no change in venous PGE2, indicating in this instance that the increase in arterial PGE2 levels is related to increased pulmonary production.

Animals↗
PubMed1991

Oleic acid induced pancreatitis in pigs.

An experimental model of edematous pancreatitis in pigs was established and measurement of pancreatic macro- and microcirculatory parameters and determinations of pancreatic enzymes (lipase, phospholipase A) and vasoactive mediators (prostanoids, kallikrein, kininogen) were performed. During general anesthesia the pancreas was isolated in situ. Pancreatic microcirculatory parameters were measured using videofluorescence microscopy after iv administration of FITC-Dextran. In hourly collected samples lipase and phospholipase A activities were determined enzymatically, concentrations of kallikrein, kininogen, and selected prostanoids were measured by radioimmunoassay. Two experimental groups were studied: (1) control (n = 9); (2) edematous pancreatitis induced by injection of oleic acid into the pancreatic artery (free fatty acid, ffa; n = 10). The animals were followed up for 6 hr. Systemic hemodynamic parameters remained constant in both groups. In the pancreatitis group pancreatic blood flow and O2-consumption decreased significantly (-55 and -49%), while pancreatic vascular resistance increased significantly (+50%). During baseline conditions 41% of all capillaries were perfused. In the pancreatitis group there were both areas with persistent stasis as well as areas with continuous perfusion. However, in the latter areas the portion of perfused capillaries decreased significantly to 27%. In the control group the portion of perfused capillaries remained constant. Liberation of lipase and phospholipase A especially into lymph and ascites fluid was measured during pancreatitis. Furthermore, considerable releases of kallikrein into lymph (+50%) and ascites (+800%) and a marked consumption of kininogen in lymph (+90%) and in ascites fluid (+80%) were measured. Activation of the arachidonic acid cascade and a significant release of prostacyclin and thromboxane A2 into pancreatic venous blood and lymph was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed2001

Redox-dependent modulation of lipid synthesis induced by oleic acid in the human intestinal epithelial cell line Caco-2.

The absorption, remodeling, and delivery of dietary lipids by intestinal cells are part of a complex multi-step process, the dynamics of which is influenced by the lipid composition of the diet and the physiological state of enterocytes. Emerging data indicate that, among the parameters known to modulate the cell functionality, the internal oxidative balance plays a pivotal role. In this study, we analyzed the effects of varying redox equilibria on the way in which the intestinal Caco-2 cell line utilize an exogenous lipid source such as oleic acid. Firstly, we manipulated the intracellular levels of soluble thiols (glutathione), and the amount of cell-associated products of lipid peroxidation, commonly regarded as two critical parameters characterizing the redox profile of the cells. Two different perturbants having opposite effects on the cell's redox profile were used: the pro-oxidizing agent CuSO4 (2.5 and 10 microM) and the antioxidant and thiol supplier N-acetylcysteine (NAC, 2.5 and 5 mM). The influence of these mild but critical manipulations on the incorporation of oleate (50 and 500 microM) into cholesterol, triacylglycerol, and phospholipid was then evaluated. We found that the emerging pro-oxidant condition induced by CuSO4 pre-exposure was associated with a significant up-regulation of phospholipid synthesis, while minor modifications were detected in that of triacylglycerols. Conversely, when a more reducing state was induced by NAC pre-treatment, there was a significant down-regulation of triacylglycerol synthesis, with minor modifications in that of phospholipids. In addition, the incorporation of oleic acid in the cholesteryl ester fraction appeared to be unmodified under all the redox conditions reported. On the whole, these results indicate that the pre-existing internal redox potential of the enterocytes is a critical factor that is able to differentially modulate lipid synthesis at the intestinal level. Thus, the adoption of a strategy designed to control/buffer the antioxidant capacity of the gastrointestinal tract could have important consequences for the modulation of lipid balance in the body.

Acetylcysteine↗
PubMedDate not supplied

Degradation of oleic acid in anaerobic filters: the effect of inoculum acclimatization and biomass recirculation.

The degradation of oleic acid in anaerobic filters was studied and the effect of an acclimated inoculum and biomass recirculation was evaluated. Three anaerobic filters (R1, R2, and R3) were operated in parallel. The anaerobic filters R1 and R2 were inoculated with nonacclimated biomass, whereas the anaerobic filter R3 was inoculated with acclimated biomass. In the anaerobic filters R2 and R3, biomass settling and recirculation were applied. The use of an acclimated inoculum and biomass recirculation (R3) was beneficial in terms of removal efficiency, which was 4 to 8% higher than in the anaerobic filters R1 and R2 when oleate was the sole carbon source fed to the reactors at an applied organic load of 12.5 kg of chemical oxygen demand (COD)/m3 x d, even with an oleate to calcium and magnesium ion molar concentration ratio of 6.8. Biomass recirculation significantly reduced the biomass washout and the toxic effect on the acetogenic and methanogenic populations. The use of an acclimated inoculum was beneficial in terms of methane yield, which was 50% greater than that observed for the reactors inoculated with nonacclimated inoculum for the highest applied organic loading rate (12.5 kg COD/m3 x d). At the end of the operation, the biomass was encapsulated by a whitish matter, which was well detected by microscopic examination. When this sludge was incubated in batch vials at 37 degrees C where no substrate was added, methane production from the adsorbed organic matter was evidenced, attaining a maximum value (at standard temperature and pressure) of 39.7 mL/g volatile solids x d for the biomass taken from R1. With stirring (150 r/min), the methane production rate was 13.8 times higher than under static conditions. When oleate was added to this sludge, methane production was delayed, suggesting that adsorbed matter can be an intermediate of oleate degradation such as stearic, palmitic, myristic, or other saturated acids.

Anaerobiosis↗