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PubMed1988

Inhibition of cell migrations by the linoleic acid oxygenation product 9S-hydroxy 10E,12Z octadecadienoic acid (9-HODE).

The linoleic acid metabolite 9S-HODE was prepared by means of tomato fruit lipoxygenase and purified by high-performance liquid chromatography (HPLC) to a high steric purity as judged by chiral-phase HPLC. 9S-HODE caused in the concentration range between 0.01 and 1 microM a strong dose-dependent inhibition of the migration of both cultured porcine aortic endothelial cells and of phytohaemagglutinin-stimulated human mononuclear cells. The effect was not observed with another polyenoic fatty acid metabolite, 15S-hydroperoxy-5Z,8Z,11Z,13E-eicosatetraenoic acid (15-HPETE). The results are discussed in the light of other biological actions of 9-HODE recently described.

Animals↗
PubMed2000

Linoleic acid diols are novel substrates for human UDP-glucuronosyltransferases.

Linoleic acid diol glucuronides have been isolated previously from urine of patients suffering from generalized peroxisomal disorders. Glucuronidation of linoleic acid and linoleic acid diols by human liver microsomes was studied to investigate the role of glucuronide conjugation in the metabolism of linoleic acid diols. Glucuronide products were isolated and analyzed by TLC and HPLC-MS. HPLC-MS showed ions with (m/z) corresponding to singly glucuronidated linoleic acid diols while TLC revealed that the glucuronidation was at a hydroxyl position. Kinetic analysis gave apparent K(m) values in the range of 50-200 microM and V(max) rates from 5 to 12 nmol/mg x min. These rates are substantially higher than activities seen for most endogenous hydroxylated substrates. Assays using each of the four individually purified linoleic acid diol enantiomers suggest that glucuronidation occurs at only one of the two hydroxyl groups of each enantiomer. These results show for the first time that hydroxylated fatty acids are actively glucuronidated by human liver microsomes and suggest that glucuronidation may play a significant role in the biotransformation of linoleic acid diols in humans.

Adolescent↗
PubMed1985

Altered levels of n-6/n-3 fatty acids in rat heart and storage fat following variable dietary intake of linoleic acid.

Fat-supplemented dies enriched with linoleic acid by the addition of 12% w/w sunflower seed oil or proportionally reduced in linoleic acid by addition of 12% mutton fat were fed to rats for 18 months before the fatty acid composition of perirenal storage fat and myocardial membranes (phospholipids) was determined. Although the fatty acid composition of perirenal fat generally reflected that of the diet, there was an inverse relationship between the consumption of n-6 and the deposition of n-9 fatty acids. In addition, enhanced deposition of oleic acid (18:1, n-9) appears to be related to the dietary intake of stearic acid (18:0). In contrast, in myocardial membranes the n-3 polyunsaturated fatty acids are found to be increased when the intake of n-6 polyunsaturated fatty acids is reduced. This is particularly evident for docosahexaenoic acid (22:6, n-3) which is significantly increased in phosphatidylcholine, phosphatidylethanolamine, and diphosphatidylglycerol fractions of myocardial membranes, when the mutton fat diet was fed. After feeding the sunflower seed oil diet, the increased consumption of linoleic acid produced only small changes in the 18:2, n-6 content of cardiac phosphatidylcholine and phosphatidylethanolamine. These major classes of membrane phospholipids also showed only small increases in 20:4, n-6. In diphosphatidylglycerol, increased 18:2, n-6 also followed increased dietary intake, but this was not accompanied by increased 20:4, n-6. These changes in myocardial phospholipid fatty acid composition are similar to those observed after short-term feeding reported previously and confirm that changes in dietary n-6/n-3 fatty acid intake affect the fatty acid composition of both myocardial membranes and storage fat. These changes persist for the duration of the feeding period.

Adipose Tissue↗
PubMed1996

Mitogenic stimulation of primary cultures of lung epithelial cells by linoleic acid.

The role of linoleic acid (18:2 n-6) in stimulating proliferation of normal lung epithelial cells in vitro is investigated. When 18:2 n-6 is present with insulin (I) and cholera toxin (CT), growth is stimulated synergistically. In the presence of indomethacin (10 mu M), an inhibition of proliferation is observed in I,CT, and 18:2 n-6, which can be reversed by the addition of exogenous prostaglandin E(2) (PGE(2)). Incorporation of [(14)C]18:2 n-6 with lipid-independent I, CT, and cortisol and lipid-dependent I, CT, and 18:2 n-6 conditions suggests differences in mobilization of 18:2 n-6 from the phospholipid (PL) fractions between 2 and 8 days. The decline of [(14)C]18:2 n-6 in PL fractions with lipid-dependent condition suggests that free 18:2 n-6 may be available for metabolism by the cyclooxygenase pathway. In non-proliferative cultures, an accumulation of the label in the PL fraction is observed. Proliferation in lipid-dependent conditions appears to be due to the mobilization of 18:2 n-6 whereas proliferation in lipid-independent conditions appears to be independently controlled.

Animals↗
PubMed2000

Intestinal absorption and postabsorptive metabolism of linoleic acid in rats with short-term bile duct ligation.

We investigated in bile duct-ligated (BDL) and sham-operated control rats whether the frequent presence of essential fatty acid deficiency in cholestatic liver disease could be related to linoleic acid malabsorption, altered linoleic acid metabolism, or both. In plasma of BDL rats, the triene-to-tetraene ratio, a biochemical marker for essential fatty acid deficiency, was increased compared with controls (0.024 +/- 0.004 vs. 0.013 +/- 0.001; P < 0.05). Net and percentage of dietary linoleic acid absorbed were decreased in BDL rats compared with control rats (1.50 +/- 0.16 mmol/day and 81.3 +/- 3.3% vs. 2.08 +/- 0.07 mmol/day and 99.2 +/- 0.1%, respectively; each P < 0.001). At 24 h after [(13)C]linoleic acid administration, BDL rats had a similar ratio of plasma [(13)C]arachidonic acid to plasma [(13)C]linoleic acid concentration compared with control rats. Delta(6)-Desaturase activity was not significantly different in hepatic microsomes from control or BDL rats. At 3 h after [(13)C]linoleic acid administration, plasma appearance of [(13)C]linoleic acid and cumulative expiration of (13)CO(2) were decreased in BDL rats, compared with controls (by 54% and 80%, respectively). The present data indicate that the impaired linoleic acid status in cholestatic liver disease is mainly due to decreased net absorption and not to quantitative alterations in postabsorptive metabolism.

Animals↗
PubMed1994

Oxidation of furan fatty acids by soybean lipoxygenase-1 in the presence of linoleic acid.

The interaction of furan fatty acids (F-acids) with lipoxygenase was investigated by incubation experiments of a synthetic dialkyl-substituted F-acid with soybean lipoxygenase-1. Originally the oxidation of furan fatty acids was assumed to be directly effected by lipoxygenase. It is now demonstrated that this reaction is a two-step process that requires the presence of lipoxygenase substrates, e.g. linoleic acid. In the first step linoleic acid is converted by the enzyme to the corresponding hydroperoxide. This attacks, probably in a radical reaction, the furan fatty acid to produce a dioxoene compound that can be detected unequivocally by gas chromatography-mass spectrometry.

Fatty Acids↗
PubMed1985

[The effect of linoleic acid intake on its concentration and resultant products in individual plasma lipids in humans].

Dietary linoleic acid enrichment in different plasma lipids was investigated in six healthy females. They were given formula diets (FD) containing no arachidonic acid, and providing a linoleic acid supply of 0% (FD0), 4% (FD4) or 20% (FD20) of total energy intake. At the end of each two weeks FD period fatty acid distribution was determined in cholesterol esters (CE) and in lecithin of LDL and HDL. The increase of linoleic acid in CE was twice that found in the lecithin of LDL and HDL. Comparing FD0 and FD20 the increase of linoleic acid in CE of LDL and HDL was 34%, and in lecithin 15%. Simultaneously oleic acid was lowered in CE (-17%) and in lecithin (-8%) of LDL and HDL. Comparing FD0 and FD20 arachidonic acid, which derives from linoleic acid, was lowered with increased linoleic acid intake in LDL-CE (-5%) and in HDL-lecithin (-8%), while no effect was found in LDL-lecithin. Our results demonstrate that dietary linoleic acid enrichment occurs preferentially in CE of LDL and HDL, but does not lead to an increase of arachidonic acid in plasma lipids. However, a decrease was found for arachidonic acid in HDL-lecithin, while in LDL-lecithin no effect could be observed. From this it is concluded that incorporation and metabolism of linoleic acid in different plasma lipids is not identical, although lipid exchange and lipid transfer have been shown for most lipoprotein fractions.

Adult↗
PubMed2005

Detection of conjugated dienoic fatty acids in human vascular smooth muscle cells treated with conjugated linoleic acid.

Conjugated linoleic acids (CLA) have attracted scientific interest due to their potential beneficial effects on atherosclerosis. Recent studies demonstrated that conjugated metabolites of CLA are found in tissues of CLA-fed animals and cultured cells treated with CLA. This observation has gained in importance since it has recently been shown that these metabolites of CLA exert specific biological activities. Therefore, the present study aimed to explore the potential formation of metabolites of cis-9, trans-11 CLA, trans-10, cis-12 CLA and trans-9, trans-11 CLA in cells of the vascular wall, which has not yet been shown. Examination of fatty acid composition of total cell lipids using Ag+-HPLC, GC-FID and GC-MS analysis revealed a significant isomer-specific formation of conjugated metabolites of CLA such as CD16:2, CD20:2 and CD22:2 in human coronary artery smooth muscle cells treated with various CLA isomers. Different CD16:2/CLA ratios between various CLA isomers as observed in the present study indicate that fatty acid metabolism is differently affected by the configuration of the double bonds. In conclusion, the observation from the present study suggests that the effects of CLA in vascular cells might not only be mediated by CLA itself but also by its conjugated metabolites. Future studies using highly purified conjugated metabolites of CLA are necessary to study their role in mediating biological effects of CLA in cell culture systems.

Animals↗
PubMed1998

Reactivity of soybean lipoxygenase-1 to linoleic acid entrapped in phosphatidylcholine vesicles.

The linoleic acids embedded in the SUVs of soy-PC, DMPC, and DPPC served as substrate for soybean lipoxygenase-1 (L-1). The initial velocity of the catalytic reaction and the concentration of the substrate showed a hyperbolic relation. The Km values of L-1 for the linoleic acids in soy-PC, DMPC, and DPPC vesicles were 0.07, 0.09, and 0.11 mM, respectively, being comparable with that for Tween-20 micellar linoleic acid. Soy-PC and DMPC competitively inhibited the enzyme with Ki values of 0.20 and 0.13 mM, respectively, whereas DPPC had no effect. DSC analysis revealed the phase separation of linoleic acid and DPPC in vesicles in the temperature range in which the enzyme reaction was carried out. This may account for the lack of inhibitory effect of DPPC on the enzyme. From the temperature dependence of the specific activity of the enzyme, the Ea values of the catalytic reaction were estimated to be 26.7 and 35.3 kJ.mol-1 for soy-PC and DPPC vesicles, respectively. For linoleic acid-DMPC vesicles, a two-phase temperature dependence of the activity across the transition temperature of the mixed vesicles was suggested.

Calorimetry, Differential Scanning↗
PubMed1993

Modulation of learning, pain thresholds, and thermoregulation in the rat by preparations of free purified alpha-linolenic and linoleic acids: determination of the optimal omega 3-to-omega 6 ratio.

Ingested polyunsaturated fatty acids are postulated to lead to changes in central nervous system activity, presumably by altering the lipid composition of neuronal membranes. In support of this hypothesis, we and other investigators have previously demonstrated cognitive effects in rats fed oils that contain both alpha-linolenic acid (18:3 omega 3) and linoleic acid (18:2 omega 6), with the relative content of alpha-linolenic acid being seen as the critical variable. The present study in rats examined the effects of preparations containing different ratios of highly purified free alpha-linolenic acid to linoleic acid (about 25 mg/kg of body weight daily) on learning performance (Morris water tank), pain thresholds (heated plate), and thermoregulatory control of d-amphetamine-induced hypothermia during 4 weeks of treatment. Preparations with omega 3-to-omega 6 ratios ranging from 1:3.5 to 1:5 (specifically a ratio of 1:4) produced significant favorable effects on all of these variables. Although the specific mode of action remains to be elucidated, these results suggest that such preparations of free fatty acids should be evaluated in the treatment of memory disorders and pain conditions.

Animals↗
PubMed1998

Linoleic acid induces relaxation and hyperpolarization of the pig coronary artery.

Linoleic acid, a polyunsaturated C18 fatty acid, is one of the major fatty acids in the coronary arterial wall. Although diets rich in linoleic acid reduce blood pressure and prevent coronary artery disease in both humans and animals, very little is known about its mechanism of action. We believed that its beneficial effects might be mediated by changes in vascular tone. We investigated whether linoleic acid induces relaxation of porcine coronary artery rings and the mechanism involved in this process. Linoleic acid and two of its metabolites, 13-hydroxyoctadecadienoic acid (13-HODE) and 13-hydroperoxyoctadecadienoic acid (13-HPODE), induced dose-dependent relaxation of prostaglandin (PG) F2alpha-precontracted rings that was not affected by indomethacin (10[-5] mol/L), a cyclooxygenase inhibitor, or cinnamyl-3,4-dihydroxy-alpha-cyanocinnamate (CDC; 10[-5] mol/L), a lipoxygenase inhibitor. Removal of endothelial cells had no effect on vasorelaxation, suggesting a direct effect on the vascular smooth muscle cells (VSMC). When rings were contracted with KCl, linoleic acid failed to induce relaxation. Although tetrabutylammonium (5 x 10[-3] mol/L), a nonselective K+ channel blocker, slightly inhibited the relaxation caused by linoleic acid, glibenclamide (10[-6] mol/L), an ATP-sensitive K+ channel blocker, and charybdotoxin (7.5x10[-8] mol/L) or tetraethylammonium (5x10[-3] mol/L), two different Ca2+-activated K+ channel blockers, had no effect. However, relaxation was completely blocked by ouabain (5x10[-7] mol/L), a Na+/K+-ATPase inhibitor, or by a K+-free solution. In addition, linoleic acid (10[-6] mol/L) caused sustained hyperpolarization of porcine coronary VSMC (from -49.5+/-2.0 to -60.7+/-4.2 mV), which was also abolished by ouabain. We concluded that linoleic acid induces relaxation and hyperpolarization of porcine coronary VSMC via a mechanism that involves activation of the Na+/K+-ATPase pump.

Animals↗
PubMed1994

Dietary linoleic acid influences desaturation and acylation of deuterium-labeled linoleic and linolenic acids in young adult males.

The purpose of this study was to investigate the effect of dietary linoleic acid (18:2(n - 6)) on the conversion of 18:2(n - 6) and 18:3(n - 3) to their respective n - 6 and n - 3 metabolites; to compare the incorporation of these fatty acids into human plasma lipids; to evaluate the importance of dietary 18:3(n - 3) as a precursor for the biosynthesis of long-chain length n - 3 fatty acids. The approach used was to feed young adult male subjects (n = 7) diets containing 2 levels of linoleic acid (SAT diet, 15 g/day; PUFA diet, 30 g/day) for 12 days. A mixture of triacylglycerols containing deuterated linolenic (18:3(n - 3)) and linoleic (18:2(n - 6)) acids was fed and blood samples were drawn over a 48 h period. Concentrations of deuterated 18:3(n - 3) in plasma total lipid ranged from 309.2 to 606.4 microgram/ml and concentrations of 18:2(n - 6) ranged from 949.2 to 1743.3 micrograms/ml. The sum of the deuterated n - 3 long-chain length fatty acid metabolites in plasma total lipid were 116 +/- 4.3 micrograms/ml (SAT diet) and 41.6 +/- 12.4 micrograms/ml (PUFA diet). The total deuterated n - 6 fatty acid metabolites were 34.6 +/- 12.2 micrograms/ml (SAT diet) and 9.8 +/- 5.9 micrograms/ml (PUFA diet). The total percent conversion of deuterated 18:3(n - 3) to n - 3 fatty acid metabolites and deuterated 18:2(n - 6) to n - 6 fatty acid metabolites were 11-18.5% and 1.0-2.2%, respectively. The percentages for deuterated 20:5(n - 3), 22:5(n - 3) and 22:6(n - 3) (6.0%, 3.5%, and 3.8%) were much higher than for 20:3(n - 6) and 20:4(n - 6) (0.9% and 0.5%). Overall, conversion of deuterated 18:3(n - 3) and 18:2(n - 6) was reduced by 40-54% when dietary intake of 18:2(n - 6) was increased from 15 to 30 g/day. Comparison of the deuterated 18:3(n - 3) and 18:2(n - 6) data for plasma triacylglycerol and phosphatidylcholine (PC) indicated that 18:2(n - 6) was preferentially incorporated into PC. Dietary 18:2(n - 6) intake did not alter acyltransferase selectivity but activity was reduced when 18:2(n - 6) intake was increased. Based on these results, conversion of the 18:3(n - 3) in the US diet (2 g) is estimated to provide 75-85% of the long-chain length n - 3 fatty acids needed to meet daily requirements for some (but not all) adults.

Acylation↗