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PubMed1990

The prominent role of thromboxane A2 formation on early pulmonary hypertension induced by oleic acid administration in sheep.

The early increase of pulmonary artery pressure observed in different models of experimentally induced lung injury have been shown to be associated with the release of vasoconstrictive agents by activated platelets. The aim of this study was to evaluate the pattern of these metabolites, in particular TxA2, and the effects of the inhibition of their production by ASA on the modifications of pulmonary hemodynamics induced by oleic acid administration in sheep. Group I (8 sheep) was infused with oleic acid (0.09 ml/kg at 0.02 ml/min) while in group II (6 sheep) ASA (10 mg/kg i.v.) was administered 30 minutes before oleic acid infusion. In group I pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR) were significantly higher at the end of the infusion while cardiac output (CO) significantly decreased in comparison to baseline values. A marked increase in plasma TxB2 levels paralleled pulmonary hemodynamic changes. Also plasma 6 keto PGF levels increased after OA infusion. The early increase in PAP and PVR was significantly lower in group II (p less than 0.005) while CO did not undergo any significant change. ASA pretreatment significantly blunted the rise of TxB2 concentrations and prevented the elevation of 6 keto PGFa. These results indicate that early pulmonary hypertension in oleic acid induced injury is mainly related to TxA2 released from platelets and leukocytes and that pulmonary hemodynamic changes are significantly inhibited by ASA pretreatment.

6-Ketoprostaglandin F1 alpha↗
PubMed1975

Exacerbating effect of dietary 12-keto oleic acid on vitamin E deficiency in the rat.

12-Keto oleic acid, possibly one of the oxidation products of long-chain, unsaturated fatty acids, was added to the feed of weanling male rats at the 1% level. Their growth curves, tissue weights, plasma alkaline phosphatase, GOT, and GPT activities, and plasma and liver lipid (cholesterol, triglyceride and phospholipid) levels were investigated and compared with those of weanlings fed a vitamin E deficient diet. Both the diet containing 12-keto oleic acid and the diet deficient in vitamin E decreased the growth rate of body weight and tissue weight, and increased the liver triglyceride and cholesterol levels. Parallel with these, increased hemolysis and stimulation of lipid peroxidation and fluorescent production in the liver homogenate were observed. Elevated plasma alkaline phosphatase and GOT activities which may be considered to be due to a functional disorder of the liver were also observed.

Alanine Transaminase↗
PubMed1994

Developing intestine is injured during absorption of oleic acid but not its ethyl ester.

Although lipids are essential nutrients in the mammalian diet, we have shown that fatty acids are injurious to epithelial cells of developing piglet intestine during luminal perfusion. Furthermore, the intestine of young animals sustains greater injury than that of older piglets. In an effort to understand the mechanism for this developmental injury, we investigated whether changes in the chemical configuration of oleic acid would alter this damage. Mucosal permeability, as quantitated by the plasma-to-lumen clearance of 51chromium EDTA, was evaluated during luminal perfusion with oleic acid as compared with its ethyl (ethyl oleate) and glyceryl (glycerol-1-mono-oleate) esters, solubilized with taurocholic acid, in jejunum of 1-d-, 3-d-, 2-wk-, and 1-mo-old piglets. 51Chromium EDTA clearance increased significantly during oleic acid and glycerol-1-mono-oleate perfusion, but did not increase during perfusion with ethyl oleate or saline. This result was not secondary to failure of absorption of ethyl oleate, as [14C]oleic acid and ethyl [1-14C]oleate were absorbed to a similar extent. Furthermore, developing intestine was able to remove the ethyl group and then re-esterify the fatty acid to form triacyglycerol. These studies indicate that oleic acid-induced mucosal injury can be abolished when the carboxylic group of the fatty acid is esterified with an ethyl, but not a glycerol, group. Since the ethyl ester is also absorbed and metabolized similarly to the free fatty acid, this may provide a means of supplying long-chain fatty acids to developing intestine without causing mucosal damage.

Animals↗
PubMed1986

Effects of micellar oleic acid on canine jejunal blood flow and neurotensin release.

The purpose of this study was to evaluate the role of neurotensin in the local regulation of the lipid-induced jejunal hyperemia. Total blood flow and the arteriovenous hormone concentration difference were measured in isolated jejunal loops of anesthetized dogs with either saline, bile (10% in normal saline), oleic acid (40 mM in normal saline), or oleic acid and bile in the lumen. The bile-oleic acid mixture produced a sustained increase (+25 +/- 3%) in jejunal blood flow, whereas neurotensin release reached a maximum (1.14 +/- 0.34 pmol X min-1 X 100 g-1) 2 min after initiation of the response and then returned to control. Venous neurotensin concentrations also reached a maximum (51 +/- 17 pmol/l) at 2 min. There were no significant changes in either blood flow or neurotensin release in response to the other test solutions. Intra-arterial infusion of neurotensin did not significantly decrease jejunal vascular resistance (-12 +/- 3%) until venous concentrations of 478 +/- 101 pmol/l were attained. It seems unlikely, then, that neurotensin plays any role in the regulation of the lipid-induced jejunal hyperemia.

Animals↗
PubMed1994

New cytochrome P450-dependent reactions from wheat: terminal and sub-terminal hydroxylation of oleic acid by microsomes from naphthalic acid anhydride and phenobarbital induced wheat seedlings.

Incubation of the microsomal fraction from etiolated wheat shoots (Triticum aestivum L. cv Etoile de Choisy) with [1-14C]oleic acid led to the formation of three polar metabolites which were identified as 18-, 17- and 16-hydroxyoleic acids by gas chromatography/mass spectra analysis. They were generated in a molar ratio of 1.4/4.6/4, respectively. Terminal and sub-terminal hydroxylation of oleic acid and the cytochrome P450 content were strongly enhanced in microsomes from wheat shoots treated with naphthalic acid anhydride and phenobarbital. The involvement of cytochrome P450 is demonstrated by the dependence of hydroxylation upon O2 and NADPH, and by their light-reversible inhibition by carbon monoxide. In addition, the hydroxylation of oleic acid, but not of lauric acid and cinnamic acid, was inhibited when microsomes where incubated with 9-octadecen-16-ynoic acid, a substrate analogue displaying an acetylenic function at the carbon position of major enzyme attack. Our results suggest that at least two different P450 enzymes are involved in the oxidation of oleic and lauric acids in wheat.

Cytochrome P-450 Enzyme System↗
PubMed2003

Image analysis, methanogenic activity measurements, and molecular biological techniques to monitor granular sludge from an EGSB reactor fed with oleic acid.

Morphological changes in anaerobic granular sludge fed with increasing loads of oleic acid were quantified by image analysis. The combination of this technique with data on the accumulation of adsorbed long chain fatty acid and with the molecular characterization of microbial community gave insight into the mechanisms of sludge disintegration, flotation and washout. It was found that the bacterial domain was more affected than the archaeal domain during this process. However, no acetoclastic activity and onlya residual hydrogenotrophic activity were detected in the sludge at the end of the operation.

Adsorption↗
PubMed1979

Bactericidal effect of oleic acid on group A streptococci: mechanism of action.

In contrast to Staphylococcus aureus and coagulase-negative staphylococci, group A streptococci are infrequently present on normal human skin, except in certain populations with endemic impetigo. This has been attributed to differences in susceptibility to the bactericidal effect of skin surface lipids, particularly unsaturated fatty acids. When an M type 6 strain group A streptococcus was exposed to 500 mug of oleic acid per ml, viable counts decreased by 4 logs in 5 min. The rank order of killing was 35 > 20 > 4 degrees C. Oleic acid did not kill a strain of S. aureus, a strain of coagulase-negative staphylococcus, or a strain of Escherichia coli, but bound rapidly to these bacteria as well as to the group A streptococcus. The loss of [(3)H]uridine from labeled oleic acid-treated group A streptococcal cells was greater than 100 times that of controls. There was no loss of [(3)H]-thymidine from group A streptococci or of [(3)H]uridine or [(3)H]thymidine from identically exposed coagulase-negative staphylococci. When [(3)H]uridine was added to group A streptococci during mid-log-phase growth, cessation of uptake occurred within 5 min of addition of 50 mug of oleic acid per ml. Electron microscopic changes seen within 5 min included condensation of the nucleoid and distortion of the streptococcal surface by numerous clumps and blebs. Coagulase-negative staphylococci, S. aureus, and E. coli similarly exposed showed no comparable electron microscopic changes. We propose that oleic acid kills group A streptococci by altering the integrity of the cell membrane with resulting loss of ribonucleic acid but not deoxyribonucleic acid.

Escherichia coli↗
PubMed1994

Segmental pulmonary vascular resistances during oleic acid lung injury in rabbits.

We studied in isolated rabbit lungs the effects of oleic acid (OA) injury on the segmental distribution of vascular resistance. Vascular occlusion pressures were measured in control and OA-injured preparations over 90 min. Capillary filtration coefficient KF,C increased from 0.61 (+/- 0.10) to 0.91 (+/- 0.14) g.min-1.mmHg-1.(100 g)-1 in OA-injured lungs whereas it remained constant in control lungs. Total pulmonary vascular resistance changed little in both control and OA-injured lungs. OA injury resulted in a 15% increase of the double occlusion capillary pressure. In addition, the contribution of the microvascular to the total vascular resistance rose from 8% to 22%. The increase in microvascular resistance was significant 15 min after OA on the arteriolar side and became significant 30 min later on the venular side. Oleic acid injury does not change the total pulmonary vascular resistance but alters the distribution of segmental resistances in the isolated rabbit lung, thereby contributing to the accumulation of lung water in this model of low pressure permeability edema.

Animals↗
PubMed1992

Microbial oxidation of oleic acid.

Resting cells of Saccharomyces cerevisiae (baker's yeast, type II; Sigma) were used to convert oleic acid into 10-hydroxyoctadecanoic acid with a 45% yield. Nocardia aurantia (ATCC 12674), Nocardia sp. (NRRL 5646), and Mycobacterium fortuitum (UI 53378) all converted oleic acid into 10-oxo-octadecanoic acid with 65, 55, and 80% yields, respectively. Structures of all metabolites were suggested by 1H and 13C nuclear magnetic resonance and by infrared and mass spectrometry. Structures of isomeric hydroxystearate and oxostearate derivatives and the stereochemical purity of hydroxystearates are difficult to prove unambiguously unless authentic standard compounds are available for spectral comparison. We describe the use of the chemical Baeyer-Villiger oxidation technique with 10-oxo-octadecanoic acid followed by mass spectral analysis of neutral extracts as a simple method to confirm the position of oxo-functional groups in the structures of fatty acid ketones. We further introduce a simple method based on 1H nuclear magnetic resonance analysis of diastereomeric S-(+)-O-acetylmandelate esters of hydroxystearates as a means of ascertaining stereochemical purities of hydroxy fatty acids.

Bacteria↗
PubMed1992

Altered platelet stearic to oleic acid ratio in malignancy.

Alteration of lipid metabolism associated with malignant disease is well-documented and some studies have suggested a reduced stearic to oleic acid ratio occurs in erythrocytes in cancer patients. In this study, the fatty acid composition was measured in platelets, which are capable of lipid synthesis and have a much shorter lifespan. While demonstrating any malignancy related change in the platelet stearic to oleic acid ratio the study aimed to assess whether it could be of value as a tumour marker. Patients with active malignancy (n = 46) had a lower ratio of stearic to oleic acid than those with malignant disease in clinical remission [mean (S.D.) 1.08 (0.22) vs. 1.26 (0.30), P less than 0.01], and 22 healthy controls [1.29 (0.24), P less than 0.001]. However in a group of 17 patients with chronic, non-malignant diseases the ratio was also lower than in normal controls and similar to that seen in the active malignancy group [0.97 (0.29)]. Thus while a reduction in platelet stearic to oleic acid ratio was found in active malignancy, it is not specific to neoplastic disease.

Adolescent↗
PubMed1983

Failure of various agents to decrease oleic acid pulmonary albumin leak.

Computerized pulmonary gamma scintigraphy has been shown to be a sensitive technique for the measurement of albumin flux in oleic acid pulmonary microvascular injury. In this technique technetium-99m-tagged human serum albumin is administered intravenously and lung:heart radioactivity ratios are constructed. This ratio remains constant unless there is a net flux of albumin from the vascular space into the lung, when a rising ratio is seen, called the "slope of injury" or SI. Gamma scintigraphy provides a method to rapidly screen the ability of various possible therapeutic agents to reduce the flux of albumin in experimental ARDS. In this study, 0.05 ml/kg oleic acid produced a significant increase in the SI. None of the agents tested (30 mg/kg methylprednisolone, 12.5 mg/kg ibuprofen, 4 mg/kg MK-447, a superoxide radical scavenger, or 140 mg/kg calcium gluconate) were able to alter the scintigraphically measured increased albumin flux produced by 0.05 ml/kg oleic acid.

Albumins↗
PubMed2003

Oxidative stress in early stage of acute lung injury induced with oleic acid in guinea pigs.

Changes in several biomarkers in bronchoalveolar lavage fluid (BALF) during an early stage of lung injury induced with oleic acid were examined in guinea pigs. In addition, a possible contribution of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and xanthine oxidase to the oxidative changes in the lung injury was investigated. An intravenous injection of oleic acid increased the levels of lipid peroxidation products, lactate dehydrogenase, and total proteins, decreased the ratio of glutathione to glutathione disulfide in the BALF, and also affected the levels of other oxidative biomarkers such as superoxide dismutase and catalase in the BALF in a dose-dependent manner. Diphenyleneiodonium chloride, a NADPH oxidase inhibitor, inhibited the oxidative changes in the BALF and the decrease in partial pressure of oxygen in artery induced with oleic acid, while allopurinol, a xanthine oxidase inhibitor, had no inhibitory effects. The results demonstrate that oxidative stress would be an important mechanism of oleic acid-induced lung injury, and indicate that the NADPH oxidase-dependent pathway contributes significantly to the generation of reactive oxygen species in oleic acid-induced lung injury.

Animals↗
PubMed2003

Role of oleic acid as a neurotrophic factor is supported in vivo by the expression of GAP-43 subsequent to the activation of SREBP-1 and the up-regulation of stearoyl-CoA desaturase during postnatal development of the brain.

We have recently reported that albumin, a serum protein present in the developing brain, stimulates the synthesis of oleic acid by cultured astrocytes by inducing stearoyl-CoA 9-desaturase, the rate-limiting enzyme in oleic acid synthesis, through activation of the sterol regulatory element-binding protein-1. In this work, we offer evidence supporting the in vivo occurrence of this process during the postnatal development of the rat brain. Our results show that albumin reaches maximal brain level by day 1 after birth, coinciding with activation of the sterol response element binding protein-1, which is responsible for the transcription of the enzymes required for oleic acid synthesis. In addition, the developmental profile of stearoyl-CoA 9-desaturase-1 mRNA expression follows that of sterol regulatory element-binding protein-1 activation, indicating that these phenomena are tightly linked. In a previous work, we showed that oleic acid induces neuronal differentiation, as indicated by the expression of growth associated protein-43. Here, we report that the expression of growth associated protein-43 mRNA peaks at about day 7 after birth, following the maximal expression of stearoyl-CoA 9-desaturase-1 mRNA that occurs between days 3 and 5 postnatally. In conclusion, our results support the hypothesis that the synthesis of oleic acid is linked to neuronal differentiation during rat brain development.

Age Factors↗
PubMed2001

Slowing of gastrointestinal transit by oleic acid: a preliminary report of a novel, nutrient-based treatment in humans.

Chronic diarrhea may occur when gastrointestinal transit is abnormally rapid. We hypothesized that oleic acid given prior to a meal would slow gastrointestinal transit and reduce diarrhea by activating nutrient-triggered inhibitory feedback mechanisms in the small intestine. Transit time was measured in eight normal subjects following ingestion of a control emulsion (0 ml oleic acid), and in 45 patients with chronic diarrhea following ingestion of emulsions containing 0, 1.6, and 3.2 ml oleic acid. Stool volume and frequency on and off treatment were compared. Transit time in normal subjects was 102.4 +/- 11.2 min (mean +/- SE). Transit times in patients was shorter at 29.3 +/- 2.8 min with the 0-ml dose (P < 0.001), but increased to 57.2 +/- 4.5 min with the 1.6-ml dose and to 83.3 +/- 5.2 min with the 3.2-ml dose (P < 0.001). In the 18 patients who provided stool records, frequency of bowel movements decreased from 6.9 +/- 0.8 to 5.4 +/- 0.9 bowel movements/24 hr (P < 0.05) and stool volume decreased from 1829.0 +/- 368.6 to 1322.5 +/- 256.9 ml/24 hr with treatment (P < 0.05). An emulsion containing oleic acid slowed gastrointestinal transit and reduced diarrhea by activating nutrient-triggered inhibitory feedback mechanisms in the small intestine.

Adolescent↗
PubMed1992

Polyamines attenuate jejunal mucosal injury induced by oleic acid.

Effects of putrescine, spermidine, and spermine on lipid-induced injury to jejunal mucosa were assessed in anesthetized rats. Mucosal epithelial integrity was continuously monitored by measuring blood-to-lumen clearance of 51Cr-labeled EDTA. Perfusion of jejunal lumen with emulsified lipid (20 mM sodium taurocholate and 40 mM oleic acid) increased 51Cr-EDTA clearance. Addition of spermidine (0.5 mM), but not putrescine (2.0 mM) or spermine (0.25 mM), to the lipid perfusate reduced the increment in 51Cr-EDTA clearance. Histological evaluation of jejunal mucosa indicated that the epithelial lining of the villous tips was damaged by emulsified oleic acid and that this injury was ameliorated by spermidine. Pretreatment of jejunal mucosa with spermidine did not prevent disruption of mucosal integrity induced by a subsequent perfusion with emulsified lipids. Intravenous infusion of spermidine to achieve an extracellular concentration of 0.5 mM did not prevent the lipid-induced increase in 51Cr-EDTA. Spermidine also ameliorated lipid-induced disruption of Caco-2 cell monolayers in culture; this protective effect was dose dependent and was observed only when spermidine was applied to the apical aspect of the monolayers. These findings indicate that spermidine must be present on the apical portion of the epithelial cell during lipid insult. Substitution of lysine or arginine for spermidine did not reduce the extent of lipid-induced injury to jejunal mucosa, indicating that spermidine's protective effects cannot simply be attributed to its cationic nature. Spermidine did not alter the turbidity of a micellar oleic acid solution, indicating that spermidine was not removing oleic acid from the soluble phase.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Anaerobic degradation of oleic acid by suspended and granular sludge: identification of palmitic acid as a key intermediate.

The aim of the present work was to study the maximum potential methane production in batch assays of sludge samples taken along the operation of two EGSB reactors (RI inoculated with granular sludge and RII inoculated with suspended sludge) fed with increasing oleic acid concentrations between 2 and 8 gCOD/l (HRT = 1 day). After removing the residual substrate, the sludge was incubated in batch vials without any added carbon source. A maximum methane production rate of 152+/-21 mlCH4(STP)/gVS.day was obtained for the suspended sludge taken on day 70, when oleate at a concentration of 2 g COD/l was fed with a co-substrate (50% COD). The maximum plateau achieved in the methane production curve was 1145+/-307 mlCH4(STP)/gVS, obtained for the suspended sludge taken on day 162, when oleate was fed as the sole carbon source at 6 g COD/I. The methanization rate of the adsorbed substrate was enhanced under stirring conditions and was inhibited by adding oleic acid. Extraction and GC analysis confirmed that the main adsorbed substrate was palmitate, and not oleate. Accumulated palmitate adsorbed onto the sludge and further beta-oxidation was inhibited when in the presence of oleic acid. If oleic acid was removed from the medium beta-oxidation proceeded with methane production. Suspended sludge was more efficient than granular sludge.

Adsorption↗
PubMed1994

Peroxidation of linoleic, arachidonic and oleic acid in relation to the induction of oxidative DNA damage and cytogenetic effects.

In the present study, the possible role of the polyunsaturated fatty acids linoleic and arachidonic acid in the chemical induction of carcinogenesis has been investigated. Analysis of 7,8-dihydro-8-oxo-2'-deoxyguanosine (8-oxodG) levels in 2'-deoxyguanosine (dG) and isolated DNA has demonstrated that linoleic and arachidonic acid are capable of inducing this specific genotoxic damage. This effect appears to be related to the degree of fatty acid unsaturation, since it was not induced by monounsaturated oleic acid. Enzymatic peroxidation of linoleic and arachidonic acid resulted in a significant increase in oxidative DNA damage. Studies on the interference of radical scavengers with the induction of 8-oxodG in combination with electron spin resonance spectroscopy demonstrated that the superoxide anion was generated during peroxidation of these fatty acids and that singlet oxygen is most likely involved in the formation of oxidative DNA damage. The level of oxidative damage in dG and single-stranded DNA was higher as compared to that in native DNA after equimolar treatment. Exposure of human lymphocytes to linoleic or arachidonic acid did not result in a significant increase in levels of 8-oxodG. This may indicate that the rate of intracellular peroxidation is relatively low and/or that nuclear DNA in intact cells is effectively protected against genetic damage induced by reactive oxygen species. It is therefore concluded that relatively short periods of linoleic or arachidonic acid administration are not likely to impose a direct genotoxic risk. It can, however, not be excluded that chronic exposure to polyunsaturated fatty acids induces oxidative DNA damage or is related to cancer risk by epigenetic mechanisms, as is also indicated by the observed cytotoxic effects of linoleic and arachidonic acid.

Animals↗