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PubMed2004

Biocatalyzed acidolysis of soybean oil triacylglycerols to increase oleic acid content.

Lipase catalyzed acidolysis of triacylglycerols (TAG) of soybean oil with oleic acid in organic solvent was studied; immobilized lipase from Rhizomucor miehei was used and the effects of reaction time, incubation temperature and enzyme load on TAG total and positional fatty acid (FA) percentage compositions were investigated. The results show that oleic acid incorporation was high after 24 and 48 h, while after 72 h a lower level of oleic acid in TAG was observed. Moreover, for the reactions carried out at 30 and 40 degrees C, it was observed that the oleic acid level was about 46.5% while ligtly higher values (about 49%) were observed at 50 degrees C; however, under this last condition, the modification of sn-2 position FA composition was higher. Finally, the variable enzyme load resulted also important on the incorporation of oleic acid; in particular, even if the value of 10% (w/w) of enzyme load resulted in a lightly lower incorporation of oleic acid in soybean oil TAG (about 45%), in this situation a minimal modification of sn-2 position FA composition was obtained.

Acids↗
PubMed1991

Intrinsic lymphatic partition rate of mepitiostane, epitiostanol, and oleic acid absorbed from rat intestine.

Mepitiostane (MP), epitiostanol (EP), and oleic acid were administered to the jejunal loop of mesenteric vein- and thoracic duct-cannulated rats, and the intrinsic lymphatic partition rate (ILPR) of the absorbed compounds was directly determined. When 14C-EP was administered to the jejunal loop, recovery of unchanged EP in the mesenteric blood and the lymph was 7.9 and 0.03% of the administered dose, respectively. In contrast, following administration of 14C-MP, recovery of unchanged MP in the mesenteric blood and the lymph was 1.2 and 15.0%, respectively. Thus, following passage through the mucosal cell, 99.6% of the unchanged EP was partitioned into the blood and 0.4% into the lymph, while for unchanged MP, 7.6% was partitioned into the blood and 92.4% into the lymph. When 14C-oleic acid was administered to the jejunal loop, most of the penetrating oleic acid was incorporated into triglycerides in epithelial cells and transferred exclusively into the lymph. However, of the unchanged oleic acid, only 37.6% was partitioned into the lymph and 62.4% into the blood. The ILPR was 92.4% for MP, 0.4% for EP, and 37.6% for oleic acid. We conclude that the ILPR values indicate the true lymphotropic property of the compounds.

Androstanols↗
PubMed1998

Oleic acid and angiotensin II induce a synergistic mitogenic response in vascular smooth muscle cells.

Oleic acid and angiotensin II (Ang II) are elevated and may interact to accelerate vascular disease in obese hypertensive patients. We studied the effects of oleic acid and Ang II on growth responses of rat aortic smooth muscle cells (VSMCs). Oleic acid (50 micromol/L) raised thymidine incorporation by 50% at 24 hours and cell number by 55% at 6 days (P<.05). Ang II (10(-11) to 10(-6) mol/L) did not significantly increase thymidine incorporation or VSMC number. Combining Ang II and 50 micromol/L oleic acid doubled thymidine incorporation and VSMC number. Losartan, an angiotensin type 1 (AT1) receptor antagonist, blocked the synergistic interaction between Ang II and oleic acid, whereas the AT2 receptor antagonist PD 123319 did not. Protein kinase C inhibition and downregulation, as well as inhibition of extracellular signal-regulated kinase (ERK) activation by PD 98059, eliminated the rise of thymidine incorporation in response to oleic acid and the synergistic interaction with Ang II. However, the response to 10% fetal bovine serum was unaffected. An antisense oligodeoxynucleotide to ERK-1 and ERK-2 reduced ERK protein expression and activation by 83% and 75%, respectively. Antisense prevented the rise of thymidine incorporation in response to oleic acid and the synergy with Ang II. Antisense reduced but did not prevent increased thymidine incorporation in response to serum. The data indicate that oleic acid and Ang II exert a synergistic mitogenic effect in VSMCs and suggest an important role for the AT1 receptor, PKC, and ERK in this synergy. The observations raise the possibility that a synergistic mitogenic interaction between oleic acid and Ang II accelerates vascular remodeling in obese hypertensive patients.

Angiotensin II↗
PubMed2000

Addition of oleic acid increases expression of recombinant human serum albumin by the AOX2 promoter in Pichia pastoris.

The addition of several kinds of fatty acid to the culture medium of a recombinant human serum albumin (rHSA)-producing yeast, Pichia pastoris, resulted in increased expression levels of the product. Among the fatty acids tested, a small amount of oleic acid (0.01% (w/v)) doubled the rHSA production level in a shake-flask culture when measured by the reversed passive hemagglutination assay method. To elucidate this phenomenon, studies were conducted using deletion mutants from the AOX2 promoter region. Deletion mutants, designed for a detailed evaluation of the methanol regulation elements (AOX2-UAS, AOX2-URS1, and AOX2-URS2) did not respond to the addition of oleic acid. However, a deletion mutant that was not lacking an upstream region from the AOX2 promoter showed a response to oleic acid. The results implied the presence of an oleic acid-responsive element between nucleotides (nt) -1529 and -803, and it may lie between nt -1411 and -1403 in the AOX2 promoter of P. pastoris. The response to oleic acid was shown to function even when the level of rHSA expression was increased by a mutation in the AOX2 promoter. Therefore addition of oleic acid to the medium is likely to play an important role, in cooperation with gene manipulation, in achieving high expression levels of rHSA for the purpose of commercial production.

Journal Article↗
PubMed1984

Intestinal absorption of free oleic acid in the unanesthetized rat: evidence for a saturable component?

The intestinal absorption of free oleic acid at low intraluminal concentrations and the influence of luminal factors on its absorption were studied in the unanesthetized rat. The relationship between oleic acid concentration (30-2500 microM) and its rate of absorptions fitted best to a rectangular hyperbola (y = x/(2.19 + 0.0015x), r = 0.94). Oleic acid's rate of absorption increased as the hydrogen ion and sodium taurocholate concentrations were increased or as the thickness and resistance of the unstirred water layer were diminished or following the addition of lysolecithin. The additions of the artificial detergent Tween-80, or lecithin and linoleic, linolenic and arachidonic acids to the perfusate decreased oleic acid's rate of absorption. It was concluded that oleic acid absorption in this range of concentrations displays apparent saturation kinetics which are due to unstirred layer effects, limited aqueous solubility of oleic acid and possible saturation of cytosol fatty acid binding proteins. Factors which increase oleic acid's protonated concentration or diminish the unstirred layer resistance, enhance its absorption rate, while factors which enhance its micellar solubility or interfere with its transfer out of the cell membrane decrease its overall rate of absorption.

Animals↗
PubMed2005

Oleic acid causes apoptosis and dephosphorylates Bad.

There is increasing evidence showing the involvement of unsaturated free fatty acids in cell death pathways, particularly in the context of apoptotic signalling. Our previous in vitro study has demonstrated that oleic acid, a monounsaturated fatty acid, reduces phosphorylation of proapoptotic Bad through activation of protein phosphatase type 2Cbeta. In the present study, we attempted to investigate the role of oleic acid in neuronal apoptosis using different types of cell cultures, and, furthermore, to explore the underlying mechanism with regard to its effect on Bad expression. As revealed by nuclear staining, oleic acid caused a concentration- and time-dependent damage with typical apoptotic features in cortical and hippocampal cultures from embryonic and neonatal rats, respectively, as well as in human neuroblastoma SH-SY5Y cells. In mixed hippocampal cultures, nearly all neurons were damaged at 24 h after the treatment, while damage of astrocytes was detected 48 h after adding this fatty acid, suggesting that neurons were more vulnerable than astrocytes. Nile blue staining showed that oleic acid and oleic acid methyl ester were both taken up by the neurons within 30 min. In contrast to oleic acid, oleic acid methyl ester did not change cell viability demonstrating that oleic acid-induced cell death was not due to an overload of the cells with lipids. Caspase-3 activity was not increased by oleic acid in cultured hippocampal cells. Western blot analysis of phospho-Ser112 Bad and the total Bad in cultured hippocampal cells revealed a significant decrease in the ratio of phospho-Ser112 Bad to total Bad in a time- and concentration-dependent manner after the exposure with oleic acid. We conclude that oleic acid induces neuronal apoptosis through a caspase-3-independent mechanism involving dephosphorylation of Bad.

Animals↗
PubMed1994

Effect of calcium and mineral waters on oleic-acid uptake by isolated hamster enterocytes.

The effect of calcium upon the uptake of oleic acid solubilized with 10 mM taurocholate was investigated using an in vitro model of isolated enterocytes. The addition of Ca2+ to the incubation medium (Hanks' medium) led to a decrease in oleic-acid uptake. This uptake inhibition was dependent on both the amount of Ca2+ and the fatty-acid concentration, since the inhibitory effect was significant for 10 microM but not 100 microM oleic acid. The determination of the monomeric activity of oleic acid indicated that the decrease in fatty-acid uptake was not linked to the formation of insoluble calcium soaps. The replacement of Hank's medium by several mineral waters containing between 0.3 and 11.7 mM Ca2+ significantly reduced the uptake of both 10 and 100 microM oleic-acid. The ionic composition of these waters was correlated with the decrease of initial rate of oleic acid uptake, but Ca2+ and other ions could interfere by synergetic effects with the fatty-acid-absorption mechanism. It is concluded that the ion-induced inhibition of oleic-acid uptake is not due to the formation of insoluble soaps but rather to a direct effect on the fatty-acid transport in membranes. Whether the fatty-acid binding protein in the plasma membrane is involved in the effect of Ca2+ on fatty-acid transport remains to be established.

Animals↗
PubMed1998

Involvement of cytochrome P450 2E1 in the (omega-1)-hydroxylation of oleic acid in human and rat liver microsomes.

In vitro techniques have been used to investigate the nature of microsomal cytochrome P450 involved in the metabolism of oleic acid, a physiological monounsaturated fatty acid. Like lauric acid, which is currently used as a model substrate of fatty acid metabolism, the alkyl chain of oleic acid is hydroxylated on its omega and (omega-1) carbons. The identity of these hydroxylated metabolites was ascertained by GC/MS and LC/MS. The omega/omega-1 ratio of oleic acid metabolites (1.22+/-0.01) was found to be similar to that obtained with lauric acid in rat liver microsomes (1.10+/-0.02), while in human liver microsomes this ratio was 0.75+/-0.5 for lauric acid and 5.2+/-2.6 for oleic acid. After treatment of rats with ethanol or clofibrate, inducers of CYP2E1 and CYP4A, respectively, the hydroxylations of oleic acid were shown to be less inducible than those of lauric acid. Five in vitro approaches were used to identify the P450 isoform(s) responsible for the microsomal (omega-1)-hydroxylation of oleic acid: effect of various inducers in rats, correlation studies between specific P450 catalytic activities in a panel of 25 human liver microsomes, chemical inhibitions, immuno-inhibitions and metabolism by cDNA-expressed human P450 enzymes. From the above results, it can be ascertained that P450 2E1 is the main enzyme involved in the (omega-1)-hydroxylation of oleic acid. Furthermore, the omega-hydroxylation of oleic acid was shown to be mainly catalyzed by P450 4A enzymes in human liver microsomes. The turnover number of (omega-1)-hydroxylation of lauric and oleic acids decreased from 7.8 to 1.5 min(-1), respectively, suggesting that the dodecane alkyl chain allows optimal binding to the active site of CYP2E1.

Animals↗
PubMed1975

Turnover of plasma-free arachidonic and oleic acids in resting and exercising human subjects.

Turnover rates and metabolism in the leg region and the splanchnic region, of free arachidonic and oleic acid have been examined in five healthy subjects at rest and during bicycle exercise. A continuous intravenous infusion of tritiated arachidonic acid and 14-C-labeled oleic acid was given. The rate constant for arachidonic acid turnover at rest was 0.44 plus or minus 0.004/min as compared to 0.29 plus or minus 0.02 for oleic acid. Significant correlations between turnover rate and arterial concentrations were observed for both acids in the resting state. The turnover of arachidonic acid was not significantly altered during exercise which caused an eight- to ninefold rise in pulmonary oxygen uptake. In contrast, the turnover of oleic acid rose markedly with exercise; its rate constant increased by approximately 90% to 0.57 plus or minus 0.05/min. The fractional uptakes of the two acids in the leg region were similar in the resting state. The splanchnic fractional uptake for arachidonic acid significantly exceeded that for oleic acid at rest. There was a net uptake of arachidonic acid in the splanchnic region in all subjects studied. In vitro incubations of whole blood deomonstrated a significant exchange of arachidonic as well as oleic acid between plasma and blood cells. We conclude that the metabolism of plasma free arachidonic acid differs from that of oleic acid in that (1) its fractional turnover at rest is about 50% higher, (2) its splanchnic fractional uptake is about 60% higher, and (3) its turnover rate is unaffected by physical exercise. It is further suggested that the high turnover rate of arachidonic acid, and to a less extent that of oleic acid, could be due in part to an exchange of fatty acids between plasma and endothelial cells.

Abdomen↗
PubMed2000

Use of oleic acid to reduce the population of the bacterial flora of poultry skin.

The effect of oleic acid on native bacterial flora of poultry skin was examined. Skin from commercial broiler carcasses was washed once or twice in solutions of 0, 2, 4, 6, 8, or 10% (wt/vol) oleic acid and rinsed in peptone water. Aerobic bacteria, Enterobacteriaceae, Campylobacter, and enterococci in the rinsates were enumerated. Significantly fewer aerobic bacteria, Enterobacteriaceae, Campylobacter, and enterococci were recovered from rinsates of skin washed in oleic acid than from control samples. Additionally, fewer bacteria were recovered from rinsates of skin washed in higher concentrations of oleic acid than from skin washed in lower concentrations of the fatty acid. In most cases, there was no significant difference in the number of bacteria recovered from rinsates of skin washed once or twice in solutions of oleic acid. Washing skin samples twice in 10% solutions of oleic acid significantly reduced the number of aerobic bacteria, Enterobacteriaceae, Campylobacter, and enterococci that remained attached to the skin. Campylobacter sp., Enterococcus faecalis, and Listeria monocytogenes isolates possessed the least resistance to the antibacterial activity of oleic acid in vitro, while Escherichia coli and Pseudomonas aeruginosa showed higher resistance. Enterobacter cloacae, Staphylococcus lentus, and Salmonella Typhimurium had the greatest resistance to the antibacterial activity of oleic acid. Findings indicate that oleic acid reduces the number of bacteria on the skin of processed broilers and that the fatty acid is bactericidal to several spoilage and pathogenic bacteria associated with poultry.

Animals↗
PubMed1997

Oleic acid inhibits gap junction permeability and increases glucose uptake in cultured rat astrocytes.

The role of oleic acid in the modulation of gap junction permeability was studied in cultured rat astrocytes by the scrape-loading/Lucifer yellow transfer technique. Incubation with oleic acid caused a dose-dependent inhibition of gap junction permeability by 79.5% at 50 microM, and no further inhibition was observed by increasing the oleic acid concentration to 100 microM. The oleic acid-mediated inhibition of gap junction permeability was reversible and was prevented by bovine serum albumin. The potency of oleic acid-related compounds in inhibiting gap junction permeability was arachidonic acid > oleic acid > oleyl alcohol > palmitoleic acid > stearic acid > octanol > caprylic acid > palmitic acid > methyloleyl ester. Oleic acid and arachidonic acid, but not methyloleyl ester, increased glucose uptake by astrocytes. Neither oleic acid nor arachidonic acid increased glucose uptake in the poorly coupled glioma C6 cells. These results support that the inhibition of gap junction permeability is associated with the increase in glucose uptake. We suggest that oleic acid may be a physiological mediator of the transduction pathway leading to the inhibition of intercellular communication.

Animals↗
PubMed1992

Stimulation of plasmin activity by oleic acid.

The amidolytic activity of plasmin with the chromogenic substrate H-D-valyl-L-leucyl-L-lysine p-nitroanilide (S-2251) is stimulated by oleic acid in a dose-dependent and saturable fashion. The activity of plasmin on S-2251 in the presence of oleic acid followed a sigmoidal kinetic pattern, with an almost 4-fold stimulation of activity at 60 microM-oleic acid. Half-maximal stimulation occurred at an oleic acid level of 19.5 microM. The amino acid analogue 6-aminohexanoic acid (AHA), which is known to bind to lysine-binding sites in plasmin, suppressed the stimulatory effect of oleic acid in a concentration-dependent manner; at 0.3 mM-AHA, about 70% of the oleic acid-dependent enhancement of plasmin activity was abolished. The l/v versus 1/[S] plot for plasmin changed in the presence of oleic acid from a linear to a non-linear curve, suggesting positive co-operativity. 14C-labelled oleic acid bound to plasmin, and the bound ligand was displaced by an excess of unlabelled oleic acid. Oleic acid also produced a marked (40-fold) stimulation of the plasminogen-dependent cleavage of S-2251 by urokinase. A half-maximal effect on plasminogen activation was obtained at 40 microM-oleic acid. The present findings suggest that the ability of oleic acid to stimulate plasmin activity and to enhance the conversion of plasminogen to plasmin depends on the interaction of oleic acid with specific lysine-binding sites in plasmin.

Aminocaproic Acid↗
PubMed1992

Dual effects of oleic acid on Ca2+ mobilization and protein phosphorylation in human platelets in presence or absence of platelet activating factor.

This laboratory demonstrated earlier that oleic acid inhibited platelet activating factor (PAF)-induced aggregation and serotonin release of rabbit platelets (M. Miwa, C. Hill, R. Kumar, J. Sugatani, M. S. Olson, and D. J. Hanahan, 1987, J. Biol. Chem. 262, 527-530). More recently, we reported that oleic acid caused a decrease in phosphatidylinositol-4-phosphate (PIP) and phosphatidylinositol-4,5-bisphosphate (PIP2), but did not affect the level of inositol-1,4,5-trisphosphate (IP3), in rabbit platelets (D. Nunez, J. Randon, C. Gandhi, A. Siafaka-Kapadai, M. S. Olson, and D. J. Hanahan, 1990, J. Biol. Chem. 265, 18330-18838). These results suggested that oleic acid did not stimulate phospholipase C. In contrast, PAF induced a decrease in PIP2 and an increase in PIP level and IP3. These effects were shown to be attenuated by oleic acid. In this current study, our experiments show that (a) oleic acid blocked PAF-induced rise in intracellular [Ca2+] (to provide a mechanism in agreement with our previous experiments which showed that oleic acid inhibited PAF-induced IP3 rise in platelets) and (b) oleic acid itself induced a gradual rise in [Ca2+]i, which would provide a mechanism for oleic acid-induced aggregation despite the fact that oleic acid did not cause the production of IP3 (Nunez et al., 1990). Oleic acid, in a dose-dependent manner, was shown to inhibit PAF-induced Ca2+ mobilization from intra- and extracellular sources. The inhibition was closely related to the suppressive effect of oleic acid on PAF-induced aggregation. Furthermore, oleic acid inhibited the PAF-stimulated phosphorylation of the 20- and 40-kDa proteins. At concentrations above 20 microM, oleic acid itself could induce platelet aggregation and Ca2+ mobilization, but the time sequence of these two responses in human platelets was significantly different from those obtained with PAF. Oleic acid alone, at 20 microM, caused a 1.4-fold increase in the cAMP level in platelets which was followed by a decline to a basal value at higher concentrations of this fatty acid. It seemed clear that elevation of adenylate cyclase activity was not associated with free fatty acid inhibition of platelet activation. Interestingly, both PAF and oleic acid added separately to human platelets induced protein-tyrosine phosphorylation, but oleic acid did not cause any inhibition of PAF-induced protein-tyrosine phosphorylation.(ABSTRACT TRUNCATED AT 400 WORDS)

Blood Platelets↗
PubMed2003

Preventive effect of phosphoenolpyruvate on hypoxemia induced by oleic acid in Guinea pigs.

Oleic acid-induced hypoxemia is an animal model of acute respiratory distress syndrome (ARDS). Increased capillary permeability is a cause of hypoxemia in lung injury. Endothelial cells form a major capillary barrier, and disruption of the barrier appears to involve a decreased level of ATP in the cells. Phosphoenolpyruvate (PEP) is an endogenous substance that is one of the ATP precursors and can cross some cell membranes via anion exchanger. We examined the effect of PEP on oleic acid-induced lung injury in guinea pigs. An intravenous injection of oleic acid (15 microl/kg) caused severe hypoxemia. Pretreatment with PEP at a dose of 2, 20, or 200 micromol/kg attenuated the oleic acid-induced decrease in the arterial partial pressure of oxygen in a dose-dependent manner. Furthermore, PEP attenuated the oleic acid-induced increase in vascular permeability in the proximal and distal bronchi, as indicated by the extravascular leakage of Evans Blue dye. The combination of PEP with ATP (4 micromol/kg) showed no additional inhibitory effect on oleic acid-induced lung injury, compared with PEP alone. We suggest that PEP is a promising candidate to prevent hypoxemia in acute lung injuries associated with increased vascular permeability, such as ARDS.

Animals↗
PubMed1988

The fatty-acid-induced conformational states of human serum albumin investigated by means of multiple co-binding of protons and oleic acid.

The binding of oleic acid to human serum albumin causes progressive changes in (a) the pK of some amino acid residues, as detected by pH-stat titration and (b) the induced molar ellipticities of albumin-bound drugs (diazepam and oxyphenbutazone), as measured by c.d. It is concluded that albumin undergoes several conformational transitions as the amount of oleic acid bound increases from 0 to about 9 molecules/molecule of protein. At least three different conformations of the protein seem to be involved. These conformations can be linked with the three classes of oleic acid-binding sites on albumin.

Binding Sites↗
PubMed1983

Apparent inhibition of the plasma membrane Ca2+ pump by oleic acid.

The effects of oleic acid (oleate) were examined using two in vitro model systems. In a concentration-dependent fashion oleate activated or inhibited the (Ca2+ + Mg2+)-ATPase, or Ca2+ pump ATPase, of membranes isolated from human red blood cells (RBC's). Concentrations of oleate which inhibited the Ca2+ pump ATPase also inhibited the Na+-K+ pump ATPase. Likewise, in a concentration-dependent fashion oleate increased or abolished ATP dependent 45Ca2+ transport into inside-out vesicles (IOV's) prepared from human RBC's. Addition of 500 microM oleate to IOV's which had already accumulated 45Ca2+ resulted in rapid loss of the ion. The effect was shown to be due to membrane disruption; a conclusion based on oleate-induced unmasking of latent acetylcholinesterase activity in IOV preparations. The results are compatible with, but do not prove, that membrane disruption caused by circulating free fatty acids and similar membrane active agents might play a role in the cellular injury associated with certain pathophysiologic states.

Acetylcholinesterase↗
PubMed1986

Release of a lectin from a fatty acid auxotroph of Saccharomyces cerevisiae grown in presence of oleic acid.

The unsaturated fatty acid-requiring mutant KD 115 of Saccharomyces cerevisiae secretes a lectin when grown in presence of oleic acid. This lectin is homogeneous on PAGE at pH 8.3, has an approximate molecular weight of 320,000, pI of 4.2 and contains about 60% sugar. It agglutinates chicken and different mammalian erythrocytes, but lyses rabbit red cells only. It is D-galactose-specific. To our knowledge, this is the first report of a hemagglutinin from yeast.

Animals↗