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PubMed1995

Oleic acid inhibits endothelial nitric oxide synthase by a protein kinase C-independent mechanism.

Many obese hypertensive individuals have a cluster of cardiovascular risk factors. This cluster includes plasma nonesterified fatty acid concentrations and turnover rates that are higher and more resistant to suppression by insulin than in lean and obese normotensive individuals. The higher fatty acids may contribute to cardiovascular risk in these patients by inhibiting endothelial cell nitric oxide synthase activity. To test this hypothesis, we quantified the effects of oleic (18:1[cis]) and other 18-carbon fatty acids on nitric oxide synthase activity in cultured bovine pulmonary artery endothelial cells by measuring the conversion of [3H]L-arginine to [3H]L-citrulline. Oleic acid (from 10 to 100 mumol/L) caused a concentration-dependent decrease in nitric oxide synthase activity at baseline and during ATP and ionomycin (Ca2+ ionophore) stimulation. At 100 mumol/L, linoleic (18:2[cis]) and oleic acids caused similar reductions of nitric oxide synthase activity, whereas elaidic (18:1[trans]) and stearic (18:0) acids had no effect. Oleic acid also inhibited the endothelium-dependent vasodilator response to acetylcholine in rabbit femoral artery rings preconstricted with phenylephrine (P < .05) but had no effect on the response to nitroprusside. The pattern of 18-carbon fatty acid effects on nitric oxide synthase activity in endothelial cells is consistent with activation of protein kinase C. Although oleic acid increased protein kinase C activity in endothelial cells, neither depletion of protein kinase C by 24-hour pretreatment with phorbol 12-myristate 13-acetate nor its inhibition with staurosporine eliminated the inhibitory effect of oleic acid on nitric oxide synthase.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1965

Effect of oleic acid on growth and cell structure of mycobacteria.

Schaefer, Werner B. (National Jewish Hospital, Denver, Colo.), and C. Willard Lewis, Jr. Effect of oleic acid on growth and cell structure of mycobacteria. J. Bacteriol. 90:1438-1447. 1965.-The growth-stimulatory effect of fatty acids on Mycobacterium kansasii and other mycobacterial species is associated with transient changes in the morphology of the bacteria. One change observed is the appearance of intracellular vacuoles separated by chromatinic crossbars. Evidence is presented that these changes are due to the rapid metabolic uptake and the accumulation of lipid in the form of globules. This process provides the cells with an internal reservoir of a preferred carbon and energy source. In certain mycobacterial species, including M. kansasii, the morphological changes are elicited by free and by esterified fatty acid; in others, only by free fatty acid. The latter strains apparently lack the enzyme to split the fatty acid ester.

Fatty Acids↗
PubMed2006

Nitric oxide-independent lipid metabolism in RAW 264.7 macrophages loaded with oleic acid.

The role of nitric oxide (NO) in the regulation of lipogenesis and lipolysis in RAW 264.7 macrophages loaded with oleic acid (OA) was investigated in this paper. Magnolol stimulated full lipolysis without affecting NO levels. Both inhibition and elevation of NO production in OA-loaded macrophages did not induce lipolysis. Besides, lipopolysaccharide (LPS)-induced increased accumulation of lipid droplets was not reduced by down-regulation of NO levels. Moreover, incubation of macrophages with sodium nitroprusside (SNP), an NO donor, stimulated significant NO production without altering the lipid droplet accumulation. All these results clearly demonstrate that NO is not involved in the modulation of lipid metabolism in macrophages loaded with OA.

Animals↗
PubMed1982

Histologic and hemodynamic effects of prostacyclin and prostaglandin E1 following oleic acid infusion.

The hemodynamic and histologic effects of exogenous prostacyclin (PGI2) and prostaglandin E1 (PGE1) on oleic acid-induced acute respiratory failure were investigated. Adult mongrel dogs infused with oleic acid were treated with saline solution, PGE1, and PGI2. Significantly lowered blood pressure, systemic and pulmonary vascular resistance, and arteriovenous oxygen difference and preservation of preoleic cardiac output were observed in the pGI2 group. Compared with the saline group, only the arteriovenous oxygen difference was improved with PGE1. Light microscopy revealed acute edema and inflammation in the saline- and PGE1-treated lungs. Histologic specimens in the PGI2 group were normal.

Animals↗
PubMed2006

The sensitivity of yeast mutants to oleic acid implicates the peroxisome and other processes in membrane function.

The peroxisome, sole site of beta-oxidation in Saccharomyces cerevisiae, is known to be required for optimal growth in the presence of fatty acid. Screening of the haploid yeast deletion collection identified approximately 130 genes, 23 encoding peroxisomal proteins, necessary for normal growth on oleic acid. Oleate slightly enhances growth of wild-type yeast and inhibits growth of all strains identified by the screen. Nonperoxisomal processes, among them chromatin modification by H2AZ, Pol II mediator function, and cell-wall-associated activities, also prevent oleate toxicity. The most oleate-inhibited strains lack Sap190, a putative adaptor for the PP2A-type protein phosphatase Sit4 (which is also required for normal growth on oleate) and Ilm1, a protein of unknown function. Palmitoleate, the other main unsaturated fatty acid of Saccharomyces, fails to inhibit growth of the sap190delta, sit4delta, and ilm1delta strains. Data that suggest that oleate inhibition of the growth of a peroxisomal mutant is due to an increase in plasma membrane porosity are presented. We propose that yeast deficient in peroxisomal and other functions are sensitive to oleate perhaps because of an inability to effectively control the fatty acid composition of membrane phospholipids.

ATPases Associated with Diverse Cellular Activitie↗
PubMed1982

Oleic acid lung damage in pigs.

With the purpose of producing a lung damage model simulating post-traumatic pulmonary insufficiency, oleic acid 0.1 ml . kg-1 body weight (b.w.) was infused intravenously into eight mechanically ventilated young pigs, and the effects were studied for 2 h. After the infusion, PaO2 during air breathing decreased to a fairly low and stable level of about 7 kPa. Venous admixture during air breathing and VD/VT showed a marked initial increase and then remained unchanged, while venous admixture during breathing of pure oxygen increased but less markedly. Haematocrit (EVF), arterial carbon dioxide tension (PaCO2) and base excess (BE) were unchanged. Mean pulmonary arterial pressure more than doubled and cardiac output decreased by 1/3, which was considered to reflect an insuperable increase in the resistance of the pulmonary blood flow. The lung model was found to resemble post-traumatic pulmonary insufficiency with respect both to the V/Q ratio displacement and to the macroscopic appearance of the lungs at autopsy.

Animals↗
PubMed1990

Interactions of serum proteins with small unilamellar liposomes composed of dioleoylphosphatidylethanolamine and oleic acid: high-density lipoprotein, apolipoprotein A1, and amphipathic peptides stabilize liposomes.

Small unilamellar liposomes composed to dioleoylphosphatidylethanolamine (DOPE) and oleic acid (OA) are stabilized by incubation with normal human serum or plasma [Liu, D., & Huang, L. (1989) Biochemistry 28, 7700-7707]. The present report describes a systematic study of interactions of purified serum proteins and lipoproteins with these liposomes. Albumin destabilized liposomes by extracting OA from the liposomes, whereas immunoglobulins and lipoproteins (HDL, LDL, and VLDL) had no effect. However, HDL and, to some extent, VLDL showed a rapid stabilization activity against the lytic effect of albumin. HDL added together with or shortly after the addition of albumin completely abolished the liposome leakage and aggregation effects induced by albumin. SDS-PAGE analysis of the HDL-stabilized liposomes revealed that apolipoprotein A1 was associated with liposomes. Purified apolipoprotein A1, but not a lipid mixture resembling the lipid composition of HDL, showed comparable liposome stabilization activity as HDL. Furthermore, synthetic peptides resembling the amphipathic helices found in apolipoprotein A1 also showed strong liposome stabilization activity. Peptides which were able to form amphipathic helixes of a wedge shape were more effective stabilizers than those which could not. These data indicate that HDL plays a major role in human serum or plasma for the liposome stabilization activity. HDL exerts its activity probably by the interactions of the amphipathic helices of apolipoprotein A1 with the hydrophobic voids found on the outer surface of the highly curved, small liposomes.

Apolipoprotein A-I↗
PubMed2002

Characterization of new acrylic bone cements prepared with oleic acid derivatives.

Acrylic bone-cement formulations were prepared with the use of a new tertiary aromatic amine derived from oleic acid, and also by incorporating an acrylic monomer derived from the same acid with the aim of reducing the leaching of toxic residuals and improving mechanical properties. 4-N,N dimethylaminobenzyl oleate (DMAO) was used as an activator in the benzoyl-peroxide radical cold curing of polymethyl methacrylate. Cements that contained DMAO exhibited much lower polymerization exotherm values, ranging between 55 and 62 C, with a setting time around 16--17 min, depending on the amine/BPO molar ratio of the formulation. On curing a commercial bone cement, Palacosreg R with DMAO, a decrease of 20 C in peak temperature and an increase in setting time of 7 min were obtained, the curing parameters remaining well within limits permitted by the standards. In a second stage, partial substitution of MMA by oleyloxyethyl methacrylate (OMA) in the acrylic formulations was performed, the polymerization being initiated with the DMAO/BPO redox system. These formulations exhibited longer setting times and lower peak temperatures with respect to those based on PMMA. The glass transition temperature of the experimental cements were lower than that of PMMA cement because of the presence of long aliphatic chains of both activator and monomer in the cement matrix. Number average molecular weights of the cured cements were in the range of 1.2x10(5). PMMA cements cured with DMAO/BPO revealed a significant (p<0.001) increase in the strain to failure and a significant (p<0.001) decrease in Young's modulus in comparison to Palacosreg R, whereas ultimate tensile strength remained unchanged. When the monomer OMA was incorporated, low concentrations of OMA provided a significant increase in tensile strength and elastic modulus without impairing the strain to failure. The results demonstrate that the experimental cements based on DMAO and OMA have excellent promise for use as orthopaedic and/or dental grouting materials.

Acrylates↗
PubMed1986

A newly discovered protein kinase C activator (oleic acid) enhances long-term potentiation in the intact hippocampus.

Protein kinase C can be activated by oleate, an unsaturated fatty acid. Since protein kinase C is activated by long-term potentiation, we wished to determine whether iontophoretic ejection of oleate into the intact hippocampal dentate gyrus of urethane-anesthetized rats would cause an enhancement of the response potentiated by high frequency stimulation of the perforant path. Oleate ejection did significantly enhance the persistence of the potentiated response. Moreover, a growth of the response beyond the initial potentiation was seen. Arachidonate, which stimulates protein kinase C to a lesser degree, had a significant preservation effect, but no effect on growth of the response. After vehicle and elaidate (trans-stereoisomer of oleate) ejections, the potentiated response decayed to baseline values. In addition, the persistence of the potentiated response observed two hours after its induction was positively correlated with the ability of an unsaturated fatty acid to activate protein kinase C in vitro. The present results support the proposal that protein kinase C activation enhances synaptic strength. It is suggested that one mechanism for this activation may be PLA2-mediated release of oleate.

Animals↗
PubMed1984

Incorporation and distribution of 3H oleic acid in the isolated, perfused guinea-pig heart made hypoxic.

Improved methods of autoradiography and lipid extraction have been used to study the influence of hypoxia on the fate of radioactive fatty acids in the isolated guinea pig heart. Evidence is provided that hypoxia causes a shift of the rate-limiting step from transport into the cell to oxidation in the mitochondria. This leads to an increased radioactivity in myocardial free fatty acid and in the cytosol. Radioactivity in the mitochondria is decreased and disappears more slowly. At the same time, there is an increased radioactivity in lipid droplets and in triacylglycerol. There is no evidence of a specific location of radioactivity in the sacroplasmic reticulum.

Animals↗