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The effects of plant oils on health are being intensively studied. Many fatty acids have attracted significant scientific attention since the studies pointed them as potential nutrients. An attempt was made to analyze the variation in three major Indian Garcinia fruits for their oils, lipid sub-classes, fatty acids and total amino acids. Solvent extraction and chromatographic techniques were used for the isolation, purification, separation and detection of these compounds. Three major Garcinia fruits G. gummi-gutta, G. indica and G. xanthochymus varied in their chemical composition. Oil content was significantly higher (p

The effect of free fatty acids (FFA) on lipid oxidation in water-in-stripped walnut oil emulsions was investigated. The formation of the primary oxidation products (hydroperoxides) and the secondary oxidation product (headspace hexanal) increased with increasing addition of oleic acid to the emulsions. However, oleic acid at high concentrations was primarily involved in accelerating hydroperoxide formation at early stage and then hydroperoxide decomposition rapidly after hydroperoxides reached the maximum point. The prooxidant effect of saturated FFA was dependent on their chain length with lipid oxidation rates being in the order of lauric acid>palmitic acid>stearic acid. The highest prooxidant activity of lauric acid among these FFA was probably due to its largest polarity and making the water droplet interface more negatively charged than the others when the aqueous phase pH was 7.0, which was above its pKa, thereby attracting prooxidant metals to the water droplet surface. The highest ability to promote lipid oxidation in water-in-oil emulsions was shown by linolenic acid, followed by linoleic and oleic acids, indicating that the oxidative capacity increased with increasing degree of unsaturation. The prooxidant effect of FFA with the cis double bonds was lower than those with the trans ones when oleic acid (18:1, cis) was compared to elaidic acid (18:1, trans) and linoleic acid (18:2, cis–cis) was compared to linoelaidic acid (18:2, trans–trans), which suggested that geometric isomeration of FFA influenced lipid oxidation rates of water-in-oil emulsions. Practical applications: FFA promote lipid oxidation in bulk oil and oil-in-water (O/W) emulsions. From the present study, it became clear that FFA were also strong prooxidants in water-in-oil (W/O) emulsions. This research pointed out the importance of using oils and fats containing minimal FFA in W/O emulsion formulation to obtain the highest quality.

Trans fatty acids (TFA) have been considered as an independent risk factor of coronary heart disease, sudden death and insulin-resistance, and different TFA isomers may have different effects on the progression of cardiovascular diseases such as atherosclerosis. The aim of the study was to investigate the effects of two major TFA, elaidic acid and linolelaidic acid which have the same number of carbons but a different number and configuration of trans bonds, on the proliferation of human umbilical vein smooth muscle cells (HUVSMC). Methyl thiazolyl tetrazolium and flow cytometry assays showed that the cell proliferation rose to 115.37 ± 0.39 and 117.5 ± 0.57 % and the cell number in the S phase of the cell cycle reached 27.7 ± 0.7 and 25.8 ± 2.8 % when treated with 50 μM elaidic acid and 20 μM linolelaidic acid, respectively. Quantitative real-time reverse transcriptase-polymerase chain reaction and Western blotting analyses showed that the two TFA increased the mRNA and protein expression levels of PCNA, CDK2 and Cyclin E in HUVSMC. Moreover, gas chromatography analysis showed that the total PUFA level of HUVSMC was lower after treatment with the two TFA, especially n-3 PUFA. These results suggested that linolelaidic acid exhibited a stronger proliferative effect on HUVSMC than elaidic acid, and regulation of CDK2 and Cyclin E may be important for the effect of the TFA on atherosclerosis.

Epidemiological data have shown an association of the intake of industrial produced trans fatty acids (TFA) and sudden cardiac death. The present study examines the impact of elaidic acid (t18:1n-9) and linoelaidic acid (t18:2n-6) on the human aortic endothelial cell functional response. Trans fatty acids predominately incorporated into the phospholipid component while only a minute fraction of the total fatty acids (FA) incorporated into triacylglycerol. Trans fatty acids incorporated into the plasma membranes at the expense of the saturated-FA, stearic, palmitic, and to a lesser extent, myristic acid. Both t18:1n-9 and t18:2n-6 induced a pro-inflammatory response by elevating surface expression of intercellular adhesion molecule-1 (ICAM-1). Neither oleic nor linoleic evoked a pro-inflammatory phenotype under the maximal 50 µM treatments. Both TFA and stearic acid increased phosphorylation of the ICAM-1 transcriptional regulator, nuclear factor-κβ (NF-κβ), while oleic and linoleic acids did not appear to alter the phosphorylation status. Elaidic acid minimally affected endothelial cell growth, whereas linoelaidic acid completely inhibited growth at 100 µM and imparted limited cytotoxicity up to 300 µM. Stearic acid induced cytotoxicity at concentrations above 75 µM, while oleic and linoleic acids evoked gradual dose-dependent growth inhibition with cytotoxicity occurring only at linoleic acid concentrations greater than 200 µM. In conclusion, t18:1n-9 and t18:2n-6 fatty acids effectively incorporated into the phospholipid component of endothelial cells and subsequently induce a pro-inflammatory phenotype.

The objectives of this study are to explore whether separate sources of trans fatty acids (TFA) have different effects on ECV304 cell line and to further elucidate the oxidation mechanism induced by TFA. ECV304 cells are used in the study because they display many endothelial features. Cell apoptosis rates increased in a dose-dependent manner following 24-h treatment with TFA from separate sources. Additionally, TFA stimulated human alpha-defensin 1 (HNP-1) expression and resulted in a significant increase in both malondialdehyde (MDA) and ROS levels. MDA levels reach their peak at 18 h. HNP-1 expression levels increase at 2 h and then reach their peak at 10 h. At the same time, the protein carbonyl (PCO) value declines slightly. After 10 h of TFA co-culture, the cells were washed and fresh low-density lipoprotein (LDL) was added. MDA generation significantly increased after 6 h and it could be inhibited by 4-aminobenzoic acid hydrazide (ABAH) or sodium ferulate. However, after the TFA co-culture for 2 h, adding LDL for 6 h just caused slight MDA generation change and the MDA generation could be inhibited by verapamil or sodium ferulate. TFA from different sources did not have different effects on ECV304. HNP-1 mediates the oxidation induced by TFA by activating ROS. Furthermore, TFA can stimulate the oxidation of LDL in ECV304 cells through both passive and active pathway. In the oxidation induced by linoelaidic acid, ABAH can decrease the MDA generation in active oxidation pathway and verapamil can decrease the MDA generation in passive oxidation pathway.

The products formed by thermally induced isomerization of trilinolein and trilinoelaidin at 250 degrees C were studied by infrared spectroscopy and gas chromatography. The triglycerides of the 9c12c and 9t12t fatty acids, linoleic and linoelaidic acid respectively, were subjected to thermal treatment under nitrogen in glass. The products were removed at regular intervals and analysed by infrared spectroscopy using a single reflectance attenuated total internal reflectance crystal accessory. Trans-esterification of the products provided the corresponding fatty acid methyl esters which were studied by gas chromatography. The results show that the samples undergo decomposition and isomerization. Thermally induced 9c12c fatty acid (linoleic acid) molecules in the trilinolein molecules isomerize into 9c12t, 9t12c and 9t12t isomers. Thermally induced 9t12t fatty acid (linoelaidic acid) molecules in the trilinoelaidin molecules isomerize into 9c12t, 9t12c and 9c12c isomers. However, the concentration profiles are different for these two triglyceride samples. The rates of formation of isomers from linoleic acid are higher than the rates of formation of isomers from linoelaidic acid. In addition, these two fatty acids also isomerize into conjugated linoleic acids (CLAs). The profiles of the CLAs are identical in both cases.

An approach based on an in silico analysis predicted that CYP77A4, a cytochrome P450 that so far has no identified function, might be a fatty acid-metabolizing enzyme. CYP77A4 was heterologously expressed in a Saccharomyces cerevisiae strain (WAT11) engineered for cytochrome P450 expression. Lauric acid (C12:0) was converted into a mixture of hydroxylauric acids when incubated with microsomes from yeast expressing CYP77A4. A variety of physiological C18 fatty acids were tested as potential substrates. Oleic acid (cis-Δ9C18:1) was converted into a mixture of ω-4- to ω-7-hydroxyoleic acids (75%) and 9,10-epoxystearic acid (25%). Linoleic acid (cis,cis-Δ9,Δ12C18:2) was exclusively converted into 12,13-epoxyoctadeca-9-enoic acid, which was then converted into diepoxide after epoxidation of the Δ9 unsaturation. Chiral analysis showed that 9,10-epoxystearic acid was a mixture of 9S/10R and 9R/10S in the ratio 33 : 77, whereas 12,13-epoxyoctadeca-9-enoic acid presented a strong enantiomeric excess in favor of 12S/13R, which represented 90% of the epoxide. Neither stearic acid (C18:0) nor linolelaidic acid (trans,trans-Δ9,Δ12C18:2) was metabolized, showing that CYP77A4 requires a double bond, in the cis configuration, to metabolize C18 fatty acids. CYP77A4 was also able to catalyze the in vitro formation of the three mono-epoxides of α-linolenic acid (cis,cis,cis-Δ9,Δ12,Δ15C18:3), previously described as antifungal compounds. Epoxides generated by CYP77A4 are further metabolized to the corresponding diols by epoxide hydrolases located in microsomal and cytosolic subcellular fractions from Arabidopsis thaliana. The concerted action of CYP77A4 with epoxide hydrolases and hydroxylases allows the production of compounds involved in plant–pathogen interactions, suggesting a possible role for CYP77A4 in plant defense.

1. Whole-cell recordings from cultured rat hippocampal neurons, from freshly dissociated dorsal root ganglion (DRG) neurons and from human embryonic kidney (HEK) 293 cells expressing the glutamate receptor GluR6 subunit were used to study the modulation of kainate receptor channels by long chain fatty acids. 2. In all three cell types, application of cis-unsaturated fatty acids caused a dose-dependent reduction in whole-cell currents evoked by kainate. Docosahexaenoic acid (DHA), arachidonic acid (AA), linolenic acid and linoleic acid all produced substantial inhibition at a concentration of 50 microM, whereas inhibition by linolenelaidic acid and linolelaidic acid was significantly weaker. Fully saturated fatty acids were essentially inactive. 3. With continuous exposure to active fatty acids, the peak current elicited by kainate declined over a time course of several minutes to reach a steady-state level less than 50 % of the initial amplitude. Recovery was slow in control solution, but was speeded up by exposure to bovine serum albumin (0.5 mg ml-1), a protein that binds fatty acids with submicromolar affinity. The inhibition in neurons was half-maximal with 5-15 microM AA or DHA, but potency was at least 10-fold greater at GluR6 in HEK 293 cells. 4. Inhibition by AA or DHA was unaffected by extracellular nordihydroguaiaretic acid (10 microM), indomethacin (10 microM), 17-octadecynoic acid (30 microM) or 1-(5-isoquinolinylsulphonyl)-2-methylpiperazine dihydrochloride (H-7; 10 microM). Furthermore, inclusion of H-7 (100 microM), BAPTA (10 mM), AA (50 microM), antioxidants, or the protein kinase C inhibitor PKC19-36 (20 microM) in the internal solution had little effect on whole-cell currents and did not prevent inhibition of currents by extracellular application of AA or DHA. 5. We conclude that the inhibition produced by cis-unsaturated fatty acids does not require conversion to oxidized metabolites or activation of PKC. Instead, active compounds may interact directly with an extracellular, or intramembraneous, site on kainate receptors.

Various fatty acids were fed to the yeast Dipodascopsis uninucleata UOFS Y 128, and the extracted samples were analyzed for the accumulation of 3-hydroxy metabolites with the help of electron impact gas chromatography-mass spectrometry. Fatty acids containing of 5Z,8Z-diene system (5Z,8Z,11Z-eicosatrienoic, 5Z,8Z,11Z,14Z-eicosatetraenoic, and 5Z,8Z,11Z,14Z,17Z-eicosapentaenoic acids) yielded the corresponding 3-hydroxy-all-Z-eicosapolyenoic acids. Moreover, linoleic acid (9Z,12Z-octadecadienoic acid) and 11Z,14Z,17Z-eicosatrienoic acid were converted to the 3-hydorxylated metabolites of shorter chain length, e,g., 3-hydroxy-5Z,8Z-tetradecadienoic acid and 3-hydroxy-5Z,8Z,11Z-tetradecatrienoic acid, respectively. In contrast, no accumulation of a 3-hydroxy metabolite was observed with oleic acid (9Z-octadecenoic acid), linolelaidic acid (9E,12E-octadecadienoic acid), gamma-linolenic acid (6Z,9Z,12Z-octadecatrienoic acid), and eicosanoic acid as substrate. These findings pinpoint that the 3-hydroxylation of a fatty acid in Dipodascopsis uninucleata requires a 5Z,8Z-diene system either directly or following initial incomplete beta-oxidation. Following analysis of the enantiomer composition, the arachidonic acid metabolite was identified as 3R-hydroxy-5Z,8Z,11Z,14Z-eicosatetraenoic acid, which rules out a normal beta-oxidation as biosynthetic route to this new class of oxylipins.

Lipid rafts were reported to play important roles in elaidic acid-induced apoptosis in human umbilical vein endothelial cells (HUVECs). Linolelaidic acid induced cell injury more seriously than elaidic acid. However, whether lipid rafts may play the same roles for linolelaidic acid- and elaidic acid-induced cell injury was unknown. Therefore, the aim of this study was to compare the effect of lipid rafts on linolelaidic acid- and elaidic acid-induced apoptosis, cell cycle arrest and inflammation in HUVECs. The cell viability was significantly decreased, the number of apoptotic cells and cell population in G1 phase were significantly increased in elaidic acid- or linolelaidic acid-treated cells, compared to methyl-β-cyclodextrin + trans-fatty acids-treated cells. In addition, the expression levels of pro-apoptotic proteins (caspase-3, -8, Bax, p53) and inflammation factors (vascular cell adhesion molecule-1, intercellular adhesion molecule, E-selectin and nitro oxide) were significantly increased, and anti-apoptotic protein like Bcl-2 decreased significantly in linolelaidic acid-treated cells, which were stronger than those in elaidic acid-treated cells. In conclusion, linolelaidic acid induces a stronger lesion effect on HUVECs through lipid rafts compared to elaidic acid. Practical applications: Different processing method generated different trans fatty acids, such as industrial hydrogenation produced amount of trans 18:1, deep frying with temperature over 200°C generated both trans 18:1 and trans 18:2. Researches reported that trans fatty acids with different saturation had diverse effect on human health, especially cardiovascular disease. This paper found that 9t12t18:2 induced a stronger lesion effect on HUVECs compared with 9t18:1 through lipid rafts, which indicated that we should pay attention to 9t12t18:2 produced from deep frying, and the deep frying temperature should be dropped to reduce the trans 18:2 level. Moreover, the involvement of lipid rafts in trans fatty acids induced apoptosis, cell cycle arrest and inflammation was demonstrated, which provided a scientific basis for the prevention and treatment of cardiovascular disease. Both linoelaidic acid and elaidic acid induced HUVECs apoptosis and increased expression of pro-apoptotic proteins. However, supplementation of TFAs to MβCD-treated cells increased the cell viability and significantly decreased the number of apoptotic cells. Moreover, linolelaidic acid induces a stronger lesion effect on HUVECs by lipid rafts mediation compared to elaidic acid.

Unsaturated fatty acid monolayers on silica gel have been autoxidized, and the rate of fatty acid disappearance and products obtained from those membrane-like assemblies have been studied. Fatty acid monolayers consisting of pure linoleic acid, linolelaidic acid, and oleic acid were autoxidized at 60 C. The rates of autoxidation of linoleic acid and linolelaidic acid monolayers followed by the disappearance of substrates are considerably faster than that in bulk phase, and the rates conform to apparent first order kinetics. Autoxidation of linoleic and linolelaidic acid monolayers, unlike bulk phase, produced only a small amount of diene conjugation, and the major products formed were identified as 9,10-epoxy and 12,13-epoxyoctadecenoic acid in roughly equal quantities. The epoxidation is stereospecific, with cis and trans olefins giving cis and trans epoxides, respectively. Oleic acid was autoxidized to only a small extent during 27 hr and produced no detectable amount of epoxide.

Male weanling rats of the Sprague-Dawley strain were made essential fatty acid (EFA)-deficient by feeding them a fat-free diet for five months. The animals were then fed a supple-ment of methyltrans-9,trans-12-octadecadienoate (methyl linoelaidate), as 5% of the dietary calo-ries (approximately 400 mg/animal/day) for 19 days, and killed by exsanguination. The com-position of the liver, kidney, epididymal and plasma lipids was determined and compared with that obtained from EPA-deficient rats given oral supplements of methylcis-9,cis-12-octadeca-dienoate (linoleate) and methylcis-9,trans-12- octadecadienoate. Linoelaidic acid was depos-ited in the phospholipids, sterol esters and tri-glycerides in all of the tissues examined. Iso-lation analysis of the fatty acids showed no evidence that linoelaidic acid was converted to higher polyunsaturated fatty acids in the EFA-deficient rat.