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PubMed2004

Diversity of oleic acid, ricinoleic acid and linoleic acid conversions among Pseudomonas aeruginosa strains.

Sixteen Pseudomonas aeruginosa strains, including patent strain NRRL B-18602, three recent isolates from composted materials amended with ricinoleic acid, and 12 randomly selected from the holdings of the ARS Culture Collection, were examined for their fatty acid converting abilities. The study examined the bioconversion of oleic acid to 7,10-dihydroxy-8( E)-octadecenoic acid (DOD) and ricinoleic acid to 7,10,12-trihydroxy-8( E)-octadecenoic acid (TOD). A new DOD-like compound from linoleic acid was observed. All strains except NRRL B-247 exhibited varying levels of DOD production. NRRL B-1000, NRRL B-18602 and NRRL B-23258 with yields up to 84% were among the best DOD producers. TOD production generally paralleled DOD production at a relatively lower yield of up to 15%. Strains NRRL B-1000 and NRRL B-23260 were the best TOD producers. A DOD-like product in low yields was obtained from linoleic acid. The fatty acid bioconversion capability was related neither to growth rate nor to variation in the greenish pigmentation of the strains. Production of significant quantities of DOD and TOD from oleic and ricinoleic acids, respectively, appeared to be a characteristic trait of P. aeruginosa strains. A number of highly effective strains for DOD production were identified.

Culture Media↗
PubMed1987

Combined chronic toxicity and carcinogenicity studies of morpholine oleic acid salt in B6C3F1 mice.

Morpholine oleic acid salt (MOAS) was administered to groups of 50 male and 50 female B6C3F1 mice in the drinking-water at levels of 0, 0.25 and 1.0%. Both sexes given 1.0% MOAS and females given 0.25% showed growth retardation. Significant increases in blood-urea nitrogen concentrations were only observed in the 1.0% male group. The incidence of squamous-cell hyperplasia of the forestomach epithelium was significantly higher in the males given 1.0% than in the controls. The male mice given 0.25% MOAS had a significantly reduced incidence of hepatocellular carcinoma in comparison with the control group and this trend was indicated also in the 1.0% group. This experiment did not demonstrate any carcinogenic effect of MOAS in mice at levels up to 1.0% in the drinking-water.

Animals↗
PubMed1977

[Release of synthesized lipids by isolated Wistar rat liver perfused by labelled oleic acid and glycerol].

After perfusions with oleic acid (9, 10-3H) and glycerol (1-14C) of isolated livers from wistar Rats, previously subjected to fasting, the study of the TG and PL synthesized by the liver and released in the circulation gives of evidence similar ways of metabolising TG and PL. Two liver pools are present: -- a storage pool, built with slow exchanges of AG of endogenous glycerolipids. In our experiments, the TG: 16 : 0 18 : 1 18: 2 and 16 : 0 18 : 1 18 : 1 and the PL: PE and PC are the glycerolipids of liver constitution: -- a pool of liver secretion. TG and PL are formed according to a rapid de novo synthesis using preferentially the exogenous substrates. They are released in the circulation. In our experiments, the TG secreted are the TG 18 : 1 18 : 1 18 : 1 and 16 : 0 18 : 1 18 : 2, the PL are the PE, AP and LPC.

Animals↗
PubMed1986

Effects of lobar pulmonary blood flow on the evolution of oleic acid lung injury in dogs.

We studied the effects of interruption of the pulmonary blood flow to the left diaphragmatic lung lobe on the evolution of canine oleic acid lung injury. We compared the morphology and edema of the left diaphragmatic lobe, whose pulmonary artery was ligated immediately after oleic acid injury, with the right diaphragmatic lobe, in which the blood supply was intact. The injury plus ligation resulted in hypoxemia and pulmonary hypertension with PaO2 falling from 98 +/- 4 to 72 +/- 21 torr (P less than 0.05) and pulmonary artery pressure increasing from 11 +/- 3 to 18 +/- 4 mm Hg (P less than 0.05). Animals were sacrificed 48 hr following the injury. Morphological examination of right and left lobes showed no consistent differences although wet/dry ratios indicated significantly greater edema (P less than 0.01) for the right diaphragmatic lobes (7.66 +/- 1.23) than the left (6.80 +/- 0.59). Both right and left lobes were substantially more edematous than our laboratory normal value of 4.74 +/- 0.54 (P less than 0.001 for both). We conclude that interruption of pulmonary arterial blood flow protects against edema formation in oleic acid injury but does not alter the morphologic evolution of the injury.

Animals↗
PubMed1989

Comparison of two formulas to calculate alveolar oxygen tension in canine oleic acid pulmonary edema.

Alveolar oxygen tension (PAO2) is calculated by either of two mathematical formulas incorporating various respiratory variables. The first formula, Equation 1, assumes a constant RQ of 0.8; the second formula, Equation 2, uses the mixing equation and requires analysis of inspired, mixed expired, and end-tidal gas samples. We tested the consistency of these formulas before and after asymmetric oleic acid pulmonary edema, then calculated and compared venous admixture values using the PAO2 value derived from each formula. Before oleic acid, Equations 1 and 2 were similar (213 +/- 22 vs. 211 +/- 22 [SD] torr, respectively), as were venous admixture values (8.7 +/- 2.9% vs. 8.5 +/- 2.9%, respectively). After oleic acid injury, Equation 1 was significantly lower than Equation 2, thus slightly but consistently underestimating venous admixture (29.9 +/- 12.2% vs. 30.2 +/- 12.3%; p less than .01). However, the venous admixture values obtained after oleic acid injury calculated from Equations 1 and 2 correlated closely (r2 = .998; p less than .001), and the clinical differences yielded by the two formulas would be minimal. We recommend using the simpler formula (Eq. 1) when calculating PAO2.

Animals↗
PubMed1993

Oxidation resistance, oxidation rate, and extent of oxidation of human low-density lipoprotein depend on the ratio of oleic acid content to linoleic acid content: studies in vitamin E deficient subjects.

The purpose of this study was to understand better the factors providing oxidation resistance to human low-density lipoprotein (LDL). Therefore, the susceptibility to copper-induced in vitro oxidation of LDL from vitamin E deficient patients and normal healthy subjects was studied. Surprisingly, the LDL of vitamin E deficient patients appeared less susceptible to oxidation than control LDL. Both oxidation rate and extent of oxidation, measured as diene production, were reduced when compared to control LDL. The lag time, a measure of resistance to oxidation, was not different from the lag time of LDL from healthy subjects. No relation was found between vitamin E content and resistance against oxidation. LDL from vitamin E deficient patients contained lower amounts of vitamin E, less cholesteryl esters, and increased amounts of triglycerides. Furthermore, its oleic acid content was increased and its linoleic acid content decreased. Linear regression analyses revealed that the ratio of oleic acid content to linoleic acid content was strongly correlated with the lag time, and inversely correlated with oxidation rate and extent of oxidation. Thus, LDL rich in oleic acid and poor in linoleic acid was less easily oxidized. It is concluded that the susceptibility of LDL to oxidation is determined not only by its antioxidant content, but also by other compositional factors, and more specifically by the ratio of oleic acid content to linoleic acid content.

Adult↗
PubMed1986

Decreased fluid tolerance, accelerated transit, and abnormal motility of the human colon induced by oleic acid.

To determine whether the presence of unabsorbed fat in the colon altered colonic motility, intraluminal pressures were recorded in the terminal ileum and proximal colon, and serial 1-min gamma camera scans were obtained while test solutions labeled with diethylenetetramine pentaacetic acid chelate of indium 111 were infused into the middle portion of the ascending colon. Seven subjects received a control solution, and 6 subjects received an emulsion of oleic acid (4.3 g/100 ml). Oleic acid accelerated colonic transit; isotope accumulated in the rectosigmoid faster in the first 120 min (4343 +/- 1175 cpm) than it did during control infusion (1236 +/- 348 cpm; p less than 0.01). Accelerated transit of oleate was accompanied by high amplitude (greater than 60 mmHg, range 60-95 mmHg), prolonged (greater than 10 s, range 10-48 s), propagated pressure waves; they originated near the ileocecal junction at a median frequency of 1.3 times/hour (mean 4.1, range 0.4-15.7). These were associated with a narrow image of the ascending colon on scintiscan and movement of 65.9% +/- 6.5% of counts from the ascending to transverse colon over the succeeding 4 min. A similar sequence was seen only once in 33 h of infusion with control solutions (p less than 0.01). Associated with these responses, the total volume of infusate tolerated before defecation was less with oleate than with control solutions (311 +/- 21 ml vs. 1049 +/- 71 ml; p less than 0.01). Long-chain fatty acids stimulated unusual motor patterns and reduced the reservoir function of the ascending colon; these effects may contribute to the diarrhea of patients with fat malabsorption.

Adult↗
PubMed1989

Pathway of alpha-linolenic acid through the mitochondrial outer membrane in the rat liver and influence on the rate of oxidation. Comparison with linoleic and oleic acids.

The movement of alpha-linolenic acid (C18:3, n-3) through the mitochondrial outer membrane to oxidation sites was studied in rat liver and compared with the movement of linoleic acid (C18:2, n-6) and oleic acid (C18:1, n-9). All differ in the degree of unsaturation, but have the same chain length and the same position of the first double bond when counted from the carboxyl end. The following results were obtained. (1) The overall beta-oxidation in total mitochondria was in the order C18:3, n-3 greater than C18:2, n-6 greater than C18:1, n-9, independent of the amount of albumin in the medium. (2) The rate of formation of acylcarnitine from acyl-CoA was higher with oleoyl-CoA than with linoleoyl-CoA, and remained very low with alpha-linolenoyl-CoA for all concentrations studied. (3) When the formation of acylcarnitines originated from fatty acids (as potassium salts) in a medium containing CoA and ATP, the conversion of alpha-linolenate was greater than that of linoleate, which in turn was greater than that of oleate. (4) Use of a more purified mitochondrial fraction, practically devoid of peroxisomes, did not modify the results obtained with alpha-linolenate. (5) alpha-Linolenoyl-CoA did not inhibit oxidation of labelled alpha-linolenate, whereas the other acyl-CoAs did. (6) Transfer to carnitine of all three fatty acids (as potassium salts) by carnitine palmitoyltransferase-I (CPT-I) was similarly inhibited by increasing concentrations of malonyl-CoA. (7) On using a fraction containing mitochondrial outer membranes, the formation of acylcarnitines from potassium salts of fatty acids was qualitatively and quantitatively similar to that found with whole mitochondria. (8) Our observations show that alpha-linolenoyl-CoA synthesized other than in the mitochondria cannot be used to any great extent by the mitochondria due to its configuration. However when added as the unactivated form, alpha-linolenate appears to be very quickly oxidized, but should first be activated by acyl-CoA synthetase in the mitochondrion itself. Then it is rapidly channelled to CPT-I. These enzymic sites are probably close together in the mitochondrial outer membrane. The different behaviour of the alpha-linolenic group compared with the other acyl groups in the studied pathway can be explained by a different spatial arrangement due to the number and position of the double bonds.

Acyl Coenzyme A↗
PubMed1991

Effects of indomethacin and PEEP on oleic acid induced pulmonary oedema in rabbits.

This study was designed to determine whether indomethacin, a suggested treatment for adult respiratory distress syndrome (ARDS), would inhibit the efficacy of positive end-expiratory pressure (PEEP) in an animal model of ARDS. Functional residual capacity (FRC), alveolar-to-arterial oxygen difference (A-aPo2) and total lung water were measured in rabbits: 30 controls and 30 with oleic acid induced pulmonary oedema. Within each group, four treatments were administered: diluent (n = 12), PEEP (n = 6), indomethacin (n = 6), or PEEP + indomethacin (n = 6). Lung injury was induced at 30 mins and treatment commenced at 45 min. Oleic acid caused a significant increase at 3 h in % increase in A-aPo2 from baseline (105 +/- 12%) attenuated by PEEP (59 +/- 17%) and indomethacin (57 +/- 7%), with the combination of PEEP + indomethacin preventing a significant increase (26 +/- 9%). PEEP increase FRC in both saline and oleic acid animals; this was not reversed by indomethacin. Oleic acid caused an increase in total lung water (5.16 to 6.58 +/- 0.16 g), not influenced by any treatment. These findings suggest that indomethacin did not inhibit the efficacy of PEEP in this model of ARDS.

Animals↗
PubMed1988

Effects of increased pulmonary vascular tone on gas exchange in canine oleic acid pulmonary edema.

Pulmonary gas exchange was investigated before and after an increase in pulmonary vascular tone induced by administration of acetylsalicylic acid (ASA), indomethacin, or almitrine in 32 pentobarbital-anesthetized and ventilated (fraction of inspired O2 0.4) dogs with oleic acid lung injury. Pulmonary vascular tone was evaluated by five-point pulmonary arterial pressure (PAP)/cardiac index (Q) plots and intrapulmonary shunt was measured using a SF6 infusion. PAP/Q plots were rectilinear in all experimental conditions. In control dogs (n = 8), oleic acid (0.09 ml/kg iv) increased PAP over the range of Q studied (1-5 l.min-1.m-2). At the same Q, arterial PO2 fell from 186 +/- 11 to 65 +/- 8 (SE) Torr and intrapulmonary shunt rose from 5 +/- 1 to 50 +/- 6% 90 min after oleic acid injection. These changes remained stable during the generation of two consecutive PAP/Q plots. ASA (1 g iv, n = 8), indomethacin (2 mg/kg iv, n = 8), and almitrine (8 micrograms.kg-1.min-1 iv, n = 8) produced a further increase in PAP at each level of Q. ASA and indomethacin, respectively, increased arterial PO2 from 61 +/- 4 to 70 +/- 3 Torr (P less than 0.05) and from 70 +/- 6 to 86 +/- 6 Torr (P less than 0.05) and decreased intrapulmonary shunt from 61 +/- 5 to 44 +/- 4% (P less than 0.05) and from 44 +/- 5 to 29 +/- 4% (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Almitrine↗
PubMed1990

Alteration of lipid methylation by oleic acid in rat heart sarcolemma.

Incubation of rat heart sarcolemma with the methyl donor S-adenosyl-L-[methyl-3H] methionine resulted in N-methylation of phosphatidylethanolamine and methylation of a heterogenous fraction of nonpolar lipids in the membrane. Oleic acid reduced the synthesis of N-methylated phospholipids and stimulated the methyl group incorporation into nonpolar lipids in a concentration-dependent manner. Both methylation reactions were not affected when oleic acid was substituted by methyl ester of oleic acid or by the detergents sodium deoxycholate or Triton X-100. This study suggests that the enzymatic biosynthesis of the N-methylated phospholipids may be altered by free fatty acids.

Animals↗
PubMed1980

Differential transport of cholesterol and oleic acid in lymph lipoproteins: sex differences in puromycin sensitivity.

Adult rats of both sexes were prepared with indwelling drainage catheters in the left thoracic lymphatic duct, and with duodenal infusion catheters. Control and puromycin-treated animals were administered an aqueous test emulsion containing [7alpha-(3)H]cholesterol and [1-(14)C]oleic acid, followed two hours later, by a tracer dose of [1-(14)C]-leucine. Successive 2-hr lymph samples were subjected to ultracentrifugal separations of the major lipoprotein classes. These were specifically extracted for lipids, and for DNA- and lipid-free protein. In both sexes, oleic acid absorption was largely associated with the d < 1.006 g/ml chylomicron fraction throughout the 6-hr experimental period. Small but consistent levels of labeled fatty acid appeared in the 1.006 < d < 1.019 g/ml VLDL fraction. However, with both sexes 25-35% of the absorbed cholesterol appearing in lymph was recovered in the VLDL fraction. Furthermore, there were statistically greater levels of cholesterol in this lymph fraction in females than in males. Cumulative protein levels and leucine incorporation into chylomicron proteins was comparable in both sexes. However, VLDL protein in the female was significantly greater than in the male and this difference was mimicked by the greater incorporation of leucine into VLDL proteins in the female. In males, there were no significant effects of puromycin on cholesterol or oleic acid absorption, despite a marked inhibition in chylomicron protein levels and leucine incorporation into this fraction. There was also no effect of the inhibitor on VLDL protein levels or on leucine incorporation into VLDL peptides. Cholesterol but not oleic acid absorption in females was significantly depressed by administration of puromycin, and this was largely attributed to a decrease in VLDL transport of the sterol. Also, unlike males, leucine incorporation into VLDL peptides was inhibited by 75% by puromycin administration. These results emphasize the importance of non-chylomicron transport of cholesterol during absorption and suggest a hormonal influence on intestinal VLDL synthesis in female rats.-Vahouny, G. V., E. M. Blendermann, L. L. Gallo, and C. R. Treadwell. Differential transport of cholesterol and oleic acid in lymph lipoproteins: sex differences in puromycin sensitivity.

Animals↗
PubMed1990

The distribution of oleic acid between chylomicron-like emulsions, phospholipid bilayers, and serum albumin. A model for fatty acid distribution between lipoproteins, membranes, and albumin.

In the process of lipoprotein lipolysis, masses of fatty acid are generated at the surface of the lipoprotein. The newly generated fatty acid may at least partly redistribute from the site of lipolysis to phospholipid-rich membranes and to albumin. We have studied the distribution of [1-13C]oleic acid in model systems consisting of chylomicron-like triacylglycerol-rich emulsions, unilamellar phosphatidylcholine vesicles, and bovine serum albumin. By using high resolution 13C NMR spectroscopy it was possible to distinguish fatty acid in each compartment (emulsion, vesicle, albumin) and quantitate the fatty acid distribution under various conditions of lipid compartment concentration and aqueous pH. When emulsions and vesicles were present in equivalent mass amounts, fatty acid exhibited a profound preference for the lipid bilayers. The release of oleic acid to phospholipid bilayers was presumably also a function of its high molar stoichiometry (5:1) with the albumin present. More equitable distributions of fatty acid between vesicles and emulsions were seen when higher concentrations of emulsion were used. The distribution of fatty acid between compartments was in good agreement with predictions made using the apparent ionization constant, expressed as pKapp, of 7.5 and the surface to core (phospholipid to triacylglycerol) distribution coefficient of 7.0, measured for unionized oleic acid in chylomicron particles (Spooner, P. J. R., Bennett Clark, S., Gantz, D. L., Hamilton, J. A., and Small, D. M. (1988) J. Biol. Chem. 263, 1444-1455). These results indicate that the affinities of fatty acid for phospholipid bilayer and chylomicron-like emulsion surfaces are equivalent. Redistribution of lipolytically generated fatty acid from chylomicron surface to cell membrane may simply be driven by the predominant quantity of the cell membrane surfaces.

Cell Membrane↗
PubMed1990

Peroxisomes induced in Candida boidinii by methanol, oleic acid and D-alanine vary in metabolic function but share common integral membrane proteins.

Peroxisomes massively proliferate in the methylotrophic yeast Candida boidinii when cultured on methanol as the only carbon and energy source. These organelles contain enzymes that catalyze the initial reactions of methanol utilization. The membranes contain abundant proteins of unknown function; their apparent molecular masses are 20, 31, 32 and 47 x 10(3) Mr and are termed PMP20, PMPs31-32 and PMP47. Recently, we reported that peroxisomes in this yeast are also induced by oleic acid and D-alanine as carbon sources, and that these peroxisomes contain increased concentrations of the enzymes of fatty acid beta-oxidation or D-amino acid oxidase, respectively. This report extends these findings and further compares the enzyme composition from peroxisomes induced by methanol, oleic acid and D-alanine. the patterns of matrix proteins represented on SDS-polyacrylamide gels from peroxisomes induced by oleic acid or D-alanine were found to be very different from those of peroxisomes induced by methanol. In order to differentiate between membrane proteins that have specific functions in pathways of substrate utilization from those with more generalized functions, peroxisomal membranes from cultures grown on methanol, oleic acid or D-alanine were purified. Analysis of these fractions demonstrated that while PMP20 is found only in peroxisomes induced by methanol, the PMPs31-32 and PMP47 were the abundant peroxisomal membrane proteins (PMP) regardless of inducing substrate. The data strongly suggest that the function of PMP20 is related to methanol metabolism. In contrast, the functions of PMPs31-32 and PMP47 are 'substrate-nonspecific'. We speculate that they may relate to the structure, assembly or general function of the organelle.

Alanine↗
PubMed1991

Toxicity of oleic acid anilide in rats.

In the present investigation, we have studied the toxic potential of oleic acid anilide (OAA) and heated oleic acid anilide (HOAA) in relation to the toxic oil syndrome (TOS). Male Sprague-Dawley rats were given 250 mg/kg of OAA or HOAA in mineral oil by gavage, on alternate days for 2 weeks (total 7 doses). The control rats received an equal volume of mineral oil only. The animals were sacrificed at days 1, 7, and 28 following the last dose. Ratio of organ-to-body weight showed increases in spleen and kidney of HOAA and OAA treated rats, respectively, at day 1 while this ratio for liver in HOAA treated group showed a decrease at day 1. Among blood parameters, white blood cells increased in HOAA treated group at day 1 and in both OAA and HOAA groups at day 28. Mean corpuscular hemoglobin (MCH) and mean cell volume (MCV) also showed increases in the HOAA treated rats at days 7 and 28. Serum lactate dehydrogenase (LDH) decreased in both OAA and HOAA treated rats at day 1, while at day 7 the decrease was confined only to the HOAA group. Serum glutamic oxalacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) activities also decreased at most of the time points. Liver mitochondrial ATPase activity decreased in the HOAA group at day 7 and in the OAA group at day 28. Among serum immunoglobulins, IgA levels increased throughout the study but the changes were more pronounced in HOAA treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Anilides↗
PubMed2002

Metabolic functions of the two pathways of oleate beta-oxidation double bond metabolism during the beta-oxidation of oleic acid in rat heart mitochondria.

Unsaturated fatty acids with odd-numbered double bonds, e.g. oleic acid, can be degraded by beta-oxidation via the isomerase-dependent pathway or the reductase-dependent pathway that differ with respect to the metabolism of the double bond. In an attempt to elucidate the metabolic functions of the two pathways and to determine their contributions to the beta-oxidation of unsaturated fatty acids, the degradation of 2-trans,5-cis-tetradecadienoyl-CoA, a metabolite of oleic acid, was studied with rat heart mitochondria. Kinetic measurements of metabolite and cofactor formation demonstrated that more than 80% of oleate beta-oxidation occurs via the classical isomerase-dependent pathway whereas the more recently discovered reductase-dependent pathway is the minor pathway. However, the reductase-dependent pathway is indispensable for the degradation of 3,5-cis-tetradecadienoyl-CoA, which is formed from 2-trans,5-cis-tetradecadienoyl-CoA by delta(3),delta(2)-enoyl-CoA isomerase, the auxiliary enzyme that is essential for the operation of the major pathway of oleate beta-oxidation. The degradation of 3,5-cis-tetradecadienoyl-CoA is limited by the capacity of 2,4-dienoyl-CoA reductase to reduce 2-trans,4-trans-tetradecadienoyl-CoA, which is rapidly formed from its 3,5 isomer by delta(3,5),delta(2,4)-dienoyl-CoA isomerase. It is concluded that both pathways are essential for the degradation of unsaturated fatty acids with odd-numbered double bonds inasmuch as the isomerase-dependent pathway facilitates the major flux through beta-oxidation and the reductase-dependent pathway prevents the accumulation of an otherwise undegradable metabolite.

Acyl Coenzyme A↗
PubMed1989

Effect of Cu2+ and Zn2+ on the inhibition of human leucocyte elastase by 6-alkyl-3-(omega-carboxyalkyl)-2-pyrone, oleic acid and sulindac sulfide.

Inhibition of human leucocyte elastase by oleic acid and the structurally related 3-(1'-oxo-7'-carboxyheptyl)-4-hydroxy-6-octyl-2-pyrone is considerably enhanced by the addition of Cu2+, Zn2+ and, to a lesser extent, Co2+ and Ca2+. Sulindac sulfide and diflunisal also respond to changes in copper concentration, while Boc-Ala-Pro-Val-NH[CH2]10CO2H does not. Binding of the -CO2H group in the vicinity of the S5 subsite is proposed for all but the last compound to account for this effect. Incubation experiments indicate that Cu2+ binds more rapidly to the enzyme than does the inhibitor. Local changes in conformation result in improved binding of the inhibitor, but do not affect the substrate (Km unchanged). Chelation by EDTA is time-dependent, indicating that the Cu2+ is shielded by the inhibitor. The results may partially explain the well-known anti-arthritic and anti-inflammatory properties of copper and zinc and their organic salts.

Copper↗