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PubMed1994

Beneficial effects of myristic, stearic or oleic acid as part of liposomes on experimental infection and antitumor effect in a murine model.

Liposomes consisting of dicetyl-phosphate, cholesterol, lecithin and stearic or myristic or oleic acid, exert a protective effect for mice against experimental infection by Salmonella typhimurium, and delay both the onset and mortality B16 melanoma in these animals. Liposomes labelled with 3H-myristic acid were used as probes in the spleen and liver. We found that the treatment schedule rather than route of administration of liposomes, is important. The results show that in order to induce protection, preventive treatment must start at least three days before. Longer treatments do not increase the degree of protection, and treatments started at the same time as, or following experimental infection or tumor transplantation, have no effect.

Animals↗
PubMed1988

Effect of oleic acid on mitochondrial oxidative phosphorylation in rat brain slices.

We tested the effect of oleic acid on oxidative phosphorylation and free fatty acid composition in rat brain slices simultaneously to investigate the relationship between the change in respiratory control ratio and the uptake of oleic acid in the brain mitochondria. The uncoupling of mitochondria was observed when the ratio of oleic acid to stearic acid in the free fatty acid fraction was nearly doubled, but was not recovered even by the addition of fatty acid-free bovine serum albumin. The data suggest that the intactness of oxidative phosphorylation of brain mitochondria is maintained by the precise control of the free fatty acid composition in the mitochondrial membranes.

Animals↗
PubMed1991

The effect of some immunomodulators administration to rats on palmitic and oleic acids incorporation into the lipids of liver cell organelles.

The incorporation of equimolar doses of [14C]-palmitic and [3H]-oleic acids into the lipid moiety of hepatocytes after muramyl dipeptide (MDP), adamantylamide dipeptide (AdDP) and levamisole (LM) administration were investigated. The utilization of [14C]-palmitic acid for the synthesis of neutral lipids and phospholipids of crude nuclear fraction increased significantly after MDP and AdDP administration and to a lesser extent after LM. While the incorporation of [3H]-oleic acid did not change significantly after MDP and AdDP, LM significantly increased the incorporation of this acid into the phospholipids of nuclear and microsomal fractions. The changes in the incorporation of saturated palmitic and unsaturated oleic acids suggest a possible influence on deacylation-reacylation mechanisms. These changes could alter the physical properties of membrane and affect certain membrane functions, including the activity of membrane bound enzymes and transport mechanisms.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1990

Proliferation and metabolic significance of peroxisomes in Candida boidinii during growth on D-alanine or oleic acid as the sole carbon source.

We have studied the induction of peroxisomes in the methylotrophic yeast Candida boidinii by D-alanine and oleic acid. The organism was able to utilize each of these compounds as the sole carbon source and grew with growth rates of mu = 0.20 h-1 (on D-alanine) or mu = 0.43 h-1 (on oleic acid). Growth was associated with the development of many peroxisomes in the cells. On D-alanine a cluster of tightly interwoven organelles was observed which made up 6.3% of the cytoplasmic volume and were characterized by the presence of D-amino acid oxidase and catalase. On oleic acid rounded to elongated peroxisomes were dominant which were scattered throughout the cytoplasm. These organelles contained increased levels of beta-oxidation enzymes; their relative volume fraction amounted 12.8% of the cytoplasmic volume.

Alanine↗
PubMed2003

Conversion of alpha-linolenic acid to palmitic, palmitoleic, stearic and oleic acids in men and women.

The purpose of this study was to determine whether adult humans can recycle carbon from alpha-linolenic acid (18:3n-3) into saturated (SFA) and monounsaturated (MUFA) fatty acids. Six men and six women consumed 700 mg [U-13C]-18:3n-3. Blood was collected over 21 days and breath over 24h. [13C]-labelled SFA and MUFA were detected in plasma phosphatidylcholine (PC) and triacylglycerol (TAG). Total labelled fatty acid incorporation into SFA and MUFA was five- and 25-fold greater in PC than TAG in men and women, respectively. [13C]-16:0 was the major labelled fatty acid in both fractions. Total [13C] incorporation into SFA and MUFA was 20% greater in men than women, and related positively (r(2) = 0.35, P<0.05) to the fractional recovery of labelled 18:3n-3 as 13CO2 on breath. These results suggest that the extent of partitioning towards beta-oxidation and carbon recycling may regulate the availability of 18:3n-3 for conversion to longer-chain fatty acids.

Adult↗
PubMed1987

Inhibition of angiotensin-converting enzyme by perindopril diacid in canine oleic acid pulmonary edema.

To test the hypothesis that angiotensin II could be a mediator of acute lung injury, we studied the effects of perindopril diacid, a new angiotensin-converting enzyme inhibitor, on hemodynamics, blood gases, lung mechanics, and extravascular lung water (EVLW). Twenty-four dogs were anesthetized, paralyzed and ventilated with a fraction of inspired oxygen of 0.4 in which pulmonary edema was induced by 0.1 ml/kg iv oleic acid. Perindopril diacid (1 mg/kg) was administered iv either before (eight dogs) or 100 min after (eight dogs) oleic acid injection. In the control group (eight dogs) not treated with perindopril diacid, 150 min after oleic acid injection, PaO2 changed from 193 +/- 7 (mean +/- SEM) to 55 +/- 4 torr, venous admixture from 3 +/- 1% to 52 +/- 5%, cardiac index from 4.1 +/- 0.3 to 3.1 +/- 0.3 L/min X m2, mean pulmonary artery pressure from 13 +/- 1 to 17 +/- 1 mm Hg, dynamic compliance from 90 +/- 8 to 46 +/- 7 ml/cm H2O, and EVLW from 165 +/- 25 to 750 +/- 92 ml/m2. Administration of perindopril diacid reduced systemic BP by 20% but did not affect other hemodynamic variables, blood gases, or dynamic compliance. Maximum increases in EVLW were from 169 +/- 16 to 615 +/- 54 ml/m2 in the pretreated group and from 188 +/- 23 to 675 +/- 56 ml/m2 in the treated group (no significant difference from the control group). However, pretreatment with perindopril diacid significantly (p less than .05) slowed the rise in EVLW, which was lower 60 and 90 min after oleic acid injection compared to untreated dogs. Plasma renin activity and angiotensin I concentration increased after oleic acid injection.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1972

Adsorption of palmitic, stearic and oleic acids in the sheep in the presence or absence of bile and-or pancreatic juice.

1. The absorption of (3)H- and (14)C-labelled palmitic, stearic and oleic acids under control conditions and in the absence of bile and/or pancreatic juice has been studied in sheep prepared with intestinal cannulae and reentrant fistulation of the thoracic lymph duct.2. Under control conditions the percentage recoveries in thoracic duct lymph of fatty acids introduced into the duodenum were: stearic acid 59.6 +/- 3.2 (mean +/- S.E. of mean), palmitic acid 71.1 +/- 1.2 and oleic acid 80.4 +/- 1.9.3. At the peak of absorption over 90% of the radioactivity was located in the triglyceride fraction.4. It was calculated that between 1900 and 3800 ml. lymph containing up to 20 g lipid flowed daily from the thoracic duct. The major fatty acids of lymph triglycerides were C(16:0) (26%), C(18:0) (39%) and C(18:1) (19%).5. In the absence of pancreatic juice, but in the presence of bile, the absorption of stearic, palmitic and oleic acids was 0.8, 4.-8.5 and 26% respectively of the dose injected into the duodenum. In the absence of bile but presence of pancreatic juice corresponding values were 0.1-0.5, 1.8 and 7.7%.6. In the absence of pancreatic juice the total lipid content of thoracic duct lymph fell from 800 to 80 mg% within 4 hr. When bile was also absent the lipid content of lymph fell further to 50 mg%.7. It is concluded that pancreatic juice functions in the lumen of the intestine probably through the production from biliary lecithin of the lysolecithin necessary for the optimum absorption of lipids.

Animals↗
PubMed2005

Compact oleic acid in HAMLET.

HAMLET (human alpha-lactalbumin made lethal to tumor cells) is a complex between alpha-lactalbumin and oleic acid that induces apoptosis in tumor cells, but not in healthy cells. Heteronuclear nuclear magnetic resonance (NMR) spectroscopy was used to determine the structure of 13C-oleic acid in HAMLET, and to study the 15N-labeled protein. Nuclear Overhauser enhancement spectroscopy shows that the two ends of the fatty acid are in close proximity and close to the double bond, indicating that the oleic acid is bound to HAMLET in a compact conformation. The data further show that HAMLET is a partly unfolded/molten globule-like complex under physiological conditions.

Humans↗
PubMed1990

Low density lipoprotein rich in oleic acid is protected against oxidative modification: implications for dietary prevention of atherosclerosis.

Oxidative modification of low density lipoprotein (LDL) enhances its potential atherogenicity in several ways, notably by enhancing its uptake into macrophages. In vivo studies in the rabbit show that inhibition of LDL oxidation slows the progression of atherosclerotic lesions. In the present studies, rabbits were fed either a newly developed variant sunflower oil (Trisun 80), containing more than 80% oleic acid and only 8% linoleic acid, or conventional sunflower oil, containing only 20% oleic acid and 67% linoleic acid. LDL isolated from the plasma of animals fed the variant sunflower oil was highly enriched in oleic acid and very low in linoleic acid. These oleate-rich LDL particles were remarkably resistant to oxidative modification. Even after 16-hr exposure to copper-induced oxidation or 24-hr incubation with cultured endothelial cells, macrophage uptake of the LDL was only marginally enhanced. The results suggest that diets sufficiently enriched in oleic acid, in addition to their LDL-lowering effect, may slow the progression of atherosclerosis by generating LDL that is highly resistant to oxidative modification.

Animals↗
PubMed1977

Effects of decreasing lung compliance with oleic acid on the cardiovascular response to PEEP.

In 12 anesthetized mongrel dogs on a constant volume ventilator, the response of the cardiovascular system to increasing positive end-expiratory pressure (PEEP) was examined before and after inducing acute lung injury with oleic acid. As PEEP was raised to approximately 16 mmHg, lung volume increased by approximately 900 ml before oleic acid and only 350 ml after. Pleural pressure increased by the same amount, indicating that both lung and chest wall compliance decreased with oleic acid. Right atrial pressure, the back pressure to venous return, also increased by the same amount. Although cardiac output at PEEP = 0 was lower after oleic acid, the relative decrements produced by increasing PEEP were the same as before oleic acid.

Animals↗
PubMed2004

Oleic acid levels regulated by glycerolipid metabolism modulate defense gene expression in Arabidopsis.

Stearoyl-acyl-carrier-protein-desaturase-mediated conversion of stearic acid (18:0) to oleic acid (18:1) is a key step, which regulates levels of unsaturated fatty acids in cells. We previously showed that stearoyl-acyl-carrier-protein-desaturase mutants ssi2/fab2 carrying a loss-of-function mutation in the plastidial glycerol-3-phosphate (G3P) acyltransferase (act1) have elevated 18:1 levels and are restored in their altered defense signaling. Because G3P is required for the acylation of 18:1 by G3P acyltransferase, it was predicted that reduction of G3P levels should increase 18:1 levels and thereby revert ssi2-triggered phenotypes. Here we show that a mutation in G3P dehydrogenase restores both salicylic acid- and jasmonic acid-mediated phenotypes of ssi2 plants. The G3P dehydrogenase gene was identified by map-based cloning of the ssi2 suppressor mutant rdc8 (gly1-3) and confirmed by epistatic analysis of ssi2 with gly1-1. Restoration of ssi2-triggered phenotypes by the gly1-3 mutation was age-dependent and correlated with the levels of 18:1. Regeneration of G3P pools by glycerol application in ssi2 and ssi2 gly1-3 plants caused a marked reduction in the 18:1 levels, which rendered these plants hypersensitive to glycerol. This hypersensitivity in ssi2 was rescued by the act1 mutation. Furthermore, overexpression of the ACT1 gene resulted in enhanced sensitivity to glycerol. Glycerol application also lowered the 18:1 content in SSI2 plants and converted these into ssi2-mimics. Our results show that 18:1 levels in plastids are regulated by means of acylation with G3P, and a balance between G3P and 18:1 is critical for the regulation of salicylic acid- and jasmonic acid-mediated signaling pathways.

Alleles↗
PubMed1989

Effect of choline esters and oleic acid on the penetration of acyclovir, estradiol, hydrocortisone, nitroglycerin, retinoic acid and trifluorothymidine across hairless mouse skin in vitro.

Five choline esters, lauroylcholine, myristoylcholine, palmitoylcholine, stearoylcholine and oleoylcholine, were evaluated as skin penetration enhancers by testing their effects on the penetration of six drugs, acyclovir, 17 beta-estradiol, hydrocortisone, nitroglycerin, all-trans-retinoic acid and trifluorothymidine, across hairless mouse skin in vitro and comparing the results to those obtained with oleic acid. The results show that the transdermal delivery of the drugs tested from propylene glycol vehicle systems, can be significantly increased by adding small amounts of choline esters and/or oleic acid to the vehicle. Lauroylcholine was a better enhancer than oleic acid for the transdermal delivery of 17 beta-estradiol and, in mixtures, lauroylcholine and oleic acid acted as synergists giving larger enhancement of the transdermal delivery of nitroglycerin and acyclovir than when used separately.

Acyclovir↗
PubMed1998

Oleic acid distribution in small intestinal epithelial cells expressing intestinal-fatty acid binding protein.

Intestinal-fatty acid binding protein (I-FABP) has been proposed to target long chain fatty acids (LCFA) to triglyceride synthesis pathways in the intestinal epithelium. In the present studies hBRIE 380i cells, which endogenously express I-FABP only when fully differentiated, were used to investigate the role of I-FABP in LCFA incorporation and targeting by examining the relative distribution of [3H]-oleic acid in cellular lipids in these cells. [3H]-oleic acid incorporation into triglyceride was significantly higher in hBRIE 380i cells expressing I-FABP than in cells not expressing I-FABP. After 15 min, 1 and 4 h of incubation, cells expressing I-FABP incorporated 24.0%, 34.0% and 43.9% of [3H]-oleic acid into triglyceride, while newly confluent cells (no I-FABP expression) incorporated 15.6%, 18.3% and 31.9%. An I-FABP negative cell line, hBRIE 380i-neg cells, was stably transfected to investigate the effect of adding I-FABP to small intestinal epithelial cell lines. No measurable differences in [3H]-oleic acid incorporation into triglyceride was detected in these transfectants. Additionally I-FABP expression had no effect on [3H]-oleic acid incorporation or distribution within phospholipid subclasses in hBRIE 380i or transfected hBRIE 380i-neg fabpi cells. Our data from hBRIE 380i cells suggest that I-FABP can target LCFA to triglyceride synthesis pathway. However, endogenous I-FABP expression was also correlated to cellular differentiation and therefore raises the possibility that other differentiation-dependent factors may have a role in LCFA targeting. Because no effects of I-FABP were detected in the transfected hBRIE 380i-neg fabpi cells, it is concluded that factors in addition to I-FABP play a major role in determining the metabolic fate of LCFA in small intestinal epithelial cells. (c) 1998 Elsevier Science B.V.

Animals↗
PubMed1994

Epidermal growth factor attenuates jejunal mucosal injury induced by oleic acid: role of mucus.

Epidermal growth factor (EGF) is present in biliary, pancreatic, and Brunner's gland secretions. The aim of the present study was to assess the effects of EGF on lipid-induced mucosal injury. The proximal jejunum of anesthetized rats was cannulated for perfusion of the lumen with emulsified oleic acid (40 mM oleic acid in 20 mM sodium taurocholate; pH 6.0). Mucosal epithelial integrity was monitored by measuring the blood-to-lumen clearance of 51Cr-labeled EDTA. Perfusion of the lumen with emulsified lipid increased EDTA clearance. Addition of EGF (0.5 ng/ml) to the lipid emulsion ameliorated the lipid-induced increase in EDTA clearance. Perfusion of the lumen with EGF alone stimulated mucus secretion from goblet cells. This effect of EGF was abolished by atropine. In addition, in atropinized animals there was 1) an exaggeration of the lipid-induced injury and 2) a loss of the protective effect of EGF. Our findings provide evidence supporting the hypothesis that EGF provides protection against lipid-induced mucosal injury, in part, by stimulating mucus production.

Animals↗
PubMed1977

Dose-dependent effect of TRH on plasma oleic acid in man.

Administered to normal subjects of either sex, the TRH enhances the plasma oleic acid after 60 minutes without any significantly marked modification in the blood concentration of total FFA. The oleic acid increase is significantly dependent on the amount of administered TRH (200 microgram and greater than or equal to 400 microgram). It is accompanied by 1) a more or less pronounced but acute release of TSH, and 2) a rise in circulating T3 but a submaximal value within the time-course of the experiment (1 h). This elevation is presumably due to a preferential liberation of oleic acid by the adipose tissue, through a direct action of TSH and/or under the permissive influence of the thyroid hormone, among other factors that may intervene in the process.

Adult↗
PubMed1988

Effects of lung congestion and oleic acid injury on the Hering-Breuer reflex.

Breathing and the Hering-Breuer (HB) reflex may be stimulated by congestion and by acute lung injury, but there is disagreement about the effects of both stimuli. This study evaluated these effects using greater stimulus isolation and control of secondary interactions than have previously been employed. Pressurization of lung vessels and left heart and oleic acid injury were individually imposed on anesthetized open-chest dogs perfused with an external pump and gas exchanger. Lungs were inflated in steps before and during those stimuli. The HB reflex was evaluated from graphs of breathing frequency (fr) vs. airway pressure. Congestion itself had no significant sustained effect on fr, but it slightly depressed the HB reflex. Oleic acid tachypnea that was depressed to pretreatment fr by inflation, implying enhancement of the HB response. Capsaicin and oleic acid had similar effects. Vagal cooling to 8 degrees C slightly depressed the effects of oleic acid and capsaicin, had no effect on the sustained fr response to congestion, and reversed the inhibitory effect of inflation. A stimulation of breathing or an enhancement of the HB reflex by congestion was not confirmed, but oleic acid increased fr and the HB reflex.

Animals↗