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PubMed1995

Changes in linoleic acid metabolism and membrane fatty acids of LLC-PK cells in culture induced by 5 alpha-cholestane-3 beta,5,6 beta-triol.

The aim of this study was to investigate the effect of the oxysterol 5 alpha-cholestane-3 beta,5,6 beta-triol (triol) on the metabolism of linoleic acid (18:2n-6) to arachidonic acid (20:4n-6) and on the cell membrane fatty acid composition. Porcine kidney cells were incubated in medium with or without 10 microgram(s)/mL of triol for 24 h, then incubated for 1, 6, or 12 h in a medium which contained 50 muM of either [14C] linoleic acid or unlabeled linoleic acid. The cellular uptake of [14C] linoleic acid was significantly higher in the triol-treated cells than in control cells. After 1- and 6-h incubations despite the increase of [14C] linoleic acid pool size in the triol-treated cells, neither total n-6 polyunsaturated fatty acids (PUFA) metabolites nor arachidonic acid were increased in the triol-treated cells as compared to the control cells, but trienoic acids accumulated to a greater extent in the triol-treated cells. Therefore, the ratios of n-6 PUFA metabolites vs. pool size of linoleic acid and of tetraenoic acids vs. dienoic acids were significantly decreased in triol-treated cells as compared to the control cells. The cellular fatty acid composition also showed that linoleic acid percentage was significantly increased while arachidonic acid percentage was significantly decreased in the triol-treated cells, and that the accumulation of trienoic acids (18:3n-6 + 20:3n-6) observed from the [14C] linoleic acid experiment was due solely to increased 20:3n-6 content. This latter finding indicates that a decrease of elongase activity by triol is unlikely. Our results also showed that the triol-treated cells had a lower level of free cholesterol but higher levels of phospholipid and triol in their membranes, suggesting that triol displaced free cholesterol from the cell membrane.

Animals↗
PubMedDate not supplied

[Kinetic mechanisms of linoleic acid oxidation by 5-lipoxygenase from Solanum tuberosum L].

Linoleic acid oxidation by 5-lipoxygenase from Solanum tuberosum has been studied as affected by sodium dodecylsulfate (Ds-Na). The reaction system consisted of 5-lipoxygenase and mixed micelles of linoleic acid and Lubrol PX. It contained varying amounts of the enzyme effector--Ds-Na. The enzyme showed a pronounced cooperativity, and the reaction was governed by the Hill equation with h = 3.7. On the other side, increasing amounts of Ds-Na added to the system caused a tremendous increase of enzyme activity and simultaneous decline of h, with was proportional to Ds-Na concentration. Ds-Na had dual effect on 5-lipoxygenase--there was an optimal concentration of the compound (0.34 mM Lubrol PX; 0.2 mM LA; 0.13 mM Ds-Na; pH = 6.3) causing the 4-fold highest activation and h = 1.6. The further increase of Ds-Na led to the enzyme inhibition. If Ds-Na was 0.5 mM, h became 1. At this point, each molecule of 5-lipoxygenase bound 3 molecules of Ds-Na and 1 molecule of linoleic acid, thus the total number of occupied binding sites was 4. A kinetic scheme of 5-lipoxygenase reaction has been proposed. It was found that the enzyme's kinetic behaviour could be explaine if assumed an existence of a special noncatalytic binding centre capable of binding several (up to 3) molecules of either substrate, or effector. Such a centre can serve as an anchoring site facilitating the enzyme binding to the surface of lipid aggregates containing insolubilized substrate molecules. Replacing linoleic acid in the binding site, Ds-Na activates the enzyme, possibly due to the much more effective translocation of 5-lipoxygenase to the surface of lipid aggregates. This mechanism can be an universal alternative to the FLAP-type regulation of 5-lipoxygenase activities.

Arachidonate 5-Lipoxygenase↗
PubMed1989

Dietary intakes and adipose tissue levels of linoleic acid in peptic ulcer disease.

Adipose tissue levels of linoleic acid were determined from biopsies of subcutaneous abdominal fat of normal healthy controls (n 40) and from two patient groups with endoscopically evaluated non-ulcer dyspepsia (n 40) or peptic ulcer disease (n 38). The level (g/100 g) of adipose tissue linoleic acid in the normal healthy controls (15.0 (SD 4.1] was significantly (P less than 0.05) greater than that in patients with non-ulcer dyspepsia (12.8 (SD 3.5] and in patients with peptic ulcer disease (11.7 (SD 2.7]. A dietary history revealed a lower intake of linoleic acid and a significantly (P less than 0.05) lower intake of dietary fibre (g/d) for both the non-ulcer dyspepsia (15.9 (SD 6.2] and peptic ulcer disease (15.2 (SD 7.8] patients compared with normal healthy controls (20.2 (SD 11.2]. Adipose tissue linoleic acid tended to increase with indices of increasing socioeconomic status, although the differences between patient and controls were not confounded by socioeconomic status. Patients with dyspepsia reported more foods causing symptoms (onion, fried foods, alcohol, citrus fruits and spices) and more foods giving relief (milk, bread) compared with control orthopaedic patients.

Adipose Tissue↗
PubMed1999

Antiplatelet effects of conjugated linoleic acid isomers.

Conjugated diene isomers of linoleic acid (CLA) are normal constituents of certain foods and exhibit anticarcinogenic and antiatherogenic properties. In the present study, the effects of several CLA isomers on human platelet aggregation and arachidonic acid metabolism were examined. It was found that 9c,11t-CLA, 10t, 12c-CLA and 13-hydroxy-9c,11t-octadecadienoic acid (13-HODE) inhibited arachidonic acid- and collagen-induced platelet aggregation with I50s in the 5-7 microM range. The nonconjugated 9c, 12c-LA was about 300% and 50%, respectively, less potent an inhibitor with these aggregating agents. Using either thrombin or the calcium ionophore A23187 as aggregating agents, a CLA isomer mix was also found to be more inhibitory than 9c,12c-LA. The 9c,11t- and 10t,12c-CLA isomers as well as the CLA isomer mix inhibited formation of the proaggregatory cyclooxygenase-catalyzed product TXA2, as measured by decreased production of its inactive metabolite [14C]TXB2 from exogenously added [14C]arachidonic acid (I50s=9-16 microM). None of the CLA isomers tested inhibited production of the platelet lipoxygenase metabolite [14C]12-HETE. The additional presence of a hydroxyl group gave opposite results: 13-HODE (I50=3 microM) was about 4-fold more potent a cyclooxygenase inhibitor than the 9c,11t-CLA isomer but 9-HODE was 2- to 3-fold less effective an inhibitor (I50=34 microM) of [14C]TXB2 formation than the corresponding 10t,12c-CLA. In both the aggregation and arachidonic acid metabolism experiments, the inhibitory effects of CLA on platelets were reversible and dependent on the time of addition of either the aggregating agent or the [14C]arachidonic acid substrate. These studies suggest that CLA isomers may also possess antithrombotic properties.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed2001

Linoleic acid induces MCP-1 gene expression in human microvascular endothelial cells through an oxidative mechanism.

Linoleic acid is a dietary fatty acid that appears to play an important role in activation of the vascular endothelium under a variety of pathological conditions, including development of atherosclerosis or cancer metastasis. Evidence indicates that inflammatory responses may be an underlying cause of endothelial cell pathology induced by linoleic acid. However, the profile of inflammatory mediators and the potential mechanisms involved in inflammatory reactions stimulated by the exposure to linoleic acid are not fully understood. The present study focused on the mechanisms of linoleic acid-induced expression of monocyte chemoattractant protein-1 (MCP-1) gene in human microvascular endothelial cells (HMEC-1). Treatment of HMEC-1 with increasing doses of linoleic acid markedly activated an oxidative stress-responsive transcription factor, nuclear factor-kappaB (NF-kappaB). In addition, exposure to linoleic acid induced a time- and concentration-dependent overexpression of the MCP-1 gene. Increased MCP-1 mRNA levels were observed in HMEC-1 treated with linoleic acid at doses as low as 10 &mgr;M. Linoleic acid-induced overexpression of the MCP-1 gene was associated with a significant elevation of MCP-1 protein levels. Most importantly, preexposure of HMEC-1 to antioxidants, such as pyrrolidine dithiocarbamate (PDTC) or N-acetylcysteine (NAC), attenuated linoleic acid-induced MCP-1 mRNA expression. The obtained results indicate that linoleic acid triggers MCP-1 gene expression in human microvascular endothelial cells through oxidative stress/redox-related mechanisms.

Journal Article↗
PubMed1992

Effects of increasing dietary linoleic acid on phospholipid fatty acid composition and eicosanoid production in leucocytes and gill cells of Atlantic salmon (Salmo salar).

Diets containing linoleic acid at 10, 25 and 45% of total dietary fatty acids were fed to three groups of post-smolt Atlantic salmon (Salmo salar) for 18 weeks. Incorporation of linoleic acid into membrane phospholipids of leucocytes and gills increased in response to dietary intake. In general, there was an increase in arachidonic acid and a decrease in eicosapentaenoic acid in the individual phospholipids of both cell types in response to increasing dietary linoleic acid. These changes in eicosanoid precursors were reflected in significantly increased plasma concentrations of 6-keto-PGF1 alpha and TXB2 in salmon given the highest dietary linoleic acid. In whole blood stimulated with the calcium ionophore A23187, LTB4, 12-HETE and TXB2 were significantly increased and 12-HEPE significantly decreased in response to increasing dietary linoleic acid. In isolated gill cells stimulated with A23187, 12-HEPE, 12-HETE, 14-HDHE and TXB2 were all decreased in response to increasing dietary linoleic acid, although the ratio of 12-HEPE/12-HETE was also decreased.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Cardiovascular actions of dihydralazine as modified by dietary linoleic acid.

The experiments were carried out in order to examine whether the hypotensive effect of dihydralazine can be augmented by concomitant ingestion of a diet enriched with linoleic acid. After prefeeding with a linoleic acid rich diet (13.3 J%) an augmented hypotensive dihydralazine effect (11-24 mm Hg) could be observed in acute experiments in conscious (1 mg/kg i.v.) and pentobarbital-anaesthetised (4 mg/kg i.v.) normotensive rats with different duration of the feeding period as well as in conscious (1 mg/kg i.v.) spontaneously hypertensive rats relative to linoleic acid poor (0.5 J%) fed animals. This effect was abolished by pretreatment with the cyclooxygenase inhibitors indomethacin (10 mg/kg i.v.) or acetylsalicylic acid (100 mg/kg i.v.). The chronotropic dihydralazine response was with one exception not different between the two dietary groups. In chronic experiments with spontaneously hypertensive rats the augmentation of the hypotensive dihydralazine effect (1 mg/kg X d, s.c.) after linoleic acid rich diet did not attain statistical significance after a 6-weak prefeeding period. The renovasodilatory action of dihydralazine (3 mg) was increased in isolated kidney preparations of linoleic acid rich fed rats. This effect was accompanied by a shift of the prostaglandin formation toward vasodepressive PGE. We conclude that the altered cardiovascular effects of dihydralazine after linoleic acid rich diet are primarily caused by changes in the formation of prostaglandins and the activity of the sympathetic nervous system.

Animals↗
PubMed2003

Production of free conjugated linoleic acid by Lactobacillus acidophilus and Lactobacillus casei of human intestinal origin.

A gas chromatographic procedure was used for analysis of conjugated linoleic acid (CLA) isomers cis-9, trans-11-octadecadienoic; trans-10, cis-12 octadecadienoic; and trans-9, trans-11-octadecadienoic (c9t11, t10c12, t9t11) produced by lactobacilli. Four different cultures, two strains each of Lactobacillus acidophilus and Lactobacillus casei were tested for their ability to produce CLA from free linoleic acid in MRS broth supplemented with linoleic acid. Different concentrations of linoleic acid (0, 0.05, 0.1, 0.2 and 0.5 mg/ml) were added to MRS broth, inoculated with the lactobacilli, and incubated at 37 degrees C. Viable counts and amounts of individual isomers of CLA (c9t11, t10c12, t9t11) were measured at 0, 24, 48, and 72 h. All the cultures were able to produce free CLA in media supplemented with linoleic acid. Maximum production of CLA (80.14 to 131.63 microg/ml) was observed at 24 h of incubation in broth containing 0.02% of free linoleic acid. No significant (P > 0.05) increases in total CLA levels were observed after 24 h of incubation. The ability of the cultures to produce CLA in skim milk supplemented with 0.02% free linoleic acid also was studied. In this medium, the total amounts of free CLA after 24 h of incubation ranged from 54.31 to 116.53 microg/ml. The use of lactic acid bacteria able to form free CLA in cultured dairy products may have potential health or nutritional benefits. Free CLA in the products likely would be more readily available for absorption from the digestive tract than if it were incorporated into the cells of the starter culture.

Animals↗
PubMed1983

The effect of membrane-bound beta-lactamase on linoleic acid sensitivity in Staphylococcus aureus.

The presence of a plasmid conferring resistance to penicillin (PC plasmid, e.g. pI258blaI-) in Staphylococcus aureus NCTC 8325 increases the sensitivity of such a bacterium to the growth inhibitory effects of linoleic acid, whereas a plasmid conferring resistance to tetracycline does not affect linoleic acid sensitivity. The increased linoleic acid sensitivity of bacteria containing a PC plasmid may be related to the penicillinase protein itself since (i) strains having inducible penicillinase show increased sensitivity only after induction, (ii) strains in which penicillinase is directed from chromosomal or plasmid-borne genes show similar increased linoleic acid sensitivity and (iii) notwithstanding the above, the linoleic acid inhibitory effect is enhanced in a strain in which penicillinase activity is greatly reduced by a point mutation in the structural gene for penicillinase. The enhanced linoleic acid sensitivity seems to require the membrane-bound penicillinase since added extracellular penicillinase does not confer this sensitivity, and there appears to be a specific interaction between the membrane-bound penicillinase activity and linoleic acid.

Cell Membrane↗
PubMed1979

Linoleic acid absorption in the unanesthetized rat: mechanism of transport and influence of luminal factors on absorption.

Linoleic acid intestinal absorption was studied in the unanesthetized rat. At low (21-1260 micrometer) intraluminal concentrations, absorption took place by facilitated diffusion; while at high (1.26-2.5 mM) concentrations, simple diffusion was the predominant mechanism of transport. At low concentrations (840 micrometer), the equimolar additions of oleic, linolenic, and arachidonic acids or lecithin inhibited the absorption of linoleic acid. Substitution of potassium for sodium in the buffer solution, substitution of Tween 80 for sodium taurocholate, or decrease in the hydrogen ion concentration all resulted in decreased rate of linoleic acid absorption. Increase in sodium taurocholate concentration, or perfusate flow rate increased linoleic acid's absorption. These experiments demonstrate that linoleic acid is absorbed by a concentration-dependent dual mechanism of transport. The absorption rate is modified by the pH, surfactant type and concentration, the simultaneous presence of other polyunsaturated fatty acids, and the thickness of the unstirred water layer.

Animals↗
PubMed2001

Different effects of conjugated linoleic acid isomers on lipoprotein lipase activity in 3T3-L1 adipocytes.

Conjugated linoleic acids (CLAs) are the positional and geometric isomers of linoleic acid. In the present study the effects of cis-9, trans-11 CLA (c9,t11 CLA) and trans-10, cis-12 CLA (t10,c12 CLA ) on intracellular and heparin-releasable (HR-) lipoprotein lipase (LPL) activity in 3T3-L1 adipocytes were investigated. Cells were exposed to the two CLA isomers and linoleic acid, which were bound to bovine serum albumin (BSA). In the adipocytes insulin up-regulated and tumor necrosis factor alpha (TNFalpha) down-regulated HR-LPL activity, which corresponds with the findings in vivo. The experimental fatty acids at low concentrations (<30 µmol/L) moderately increased intracellular and HR-LPL activity. At a concentration of 100 µmol/L, c9,t11 CLA and t10,c12 CLA suppressed HR-LPL activity to 20 and 24% below the BSA control level, respectively, while linoleic acid had no effect unless its concentration was as high as 1000 µmol/L. Insulin abolished the inhibitory effect of c9,t11 CLA, but not of t10,c12 CLA. In the presence of insulin, t10,c12 CLA inhibited HR-LPL activity by 41% compared to BSA control. In contrast to TNFalpha, which suppressed both intracellular LPL and HR-LPL activity, CLAs suppressed HR-LPL activity without decreasing intracellular LPL activity. Additionally, t10,c12 CLA (100 µmol/L) partially prevented TNFalpha-induced decrease of intracellular LPL activity. These results indicate that CLAs differ from linoleic acid in regulating HR-LPL activity, and t10,c12 CLA appeared to be more effective than c9,t11 CLA.

Journal Article↗
PubMed1981

Chemical sympathectomy abolishes the increase in blood pressure of linoleic acid deficient fed rats induced by salt loading.

In previous experiments an altered PG biosynthesis as well as an increase in blood pressure, heart rate and plasma epinephrine could be found after a linoleic acid deficient diet compared with a linoleic acid rich diet in rats with a high salt intake. We injected rats with 200 micrograms 6-hydroxydopamine into the right and left cerebral ventricles 17 days before a four-week linoleic acid deficient diet (0.5 J% linoleic acid) and salt loading (1.5% NaCl). In these rats the elevation of blood pressure and plasma epinephrine compared with linoleic acid rich fed rats (13.3 J+ linoleic acid) was abolished and heart rate was reduced. PG biosynthesis in aorta and kidney medulla homogenate (PGE and PGF) and stomach fundus homogenate (6-Keto-PGF1 alpha) was not influenced by chemical sympathectomy, neither were the food and fluid intakes. We conclude that an enhanced adrenergic activity (via alterations in PG metabolism?) is involved in the blood pressure increase after a linoleic acid deficient diet under high salt intake.

Animals↗
PubMed2007

Familial adenomatous polyposis patients have high levels of arachidonic acid and docosahexaenoic acid and low levels of linoleic acid and alpha-linolenic acid in serum phospholipids.

Familial adenomatous polyposis (FAP) provides a model of APC inactivation as an early genetic event for the approximately 85% of colorectal cancers that develop from polyps. Abnormal fatty acid composition of tissues and serum phospholipids has been linked to cancer risk. Our aim was to describe the composition of fatty acids in serum phospholipids in 38 colectomized FAP patients as compared to 160 healthy subjects. Mean fatty acid intakes were similar between the groups. Colectomy was done on average 16 years prior to inclusion, and 18% were diagnosed with colorectal cancer at colectomy. The levels (weight %) of linoleic and alpha-linolenic acid were higher among the reference subjects (difference: 3.96, 95% confidence interval (CI) = 2.87, 5.04, and difference: 0.06, 95% CI = 0.04, 0.08, respectively), and the levels of arachidonic and docosahexaenoic acid were lower (difference: -3.70, 95% CI = -4.35, -3.06, and difference: -5.26, 95% CI = -6.25, -4.28, respectively) as compared to the FAP patients (all p < or = 0.0001). The abnormal fatty acid composition was not related to time since colectomy, intestinal reconstruction or history of colorectal cancer for any of the fatty acids assessed. Compositional differences in the fatty acid profile of serum phospholipids have not been described before in FAP patients. Further studies are needed to confirm these findings and assess clinical significances of a possible distorted fatty acid metabolism, including a potentially different dietary need of essential fatty acids. The relevance of these findings for APC induced cancers remains unclear.

Adenomatous Polyposis Coli↗
PubMed2003

Trans10, cis12-conjugated linoleic acid prevents triacylglycerol accumulation in adipocytes by acting as a PPARgamma modulator.

A group of polyunsaturated fatty acids called conjugated linoleic acids (CLAs) are found in ruminant products, where the most common isomers are cis9, trans11 (c 9,t11) and trans10, cis12 (t10,c12) CLA. A crude mixture of these isomers has been shown in animal studies to alter body composition by a reduction in body fat mass as well as an increase in lean body mass, with the t10,c12 isomer having the most pronounced effect. The objective of this study was to establish the molecular mechanisms by which t10,c12 CLA affects lipid accumulation in adipocytes. We have shown that t10,c12 CLA prevents lipid accumulation in human and mouse adipocytes at concentrations as low as 5 microM and 25 microM, respectively. t10,c12 CLA fails to activate peroxisome proliferator-activated receptor gamma (PPARgamma) but selectively inhibits thiazolidinedione-induced PPARgamma activation in 3T3-L1 adipocytes. Treatment of mature adipocytes with t10,c12 CLA alone or in combination with Darglitazone down-regulates the mRNA expression of PPARgamma as well as its target genes, fatty acid binding protein (aP2) and liver X receptor alpha (LXRalpha). Taken together, our results suggest that the trans10, cis12 CLA isomer prevents lipid accumulation in adipocytes by acting as a PPARgamma modulator.

Adaptor Protein Complex 2↗
PubMed1994

Cytokine production and DNA synthesis by human peripheral lymphocytes in response to palmitic, stearic, oleic, and linoleic acid.

Effects of palmitic, stearic, oleic, and linoleic acid on mitogen-induced DNA synthesis, on production of IL-1 beta, IL-2, IFN-gamma, and TNF-alpha, and on IL-2R expression were determined in human peripheral lymphocytes. Free fatty acids (FFA) were added over a wide range of concentrations to cells cultured under serum free conditions with fatty acid free albumin. DNA synthesis was stimulated by low and inhibited by high FFA concentrations. Physiological concentrations were stimulatory, except for linoleic acid. Cytokine production became affected by all FFA tested. Palmitic acid enhanced the release of IFN-gamma at concentrations that diminished TNF-alpha production. Saturated fatty acids were significantly more potent than unsaturated fatty acids in affecting cytokine production. IFN-gamma secretion was significantly more stimulated or inhibited by the various FFA compared with the other cytokines. IL-2R expression correlated with the production of IL-2. When tested in combination, stimulatory as well as inhibitory effects of the individual FFA became attenuated. It is suggested that palmitic, stearic, oleic, and linoleic acid are physiological regulators of DNA synthesis and cytokine release in human peripheral lymphocytes. Modulation of FFA ratios may be an effective means for the fine tuning of the immune system. As secretory mechanisms of cytokines appear to exhibit substrate specificity for FFA, the release of individual cytokines may be selectively influenced by FFA.

Animals↗
PubMed2001

Effect of dietary lipid source on conjugated linoleic acid concentrations in milk fat.

Conjugated linoleic acids (CLA) found in ruminant milk fat are a byproduct of incomplete biohydrogenation of lipids by ruminal bacteria. We examined the effect of different dietary fat supplements and processing methods on CLA. In trial 1, dietary supplements of Ca salts of fatty acids from canola oil, soybean oil, and linseed oil increased CLA content of milk fat by three- to fivefold over the control diet. Trials 2 and 3 examined the effect of processing methods for heat treatment of full fat soybeans. In trial 2, extrusion, micronizing, and roasting resulted in two- to threefold greater concentrations of CLA in milk fat than the control diet (raw ground soybeans). In trial 3, different temperatures of extrusion (120, 130, and 140 degrees C) increased the CLA content of milk fat to a similar extent; CLA averaged 19.9 mg/g of fatty acids for the extrusion treatments compared with 4.2 mg/g of fatty acids for the control diet (raw ground soybeans). Fish oil (200 and 400 ml/d) was examined in trial 4 and both levels resulted in CLA concentrations in milk fat that were about threefold greater than the control diet. In trial 5, grain and silage from a high oil corn hybrid increased the CLA content of milk fat; however, responses were modest with the CLA concentration (mg/g of fatty acids) averaging 4.6 and 2.8 for diets with high oil hybrid and normal hybrid, respectively. Similarly, dietary supplements of animal fat byproducts (tallow plus yellow grease; trial 6) resulted in modest increases in the CLA content of milk fat. Overall, several dietary manipulations involving lipid sources and processing methods were identified that allow for a marked increase in the conjugated linoleic acid content of milk fat.

Animal Feed↗
PubMed2006

Dual positional and stereospecificity of lipoxygenase isoenzymes from germinating barley (green malt): biotransformation of free and esterified linoleic acid.

The lipoxygenase isoenzymes LOX1 and LOX2 from green malt were separated by isoelectric focusing, and their catalytic properties regarding complex lipids as substrates were characterized. The regio- and stereoisomers of hydroperoxy octadecadienoates (HPODE) resulting from LOX1 and LOX2 enzymatic transformations of linoleic acid, methyl linoleate, linoleic acid glycerol esters monolinolein, dilinolein, and trilinolein, and 1-palmitoyl-2-linoleoyl-glycero-3-phosphocholine (PamLinGroPCho) were determined. In addition, biotransformations of polar and nonpolar lipids extracted from malt were performed with LOX1 and LOX2. The results show that LOX2 catalyzes the oxidation of esterified fatty acids at a higher rate and is more regioselective than LOX1. The dual position specificity of LOX2 (9-HPODE:13-HPODE) with trilinolein as the substrate (6:94) was higher than the resultant ratio (13:87) when free linoleic acid was transformed. A high (S)-enantiomeric excess of 13-HPODE was analyzed with all esterified substrates confirming the formation of 13-HPODE through the LOX2 enzyme; however, 9-HPODE detected after LOX2 biotransformations showed (R)-enantiomeric excesses. PamLinGroPCho was oxygenated by LOX1 with the highest regio- and stereoselectivities among the applied substrates.

Esterification↗