Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “OLEIC ACID”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,495 records · Page 83Linked to original sources
PubMedDate not supplied

Sequential appearance of inflammatory mediators in rat bronchoalveolar lavage fluid after oleic acid-induced lung injury.

The oleic acid (OA) model of rat lung injury was originally developed as a model of fat embolism syndrome. A single intravenous dose of pure OA causes an acute diffuse lung injury, which, in its initial stages, histologically and physiologically resembles human ARDS. Rat lungs acutely injured by intravenous OA manifest increased levels of ICAM-1 within 30-60 min. This study shows that human umbilical vein endothelial cells (HUVEC) can be used in a bioassay to reveal some of the adhesion molecule stimulating activities present in bronchoalveolar lavage fluid (BALF) from post-OA-injected rats: (1) There is an as yet unidentified ICAM-1 and ELAM (E Selectin) inducing activity in BALF within 15 min of OA injection that is not TNF alpha; there is very little measurable tumor necrosis factor-alpha (TNF alpha) in 15 min BALF (BALF15). (2) BALF15 also stimulates cultured macrophage derived from BALF of normal rat lungs to produce TNF alpha. (3) By 60 min after OA injection, 50-75% of the ICAM-1 and ELAM inducing activity in BALF (BALF60) is TNF alpha; BALF60 contains about 250-280 pg/mL TNF alpha. The other 25-50% adhesion molecule-inducing activity in BALF60 is unidentified. (4) The ICAM-1-inducing activity of pure TNF alpha was equal to that of BALF60 containing equivalent concentrations of TNF alpha. The ELAM inducing activity of pure TNF alpha, however, was about 1/2 that of BALF60 containing equivalent concentrations of TNF alpha. The time courses for ICAM and ELAM stimulation with pure TNF alpha or BALF60 containing equivalent levels of TNF alpha were the same. The identity of the mediators in BALF15 and BALF60 that are not TNF alpha and the mechanisms by which OA injection stimulates cytokine production remain to be elucidated.

Animals↗
PubMed1998

Diets enriched in (n-3) fatty acids affect rat coagulation factors dependent on vitamin K.

The effects of dietary lipids on haemostasis were investigated in rats fed high fat diets enriched in saturated fatty acids (SAT), oleic acid (OLEIC), MaxEPA oil (MaxEPA), eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA) and results were compared to those for rats fed standard chow (ST). Coagulant activities of factor IIc and factor VII-Xc were reduced by about 70% in the MaxEPA group and 50% in the EPA and DHA groups relative to the OLEIC, SAT and ST groups. Liver vitamin K levels were five times lower in the experimental groups than in the ST group, which would indicate an effect of high fat diets on vitamin K metabolism. However, only (n-3) fatty acids prolonged the prothrombin time. These components could act at the post-translational modification level of vitamin K-dependent plasma clotting factors. The changes in haemostatic factors found in the MaxEPA group were counteracted by vitamin K supplementation.

Animals↗
PubMed1988

Oleic acid-induced pulmonary injury in rats: potential role of sulfidopeptide leukotrienes.

Lung injury following intravenous oleic acid is characterized by pulmonary edema, leukopenia and hypoxemia. Because leukotrienes can increase permeability and cause leukocyte adherence, we evaluated their potential role in oleic acid-induced lung injury in the anesthetized rat using a selective LTD4/E4 antagonist, LY171883. 99mTc-albumin and 99mTc-red blood cells (99mTc-RBC) were used to measure changes in the pulmonary permeability index and intravascular space by non-invasive scintigraphy. Intravenous oleic acid (0.06 ml/kg) increased the pulmonary permeability index 11 (P less than 0.01) and 5.8 fold (P less than 0.01) at 5 and 50 min after its injection compared to baseline, but had no effect on mean pulmonary arterial pressure or pulmonary distribution of 99mTc-RBC. Oleic acid also induced arterial hypoxemia, and increased bronchoalveolar lavage-fluid levels of immunoreactive (i) leukotriene LTC4 from 0.40 +/- 0.14 ng/ml to 2.27 +/- 0.55 ng/ml (mean +/- S.E.M., n = 4, P less than 0.05) and iLTB4 (from 0.42 +/- 0.05 ng/ml to 1.91 +/- 0.63 ng/ml, n = 5-7, P less than 0.01). LY171883 attenuated the elevated permeability by 24% and 68% at 5 (P less than 0.05) and 50 min (P less than 0.01), but did not alter the hypoxemia. These results support the hypothesis that oleic acid elevates leukotriene levels which may increase pulmonary vascular permeability. Furthermore, they suggest that the prevention of elevated pulmonary vascular permeability and edema may be necessary, but are clearly not sufficient to prevent arterial hypoxemia following oleic acid injury in the rat.

Acetophenones↗
PubMed2004

Effects of N-acetylcysteine on oxidant-antioxidant balance in oleic acid-induced lung injury.

The antioxidant and anti-inflammatory properties of N-acetylcysteine has been documented in many experimental lung injury models. Because intravenous injection of oleic acid induces histopathologic changes similar to those seen in human acute lung injury or acute respiratory distress syndrome, the authors evaluated the effects of N-acetylcysteine (NAC) on oxidative stress and lung damage in an oleic acid (OA)-induced lung injury model. Thirty-five rats were divided into 5 groups as sham, NAC, OA, pre-OA-NAC, and post-OA-NAC. Lung damage was induced by intravenous administration of oleic acid. Pre-OA-NACgroup received intravenous (IV) N-acetylcysteine 15 minutes before oleic acid infusion and post-OA-NAC group received IV N-acetylcysteine 2 hours after oleic acid infusion. In both of the N-acetylcysteine treatment groups, blood and tissue samples were collected 4 hours after oleic acid infusion, independent from the time of N-acetylcysteine infusion. In other groups, blood and tissue samples were collected 4 hours after ethanol, NAC, or OA infusions. Serum myeloperoxidase activity, total antioxidant capacity, malondialdehyde levels, and lung tissue Na+ - K+ ATPase activity were measured and light microscopic analyses of lung specimens were performed. The administration of N-acetylcysteine significantly restored Na+ - K+ ATPase activity and total antioxidant capacity levels and ameliorated lung architecture. N-acetylcysteine has been shown to have some attenuating effects in experimental animal studies. However, further investigations are necessary to suggest N-acetylcysteine as a treatment agent in critically ill patients with lung injury.

Acetylcysteine↗
PubMed2004

Influence of harvest date and crop yield on the fatty acid composition of virgin olive oils from cv. Picual.

In this study was analyzed the effect of crop year and harvesting time on the fatty acid composition of cv. Picual virgin olive oil. The study was carried out during the fruit ripening period for three crop seasons. The mean fatty acid composition of Picual oils was determined. The oils contained palmitic acid (11.9%), oleic acid (79.3%), and linoleic acid (2.95%). The content of palmitic acid and saturated fatty acids decreased during fruit ripening while oleic and linoleic acids increased. The amount of stearic and linolenic acids decreased. The amount of saturated acids, palmitic and stearic, and the polyunsaturated acids linoleic and linolenic was dependent on the time of harvest, whereas the amount of oleic acid varied with the crop year. The differences observed between crop years for both palmitic and linoleic acid may be explained by the differences in the temperature during oil biosynthesis and by the amount of summer rainfall for oleic acid content. A significant relationship was observed between the MUFA/PUFA ratio and the oxidative stability measured by the Rancimat method.

Climate↗
PubMed1998

Reactive oxygen species are critical in the oleic acid-mediated mitogenic signaling pathway in vascular smooth muscle cells.

Obese hypertensive patients with cardiovascular risk factor clustering have increased plasma nonesterified fatty acid levels and are at high risk for atherosclerotic events. Our previous studies demonstrated that oleic acid induces a mitogenic response in rat aortic smooth muscle cells (RASMCs) through protein kinase C (PKC)- and extracellular signal-regulated kinase (ERK)-dependent pathways. In the present study we investigated the possibility that the generation of reactive oxygen species (ROS) constitutes a critical component of the oleic acid-induced mitogenic signaling pathway in RASMCs. We studied the effect(s) of oleic acid on the generation of ROS using the oxidant-sensitive fluoroprobe 2',7'-dichlorofluorescin diacetate. Relative fluorescence intensity and fluorescent images were obtained with laser confocal scanning microscopy from 1 to 5 minutes, since preliminary studies demonstrated that the peak fluorescence intensity occurred within 5 minutes. Oleic acid (100 micromol/L) induced a time-dependent increase of cell fluorescence that was >8-fold of that seen in control cells at 5 minutes. This was blocked by catalase, which suggests that H2O2 was the principal ROS. The oleic acid-induced increases in H2O2 were blocked when PKC was inhibited with the use of bisindolylmaleimide and when PKC activity was downregulated by exposing RASMCs to phorbol 12-myristate 13-acetate for 24 hours. Stearic and elaidic acids, which are weak PKC activators, did not significantly increase H2O2 production. The increase of H2O2 in response to oleic acid was inhibited by the antioxidant N-acetylcysteine. N-Acetylcysteine also completely blocked ERK activation and the increase of thymidine incorporation in response to oleic acid. The data suggest that generation of H2O2 in RASMCs exposed to oleic acid is PKC dependent. Moreover, H2O2 production emerges as a critical intermediary event in the oleic acid-mediated mitogenic signaling pathway between the activation of PKC and ERK. These observations raise the possibility that the elevated plasma nonesterified fatty acids, including oleic acid, in obese hypertensive patients contribute to vascular growth and remodeling by a PKC-dependent mechanism to generate ROS that subsequently activate ERK.

Acetylcysteine↗
PubMed1992

Metabolic effects of dietary stearic acid in mice: changes in the fatty acid composition of triglycerides and phospholipids in various tissues.

The fatty acid patterns of triglycerides and phospholipids extracted from adipose tissue, liver, heart, kidney, spleen, and lung of 3 groups of C57BL/6 mice were determined after feeding diets rich in palmitic acid (16:0) (high palmitic: 16:0 = 45.1% of total fatty acids), stearic acid (18:0) (high stearic: 18:0 = 42.9% of total fatty acids) and oleic acid (18:1) (high oleic: 18:1 = 79.7% of total fatty acids) for 9 months. Triglyceride content of adipose, liver, heart, kidney, lung and spleen tissues was significantly enriched in palmitic acid in mice fed the high palmitic diet (range among all tissues: 19.9% +/- 0.2% to 29.0% +/- 1.9% of total fatty acids) and in oleic acid in mice fed the high oleic diet (range 56.0% +/- 1.9% to 71.6% +/- 1.2%). The stearic acid content of organ triglycerides in mice fed the high stearic diet ranged from 3.7% +/- 0.3% to 10.8% +/- 1.2%; however, the content of oleic acid on this diet (range: 57.0% +/- 1.8% to 71.4% +/- 1.7%) was similar to the one observed in mice fed the high oleic diet. In all organs, phospholipids had a significantly higher percentage of stearic acid (range: 23.5% +/- 0.9% to 51.5% +/- 6.6%) than triglycerides, regardless of diet. To evaluate the production of oleate from stearate and palmitate, 2 groups of mice were fed the high palmitic and the high stearic diets for 1 week and then injected intravenously with [1-14C]palmitate and [1-14C]stearate and the amount of labelled oleate in liver triglycerides was measured.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1981

Effect of atropine on bile-oleic acid-induced alterations in dog jejunal hemodynamics, oxygenation, and net transmucosal water movement.

The effects of intraluminal bile-oleic acid on jejunal blood flow, oxygen uptake, net transmucosal fluid flux, and mucosal ultrastructure were studied in isolated autoperfused jejunal segments before and after cholinergic blockage with atropine. Bile-oleic acid increased jejunal blood flow (40%), decreased oxygen extraction (24%), and increased oxygen uptake (15%). Cholinergic blockade did not abolish the bile-oleic acid-induced changes in these parameters. Bileoleic acid induced net fluid secretion or significantly depressed absorption. Cholinergic blockade reversed net volume secretion to absorption or attenuated the depression of absorption produced by bile-oleic acid. Ultrastructural analyses of tissue samples taken during bile-oleic acid-induced secretion indicate major structural damage to the mucosal membrane which was not affected by cholinergic blockade. The physiologic and ultrastructural data acquired in this study suggest that: (a) the effects of bile-oleic acid on net transmucosal water movement are reversed by cholinergic blockade and (b) the hyperemia, increased oxygen consumption, and morphologic alterations induced by bile-oleic acid are not affected by cholinergic blockade. The results of this study may have important implications in steatorrheal diseases in that, atropine may alleviate the diarrhea induced by the presence of excess lipid in chyme without compromising the intestinal hyperemia and enhanced oxygen delivery required to meet the increased metabolic demands during nutrient absorption.

Animals↗
PubMed2005

In chronic fatigue syndrome, the decreased levels of omega-3 poly-unsaturated fatty acids are related to lowered serum zinc and defects in T cell activation.

There is now evidence that major depression is accompanied by decreased levels of omega3 poly-unsaturated fatty acids (PUFA), such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). There is a strong comorbidity between major depression and chronic fatigue syndrome (CFS). The present study has been carried out in order to examine PUFA levels in CFS. In twenty-two CFS patients and 12 normal controls we measured serum PUFA levels using gas chromatography and mass spectrometry. We found that CFS was accompanied by increased levels of omega6 PUFAs, i.e. linoleic acid and arachidonic acid (AA), and mono-unsaturated fatty acids (MUFAs), i.e. oleic acid. The EPA/AA and total omega3/omega6 ratios were significantly lower in CFS patients than in normal controls. The omega3/omega6 ratio was significantly and negatively correlated to the severity of illness and some items of the FibroFatigue scale, i.e. aches and pain, fatigue and failing memory. The severity of illness was significantly and positively correlated to linoleic and arachidonic acid, oleic acid, omega9 fatty acids and one of the saturated fatty acids, i.e. palmitic acid. In CFS subjects, we found significant positive correlations between the omega3/omega6 ratio and lowered serum zinc levels and the lowered mitogen-stimulated CD69 expression on CD3+, CD3+ CD4+, and CD3+ CD8+ T cells, which indicate defects in early T cell activation. The results of this study show that a decreased availability of omega3 PUFAs plays a role in the pathophysiology of CFS and is related to the immune pathophysiology of CFS. The results suggest that patients with CFS should respond favourably to treatment with--amongst other things--omega3 PUFAs, such as EPA and DHA.

Analysis of Variance↗
PubMed1986

Evaluation of (1-sarcosine, 8-isoleucine) angiotensin II as a therapeutic agent for oleic acid-induced pulmonary edema.

(1-Sarcosine, 8-isoleucine) angiotensin II was assessed as a therapeutic agent for acute respiratory distress syndrome with oleic acid pulmonary edema in sheep used as an experimental model. Under general anesthesia with controlled mechanical ventilation with 100% oxygen, 32 sheep received oleic acid (0.075 ml/kg) intravenously. After oleic acid infusion, 20 animals were treated with continuous intravenous infusion of the angiotensin II analogue; nine received 300 ng/kg/min, six received 600 ng/kg/min, and five received 2000 ng/kg/min. Cardiopulmonary measurements were repeated every 30 minutes for 270 minutes. According to time-integrated PaO2, six of 15 animals of the groups given 300 and 600 ng/kg/min (43%) did not respond to the treatment. All animals responded in the group given 2000 ng/kg/min. Animals in the latter group had lower Qs/Qt, PaCO2, and airway resistance than had the control animals. Elevation of pulmonary vascular resistance was limited and mean arterial blood pressure was well maintained. These results reveal that (1-Sar, 8-Ile) angiotensin II is effective in the treatment of oleic acid-induced pulmonary edema.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1978

Toxicity of free fatty acids for cultured rat heart muscle and endothelioid cells. II. Unsaturated long-chain fatty acids.

Oleic (C18:1), linoleic (C18:2), linolenic (C18:3) and arachidonic (C20:4) acids were compared for their toxic effects upon cultured rat heart muscle and endothelioid cells. The free fatty acids (FFA) were bound to albumin (6:1) and tested at concentrations from 5 x 10(-5)M to 5 x 10(-4)M. Reduction of cell viability (51Cr release) and in situ mitochondrial and lysosomal labilization were used as indices of injury. Oleic acids was non-toxic at all times and concentrations tested while linoleic acid increased cell death only in muscle cells after 32 h. Arachidonic acid, by contrast, demonstrated significant toxicity as early as 2 h while both linolenic and arachidonic acids produced major injury at longer durations. A detergent effect was excluded as the injury mechanism because of marked differences in the toxicities of the individual FFA. The similarity in the effects of linolenic and arachidonic acids would appear to exclude prostaglandins as responsible toxic products.

Acid Phosphatase↗
PubMed1999

Effect of fatty acid chain length and saturation on the gastrointestinal handling and metabolic disposal of dietary fatty acids in women.

The gastrointestinal handling and metabolic disposal of [1-13C]palmitic acid, [1-13C]stearic acid and [1-13C]oleic acid administered within a lipid-casein-glucose-sucrose emulsion were examined in normal healthy women by determining both the amount and nature of the 13C label in stool and label excreted on breath as 13CO2. The greatest excretion of 13C label in stool was in the stearic acid trial (9.2% of administered dose) whilst comparatively little label was observed in stool in either the palmitic acid (1.2% of administered dose) or oleic acid (1.9% of administered dose) trials. In both the palmitic acid and oleic acid trials, all of the label in stool was identified as being present in the form in which it was administered (i.e. [13C]palmitic acid in the palmitic acid trial and [13C]oleic acid in the oleic acid trial). In contrast, only 87% of the label in the stool in the stearic acid trial was identified as [13C]stearic acid, the remainder was identified as [13C]palmitic acid which may reflect chain shortening of [1-13C]stearic acid within the gastrointestinal tract. Small, but statistically significant, differences were observed in the time course of recovery of 13C label on breath over the initial 9 h of the study period (oleic acid = palmitic acid > stearic acid). However, when calculated over the 24 h study period, the recovery of the label as 13CO2 was similar in all three trials (approximately 25% of absorbed dose). These results support the view that chain length and degree of unsaturation may influence the gastrointestinal handling and immediate metabolic disposal of these fatty acids even when presented within an emulsion.

Adult↗
PubMed1982

Propionyl-Coa induced synthesis of even-chain-length fatty acids by fatty acid synthetase from Brevibacterium ammoniagenes.

The product distribution of Brevibacterium ammoniagenes fatty acid synthetase has been investigated using propionyl-CoA instead of acetyl-CoA as the primer. The synthetase produces not only an odd-numbered fatty acid (heptadecanoic acid) but also even-numbered fatty acids (stearic and oleic acids) in the presence of propionyl-CoA. The amounts of heptadecanoic, stearic and oleic acids increased with increasing concentration of propionyl-CoA. However, the formation of heptadecenoic acid (C17:1) was not observed under any conditions tested. The failure of C17:1 synthesis suggested that the enzyme component catalyzing the beta, gamma-dehydration, which is responsible for the synthesis of unsaturated fatty acids, has a high degree of chain length specificity. Under standard assay conditions, stearic acid predominated and heptadecanoic and oleic acids were found in lesser amounts. Mass spectrometric analyses of fatty acids synthesized either from [2H]propionyl-CoA or in 2H2O revealed that propionyl-CoA is utilized as the priming substrate for the synthesis of heptadecanoic acid and that an acetyl residues, which is formed by the decarboxylation of malonyl-CoA, served as the priming substrate for the syntheses of stearic and oleic acids. No evidence was obtained for the direct decarboxylation of malonyl-CoA to acetyl-CoA in this reaction. It is concluded that the decarboxylation of the malonyl moiety bound to the synthetase occurs efficiently only in the course of fatty acid synthesis. A hypothetical scheme is presented to explain the propionyl-CoA-dependent decarboxylation of the malonyl moiety.

Acetyl Coenzyme A↗
PubMed1995

Tetradecylthioacetic acid (a 3-thia fatty acid) decreases triacylglycerol secretion in CaCo-2 cells.

The effects of the hypolipidemic fatty acid analogue tetradecylthioacetic acid (TTA) on synthesis and secretion of lipoproteins in CaCo-2 cells were studied. Radiolabeled tetradecylthioacetic acid was absorbed and metabolized as efficiently as oleic acid, although a discrepancy in the metabolic fate was evident. Whereas tetradecylthioacetic acid was incorporated into cell-associated triacylglycerol to the same extent as normal fatty acids (e.g., oleic acid and palmitic acid), the amount of triacylglycerol secreted from cells incubated with tetradecylthioacetic acid was 8 to 10 times lower than the amount secreted from cells incubated with palmitic acid and oleic acid, respectively. On the other hand, there was an enhanced incorporation of tetradecylthioacetic acid into cell-associated and secreted phospholipids. Despite incorporation of tetradecylthioacetic acid into cellular triacylglycerol, unlike oleic acid, tetradecylthioacetic acid did not stimulate production of triacylglycerol-rich particles. Ultracentrifugation of basolateral media from cells incubated with tetradecylthioacetic acid revealed low amounts of triacylglycerol in the triacylglycerol-rich fraction (p < 1.006 g/ml), suggesting secretion of lipoproteins with a higher density than chylomicrons. However, the present study shows that the stimulated triacylglycerol secretion caused by oleic acid was inhibited in the presence of TTA. The decreased rate of triacylglycerol secretion from these cells was not accompanied by a stimulation of fatty acid oxidation. Based on these findings, we therefore suggest that tetradecylthioacetic acid mainly affects secretion of lipoproteins in CaCo-2 cells.

Cell Line↗
PubMed2003

End-expiratory lung volumes and density distribution patterns during partial liquid ventilation in healthy and oleic acid-injured sheep: a computed tomography study.

OBJECTIVE: To determine end-expiratory lung volumes (EELVs) and the distribution of gas and perflubron during low- and high-dose partial liquid ventilation (PLV) in healthy and oleic-acid-injured lungs. DESIGN: A prospective, randomized study. SETTING: A university medical school laboratory approved for animal research. SUBJECTS: Adult sheep. INTERVENTIONS: A total of 18 sheep were randomly divided into two groups (healthy and oleic acid lung injury) and received PLV with perflubron at incremental doses. MEASUREMENTS AND MAIN RESULTS: Animals were ventilated in a volume-control mode with a positive end-expiratory pressure of 5 cm H2O. Baseline computed tomographic scans of the entire lung were obtained during end-expiratory hold. Thereafter, the animals were randomized to undergo either PLV alone (healthy group) or after oleic acid lung injury was introduced (injury group). In both groups, PLV was induced by instilling 10 mL/kg perflubron into the endotracheal tube over 5 mins (low-dose PLV). At 60 mins after dosing, another set of computed tomographic scans during end-expiratory hold was obtained. Thereafter, another 20 mL/kg perflubron was instilled in both groups (cumulative dose, 30 mL/kg perflubron, high-dose PLV), and computed tomographic scanning was repeated 60 mins later. EELVs were calculated. To study density distribution patterns, the lungs were divided into nine segments, and the mean Hounsfield attenuation number was calculated for each segment. In healthy animals, low-dose PLV did not change EELV (47.5 +/- 8.1 mL/kg vs. 44.5 +/- 6.1 mL/kg at 10 mL/kg perflubron), whereas high-dose PLV significantly increased EELV (58.1 +/- 3.3 mL/kg, p <.01). Oleic acid lung injury significantly reduced EELV (53.9 +/- 7.5 mL/kg vs. 43.9 +/- 8.7 mL/kg, p <.01). Low-dose PLV reestablished baseline EELV (59.8 +/- 10.5 mL/kg), and high-dose PLV resulted in a significant increase in EELV (89.2 +/- 12 mL/kg, p =.003). PLV increased the mean Hounsfield attenuation number along the ventrodorsal axis in the three coronal blocks in a dose-dependent manner. In the oleic acid lung injury group, PLV produced a more homogeneous pattern of density distribution, with the highest Hounsfield attenuation numbers observed in the medial segments. CONCLUSION: High-dose PLV significantly increased EELV in both states, indicating lung distention. Healthy lungs were filled in a dose-dependent, gravity-governed fashion, showing steep craniocaudal and ventrodorsal gradients. In the oleic acid lung injury model studied, perflubron tended to accumulate on top of the most severely injured dorsal and diaphragmatic parts, rendering effective recruitment by liquid positive end-expiratory pressure in these regions questionable.

Animals↗
PubMed2001

Comparative quantitative fatty acid analysis of triacylglycerols using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry and gas chromatography.

Quantitative analyses of fatty acids from five triacylglycerol products, coconut oil, palm kernel oil, palm oil, lard and cocoa butter, were carried out using two analytical methods: matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOFMS) and gas chromatography (GC), in an effort to validate the application of MALDI-TOFMS in quantitative fatty acid analysis. For the GC analysis, transmethylated products were used, whereas, for the MALDI-TOF analysis, saponified products were used. Under MALDI-TOF conditions, the acids were detected as sodiated sodium carboxylates [RCOONa + Na](+) consistent with the mode of ionization that was previously reported. Thus, the MALDI-TOF mass spectrum of saponified coconut oil showed the presence of sodiated sodium salts of caprylic acid (7.5 +/- 0.67, m/z 189), capric acid (6.9 +/- 0.83, m/z 217), lauric acid (47.8 +/- 0.67, m/z 245), myristic acid (20.4 +/- 0.51, m/z 273), palmitic acid (9.8 +/- 0.47, m/z 301), linoleic acid (0.9 +/- 0.07, m/z 325), oleic acid (4.8 +/- 0.42, m/z 327) and stearic acid (2.0 +/- 0.13, m/z 329). Saponified palm kernel oil had a fatty acid profile that included caprylic acid (3.5 +/- 0.59), capric acid (4.7 +/- 0.82), lauric acid (58.6 +/- 2.3), myristic acid (20.9 +/- 1.5), palmitic acid (7.2 +/- 1.1), oleic acid (3.8 +/- 0.62) and stearic acid (1.2 +/- 0.15). Saponified palm oil gave myristic acid (0.83 +/- 0.18), palmitic acid (55.8 +/- 1.7), linoleic acid (4.2 +/- 0.51), oleic acid (34.5 +/- 1.5), stearic acid (3.8 +/- 0.26) and arachidic acid (0.80 +/- 0.22). Saponified lard showed the presence of myristic acid (1.5 +/- 0.24), palmitic acid (28.9 +/- 1.3), linoleic acid (13.7 +/- 0.67), oleic acid (38.7 +/- 1.4), stearic acid (12.8 +/- 0.64) and arachidic acid (2.4 +/- 0.35). Finally, for saponified cocoa butter, the fatty acid distribution was: palmitic acid (32.3 +/- 1.0), linoleic acid (2.6 +/- 0.35), oleic acid (34.9 +/- 1.7) and stearic acid (30.3 +/- 1.6). Quantitative gas chromatographic analysis of the corresponding methyl esters from these triacylglycerol products yielded data that were mostly in agreement with the MALDI-TOFMS data. The MALDI-TOF experiment, however, proved to be superior to the GC experiment, particularly with regard to baseline resolution of unsaturated acids. Furthermore, the ability of MALDI-TOFMS to detect low concentrations of fatty acids rendered it more sensitive than the GC methodology.

Animals↗
PubMed2003

Monounsaturated fatty acids prevent the deleterious effects of palmitate and high glucose on human pancreatic beta-cell turnover and function.

Glucotoxicity and lipotoxicity contribute to the impaired beta-cell function observed in type 2 diabetes. Here we examine the effect of saturated and monounsaturated fatty acids at different glucose concentrations on human beta-cell turnover and secretory function. Exposure of cultured human islets to saturated fatty acid and/or to an elevated glucose concentration for 4 days increased beta-cell DNA fragmentation and decreased beta-cell proliferation. In contrast, the monounsaturated palmitoleic acid or oleic acid did not affect DNA fragmentation and induced beta-cell proliferation. Moreover, each monounsaturated fatty acid prevented the deleterious effects of both palmitic acid and high glucose concentration. The cell-permeable ceramide analogue C(2)-ceramide mimicked both the palmitic acid-induced beta-cell apoptosis and decrease in proliferation. Furthermore, the ceramide synthetase inhibitor fumonisin B1 blocked the deleterious effects of palmitic acid on beta-cell turnover. In addition, palmitic acid decreased Bcl-2 expression and induced release of cytochrome c from the mitochondria into the cytosol, which was prevented by fumonisin B1 and by oleic acid. Finally, each monounsaturated fatty acid improved beta-cell secretory function that was reduced by palmitic acid and by high glucose. Thus, in human islets, the saturated palmitic acid and elevated glucose concentration induce beta-cell apoptosis, decrease beta-cell proliferation, and impair beta-cell function, which can be prevented by monounsaturated fatty acids. The deleterious effect of palmitic acid is mediated via formation of ceramide and activation of the apoptotic mitochondrial pathway, whereas Bcl-2 may contribute to the protective effect of monounsaturated fatty acids.

Adult↗
PubMed1985

Fluorescent pigments by covalent binding of lipid peroxidation by-products to protein and amino acids.

The fluorescent products formed on reaction of 12-oxo-cis-9-octadecenoic acid (12-keto-oleic acid) with about 20 different amino acids, polylysine and bovine serum albumin (BSA) were studied. Besides glycine, only the basic amino acids histidine, lysine and arginine gave products with strong fluorescence. N-Acetylation of amino acids greatly reduced the fluorescence of their reaction products. The formation of fluorescent products was inhibited strongly by SH-amino acids such as N-acetyl-cysteine and glutathione. Polyacrylamide gel electrophoresis showed that BSA treated with 12-keto-oleic acid was more acidic than untreated or ricinoleic acid-treated BSA, indicating that basic amino acid residues in BSA were modified by reaction with the keto fatty acid. None of the structural analogs of 12-keto-oleic acid tested--12-oxo-trans-10-octadecenoic acid, 12-oxo-octadecanoic acid, 12-hydroxy-cis-9-octadecenoic acid (ricinoleic acid), cis-9-octadecenoic acid (oleic acid) and linoleic acid--reacted with glycine to give a fluorescent product. The fluorescent products formed on reaction of 12-keto-oleic acid methyl ester with benzyl amine and glycine methyl ester were shown to be 8-(N-substituted-4,5-dihydro-4-oxo-5-hexyl-5-hydroxy-2-pyrrolyl) octanoic acid methyl esters. The fluorescence properties of these compounds were attributed to the chromophobic system NC = CC = O which contains 6 pi electrons. This investigation contributes to insight of the mechanism of formation of fluorescent pigments, probably by a similar reaction of other compounds of the beta, gamma-unsaturated carbonyl type.

Amino Acids↗