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PubMed2004

Conjugated linoleic acid prevents the development of essential hypertension in spontaneously hypertensive rats.

Conjugated linoleic acid (CLA) is a mixture of positional and geometric isomers of linoleic acid found in beef, lamb, and dairy products. CLA has attracted considerable attention over the past several decades because of its potentially beneficial biologic effects, including protective effects against several cancers, atherosclerosis, and obesity. In previous studies, we provided evidence that dietary CLA could prevent the development of obesity-related hypertension in obese animals. Here, we show that CLA suppresses the development of non-obese essential hypertension in spontaneously hypertensive rats (SHRs). After 4 weeks of feeding with CLA, the increase of systolic blood pressure was significantly suppressed compared with rats fed linoleic acid. Abdominal adipose tissue weight was also significantly lowered in CLA-fed SHRs. Content of arachidonic acid, the substrate of eicosanoid production, was not changed, but accumulation of oleic acid, the lipogenesis end-product, was markedly decreased in the membrane phospholipids of CLA-fed SHRs. In addition, we found increased level of plasma adiponectin, suggested as a regulatory factor of hypertension, through the enhancement of mRNA expression in CLA-fed SHRs. We speculate that the antihypertensive effect of dietary CLA may be due to the increase of plasma adiponectin level and associated with the alleviation of membrane abnormality in SHRs.

Adiponectin↗
PubMed2004

Effects of paprika pigments on oxidation of linoleic acid stored in the dark or exposed to light.

We examined the antioxidant effects of paprika pigments on oxidation of linoleic acid and on decoloration of the sample when stored at 37 degrees C in the dark or exposed to fluorescent light for 8 h per day. (1)H nuclear magnetic resonance with dioxane as an external proton reference was used to estimate the oxidative deterioration of linoleic acid. Oxidation was estimated by observing the ratio of the divinylmethylene proton signal area in linoleic acid vs the proton signal area in dioxane. The addition of paprika pigments suppressed the oxidation of linoleic acid during storage in the dark, and the effect was markedly increased with increasing concentrations (0.02, 0.2, and 2%). When the linoleic acid with added paprika pigments was exposed to light, only a slight suppression of oxidation was observed, and the color of the sample disappeared more rapidly than that in the dark. At the time of decoloration of the sample with added pigments, considerable oxidation of linoleic acid occurred. As the color change is due to degradation of the pigment, an increase in oxidation at the time of discoloration is consistent with the pigments functioning as antioxidants. The addition of alpha-tocopherol to paprika pigments stabilized degradation of the pigments by light. Although the addition of alpha-tocopherol to linoleic acid with added paprika pigments prolonged the decoloration of the sample under light, the prevention of oxidation under the light condition was not as effective as for the samples stored in the dark.

Antioxidants↗
PubMed1992

Toxic response of linoleic acid anilide in female rats.

The toxicity of linoleic acid anilide (LAA) and heated linoleic acid anilide (HLAA) was studied in female rats. Female Sprague-Dawley rats were given 250 mg/kg of LAA or HLAA in mineral oil, by gavage, on alternate days for two weeks. Control rats received an equal volume of mineral oil. The animals were sacrificed at day 1, 7 and 28 following the last dose. Organ-to-body weight ratio was increased for spleen in both LAA and HLAA treated rats at day 1. Lung, kidney and brain showed increases in this ratio at some time point, whereas, thymus in the HLAA group showed a decrease at day 28. Among blood parameters, red blood cells and hemoglobin content decreased in both LAA and HLAA treated groups at day 1 and in the LAA group at day 7. Serum IgA levels increased throughout the study in both treatment groups and were more pronounced in HLAA treated rats. Splenic T-helper lymphocyte numbers decreased in the HLAA group at day 1, whereas, other cell types were not affected. The changes observed in female rats are comparable to our previous findings in male rats and relatively minor in relation to sex differences. These results further support that hemopoietic system is an early target of fatty acid anilide toxicity.

Anilides↗
PubMed2005

Effects of rhodium heterogeneous catalyst and isomerization conditions on linoleic acid conjugation of soybean oil.

Rhodium heterogeneous catalyst was used to catalyze isomerization of linoleic acid in soybean oil to conjugated linoleic acid (CLA). A central composite rotatable design with five levels of three variables, namely, reaction temperature, stirring speed, and reaction time, was used to determine the maximum CLA yield. The formation of CLA during isomerization was greatly dependent on the reaction temperature and time. The CLA content of soybean oil increased from 0.63 to 202.42 mg/g oil when isomerization was done at 200 degrees C, with a stirring speed of 200 rpm for 49 min. Analysis of triacylglycerol positions showed that linoleic acid at any position in a triacylglyceride could possibly be isomerized to CLA.

Catalysis↗
PubMed1981

Utilization of arachidonic and linoleic acids by cultured human endothelial cells.

When cultured human umbilical vein endothelial cells are supplemented with linoleic acid, the arachidonic acid content of the cellular phospholipids is reduced approximately 35%. Most of the fatty acid compositional change occurs during the first 24 h. One factor responsible for this effect is the inability of the endothelial cells to convert appreciable amounts of linoleic to arachidonic acid, due to a fatty acid delta 6-desaturase deficiency. By contrast, these endothelial cultures contain delta 5- and delta 9-desaturase activity and are able to elongate long-chain polyunsaturated fatty acids. The other factor that contributes to the decrease in arachidonic acid is that high concentrations of linoleic acid reduce the incorporation of arachidonate into cellular phospholipids. Stearic acid, a long-chain saturate, does not produce any reduction, whereas eicosatrienoic acid is an even more effective inhibitor than linoleic acid. In spite of the fact that high concentrations of these polyunsaturates produced inhibition, the endothelial cells were found to efficiently incorporate exogenous arachidonic acid into cellular phospholipids and triglycerides. This may serve to compensate for the inability of these cells to synthesize arachidonic acid from linoleic acid. These findings suggest that the endothelium obtains arachidonic acid from an extracellular source, that this cannot be provided in the form of linoleic acid and, in fact, that high concentrations of linoleic acid actually may interfere with the ability of the endothelium to maintain an adequate supply of intracellular arachidonic acid.

Arachidonic Acid↗
PubMed1990

In vitro linoleic acid activation of protein kinase C.

The importance of membrane fluidity in the activation of protein kinase C (PKC) was examined using the membrane fluidizer, linoleic acid, in a well-defined model membrane system. Biochemical and biophysical properties of the system were monitored. Linoleic acid activated PKC to a level of 50% of that observed for diacylglycerol. In contrast, linoleic acid did not directly interact with the phorbol ester binding site as did diacylglycerol. This was determined by the lack of involvement of the ionizable group of the fatty acid with activity and the enhancement of phorbol ester binding by linoleic acid and its ester analogs. The membrane fluidity of this model membrane system in the presence of linoleic acid was increased as determined by fluorescence polarization. This increased the availability of phospholipids, thus, explaining the linoleic acid-induced enhancement of phorbol ester binding. The PKC conformation as determined from intrinsic tryptophan fluorescence spectra was different for lipid mixtures containing linoleic acid or diacylglycerol correlating with the difference in biochemical activation properties. This study provides evidence that membrane fluidization is not the predominant function of the lipid activator in PKC activation, but may play a role in obtaining the preferred membrane state for maximal activation.

Animals↗
PubMed1994

Feeding conjugated linoleic acid to animals partially overcomes catabolic responses due to endotoxin injection.

The ability of conjugated linoleic acid to prevent endotoxin-induced growth suppression was examined. Mice fed a basal diet or diet with 0.5% fish oil lost twice as much body weight after endotoxin injection than mice fed conjugated linoleic acid. By 72 hours post injection, mice fed conjugated linoleic acid had body weights similar to vehicle injected controls; however, body weights of basal and fish oil fed mice injected with endotoxin were reduced. Conjugated linoleic acid prevented anorexia from endotoxin injection. Splenocyte blastogenesis was increased by conjugated linoleic acid.

Animals↗
PubMed1988

Selective channelling of arachidonic and linoleic acids into glycerolipids of rat hepatocytes in primary culture.

Rat hepatocytes in primary culture were incubated with a mixture of linoleic and arachidonic acid at various total fatty acid/serum albumin molar ratios. Mixed fatty acids were taken up at the same rate and distributed with the same pattern as fatty acids added separately. The rates of total uptake, incorporation into hepatocyte and secreted triacylglycerols and beta-oxidation were linearly related to the fatty acid/albumin ratios, whereas the rate of incorporation into phospholipids was saturable. Neither the uptake rate nor the distribution of both fatty acids considered together varied with the arachidonic acid/linoleic acid molar ratio. Changes in this ratio and in the uptake rate led to significant variations in the respective fate of the fatty acids. The preferential channelling of arachidonic acid versus linoleic acid into beta-oxidation and phosphatidylinositol was greatest at a low uptake rate and then decreased as the uptake rose. Conversely, the preferential channelling of arachidonic acid versus linoleic acid into phosphatidylcholine, but not phosphatidylethanolamine, increased with the uptake rate. Moreover, both arachidonic acid and linoleic acid were preferentially incorporated into the 1-palmitoyl molecular species of phosphatidylcholine and phosphatidylethanolamine at a low uptake rate, and of phosphatidylcholine at a high uptake rate. This could be related to the synthesis of biliary phosphatidylcholine, of which 1-palmitoyl-2-linoleoyl and 1-palmitoyl-2-arachidonoyl are the main molecular species. Linoleic and arachidonic acid were selectively distributed into distinct metabolic pools of triacylglycerol, the intrahepatocyte pool which preferentially incorporated linoleic acid at a low uptake rate and the secreted pool in which the relative enrichment of arachidonic acid increased with the uptake rate. This strengthens the central role of hepatic secretion in the supply of arachidonic acid to peripheral tissues.

Animals↗
PubMed1982

Linoleic acid absorption in children with cystic fibrosis.

When safflower oil (triglyceride) was consumed without pancreatic enzymes by children with cystic fibrosis (CF), there was no rise in mean plasma linoleic acid levels over the next 4 h. When linoleic acid monoglyceride (LAM) was consumed, the increase in plasma linoleic acid levels was significantly greater than for safflower oil at 2 (p less than 0.02), 3 (p less than 0.01), and 4 h (p less than 0.01). When free fatty acid (hydrolyzed safflower oil) was ingested, there was almost no increase in plasma linoleic acid levels in CF or control children. The absorption of linoleic acid from triglyceride, but not from LAM, was greater when the CF children also took pancreatic enzymes. Three children with CF had greater increases in plasma linoleic acid levels following ingestion of safflower oil when they took antacid and cimetidine with their pancreatic capsules, compared to when they only took the pancreatic capsules.

Antacids↗
PubMed1990

Suppressive effects of linoleic acid on neutrophil oxygen metabolism and phagocytosis.

On the basis of recent reports that the proportion of linoleic acid (C18:2Cis 9,12), a free fatty acid, is markedly decreased in acne comedones and that tetracycline is effective against acne comedones by acting directly as an antioxidant on infiltrating neutrophils, we investigated the effect of linoleic acid on several inflammatory parameters of neutrophils, including neutrophil chemotaxis, phagocytosis, and generation of reactive oxygen species (ROS). Linoleic acid significantly decreased phagocytosis and the generation of O2-, H2O2, and OH.by neutrophils, whereas it did not significantly inhibit neutrophil chemotaxis or decrease the ROS levels generated in a cell-free, xanthine-xanthine oxidase system. The present study seems to suggest that decreased levels of linoleic acid in acne comedones contribute, in part, to the worsening of acne inflammation by the failure of low levels of linoleic acid to suppress neutrophil phagocytosis and ROS generation.

Acne Vulgaris↗
PubMed2006

Identification of linoleic acid free radicals and other breakdown products using spin trapping with liquid chromatography-electrospray tandem mass spectrometry.

Linoleic acid radical products formed by radical reaction (Fenton conditions) were trapped using 5,5-dimethyl-1-pyrrolidine-N-oxide (DMPO) and analysed by reversed-phase liquid chromatography coupled to electrospray mass spectrometry (LC-MS). The linoleic acid radical species detected as DMPO spin adducts comprised oxidized linoleic acid and short-chain radical species that resulted from the breakdown of carbon and oxygen centred radicals. Based on the m/z values, the short-chain products were identified as alkyl and carboxylic acid DMPO radical adducts that exhibited different elution times. The ions identified as DMPO radical adducts were studied by liquid chromatography-tandem mass spectrometry (LC-MS/MS). The LC-MS/MS spectra of linoleic acid DMPO radical adducts exhibited the fragment ion at m/z 114 and/or the loss of neutral molecule of 113 Da (DMPO) or 131 Da (DMPO + H2O), indicated to be DMPO adducts. The short-chain products identified allowed inference of the radical oxidation along the linoleic acid chain by abstraction of hydrogen atoms in carbon atoms ranging from C-8 to C-14. Other ions containing the fragment ion at m/z 114 in the LC-MS/MS spectra were attributed to DMPO adducts of unsaturated aldehydes, hydroxy-aldehydes and oxocarboxylic acids. The identification of aldehydic products formed by radical oxidation of linoleic acid peroxidation products, as short-chain product DMPO adducts, is a means of identifying lipid peroxidation products.

Chromatography, Liquid↗
PubMed1994

Pseudo-acylceramide with linoleic acid produces selective recovery of diminished cutaneous barrier function in essential fatty acid-deficient rats and has an inhibitory effect on epidermal hyperplasia.

Pseudo-acylceramides with different acyl properties were investigated for their capacity to restore diminished barrier function in essential fatty acid-deficient rats. Daily topical applications of synthetic pseudo-acylceramides containing ester-linked linoleic acid caused a dose-dependent, significant reduction of transepidermal water loss (TEWL). Both other pseudo-acylceramides with ester-linked oleic acid or saturated alkyl chains and ordinary ceramides exhibited a poor effect on recovery of TEWL. Furthermore, pseudoceramide containing ether-linked linoleic acid, which is biologically inactive in terms of degradation by hydrolytic enzymes, also induced a significant and similar increase in the barrier function. This restoration of barrier function by pseudo-acylceramides with linoleic acid was accompanied by suppressed DNA synthesis in the EFAD rat epidermis. In UVB-irradiated guinea pig skin, topical applications of the pseudo-acylceramides with linoleic acid immediately after the exposure significantly reduced epidermal hyperplasia, secondary to markedly diminished barrier disruption, whereas linoleic acid itself did not. A comparison of both the anti-hyperplasia and the barrier recovery effects in the series of pseudo-ceramide derivatives examined revealed that the suppressive effect on the induced epidermal hyperplasia was paralleled by the recovery of the barrier defect in EFAD rats. These findings directly suggest that acylceramide with an ester-linked linoleic acid has an essential role in the epidermal permeability barrier.

Animals↗
PubMed1983

The effect of aspirin and linoleic acid on platelet aggregation, platelet fatty acid composition and haemostasis in man.

The effect of linoleic acid and of aspirin on platelet aggregation has been measured in six healthy volunteers with a new platelet aggregometer (Wellcome) designed to be used with whole blood. The subjects were given a controlled diet for 6 weeks during which their platelet aggregation, platelet fatty acid composition, dilute blood clot lysis time, bleeding time and serum cholesterol and triglycerides were measured. A basal diet typical of that normally eaten in the UK was fed for 3 weeks, then for a further 2 weeks 60 ml/d of safflower seed oil was added to the diet. Finally there was a further week on the basal diet and on the last day the subjects each took 900 mg of aspirin. The effects of the safflower seed oil was to increase platelet linoleic acid (C18:2 omega 6) content from 5.53 +/- 0.52 micrograms to 10.1 +/- 0.92 micrograms/100 micrograms total fatty acids (P less than 0.001), to decrease platelet aggregation to ADP, and to decreased serum cholesterol. Fibrinolysis and bleeding times were unaltered. Aspirin decreased platelet aggregation, prolonged bleeding time and increased platelet arachidonic acid (C20:4 omega 6) from 24.7 +/- 0.38 micrograms to 25.8 +/- 0.61 micrograms/100 micrograms total fatty acids (P less than 0.01). The Wellcome whole blood aggregometer is a sensitive test of platelet function and using it linoleic acid has been shown to reduce aggregation in conjunction with an increase in polyunsaturated fatty acid content of the platelet membrane.

Adult↗
PubMed2005

The effects of conjugated linoleic acid supplementation on immune function in healthy volunteers.

OBJECTIVE: To assess the effects of dietary supplementation using two isomeric blends of conjugated linoleic acid (CLA) on immune function in healthy human volunteers. DESIGN: Double-blind, randomised, placebo-controlled intervention trial. SUBJECTS AND INTERVENTION: A total of 55 healthy volunteers (n=20 males, n=35 females) were randomised into one of three study groups who received 3 g/day of a fatty acid blend containing a 50:50 cis-9, trans-11: trans-10, cis-12 CLA isomer blend (2 g CLA), and 80:20 cis-9, trans-11: trans-10, cis-12 (80:20) CLA isomer blend (1.76 g CLA) or linoleic acid (control, 2 g linoleic acid) for 8 weeks. RESULTS: Supplementation with the 80:20 CLA isomer blend significantly (P< or =0.05) enhanced PHA-induced lymphocyte proliferation. CLA decreased basal interleukin (IL)-2 secretion (P< or =0.01) and increased PHA-induced IL-2 and tumor necrosis factor alpha (TNF(alpha)) production (P< or =0.01). However, these effects were not solely attributable to CLA as similar results were observed with linoleic acid. CLA supplementation had no significant effect on peripheral blood mononuclear cells IL-4 production, or on serum-soluble intercellular adhesion molecule-1 (sICAM-1) or plasma prostaglandin E2 (PGE2) or leukotreine B4 (LTB4) concentrations. CONCLUSIONS: This study shows that CLA supplementation had a minimal effect on the markers of human immune function. Furthermore, supplementation with CLA had no immunological benefit compared with linoleic acid.

Adult↗
PubMed2002

The effect of conjugated linoleic acid on arachidonic acid metabolism and eicosanoid production in human saphenous vein endothelial cells.

The effects of a conjugated linoleic acid (CLA) mixture of single isomers (50:50, w/w, cis9,trans11:trans10,cis12) and the individual isomers on (a) the production of resting and calcium ionophore stimulated (14)C-eicosanoids and (b) the incorporation of (14)C-arachidonic acid (AA) into membrane phospholipids of human saphenous vein endothelial cells were investigated. The CLA mixture and the individual isomers were found to inhibit resting production of (14)C-prostaglandin F(2a) by 50, 43 and 40%, respectively. A dose dependent inhibition of stimulated (14)C-prostaglandins was observed with the CLA mixture (IC(50) 100 microM). The cis9,trans11 and trans10,cis12 (50 microM) isomers individually inhibited the overall production of stimulated (14)C-prostaglandins (between 35 and 55% and 23 and 42%, respectively). When tested at a high concentration (100 microM), cis9,trans11 was found to inhibit eicosanoid production in contrast to trans10,cis12 that caused stimulation. The overall degree of (14)C-AA incorporation into membrane phospholipids of the CLA (mixture and individual isomers) treated cells was found to be lower than that of control cells and the cis9,trans11 isomer was found to increase the incorporation of (14)C-AA into phosphatidylcholine. Docosahexaenoic acid, eicosapentaenoic acid and linoleic acid did not alter the overall degree of incorporation of (14)C-AA. The results of this study suggest that both isomers inhibit eicosanoid production, and although trans10,cis12 exhibits pro-inflammatory activity at high concentrations, the CLA mixture maintains its beneficial anti-inflammatory action that contributes to its anti-carcinogenic and anti-atherogenic properties.

Arachidonic Acid↗
PubMed2005

Clinical linoleic acid deficiency in Dahl salt-sensitive (SS/Jr) rats.

Male SS/Jr rats were placed on a specially formulated, high-cholesterol, low-sodium diet at 3 weeks of age. Of the 50 animals on the diet, 40 developed skin lesions ranging from focal areas of alopecia to diffuse areas of moist dermatitis on the head, face, ear pinnae, and neck. Similar lesions were noted later in 17 of 36 SS/Jr rats in a second study group. Histopathologic findings from two affected animals revealed diffuse, hyperplastic, ulcerative dermatitis, with bacterial colonies of cocci in superficial crusts, as well as chronic hepatic inflammation with hepatocellular glycogen and sinusoidal macrophage aggregates suggestive of lipidosis. Results of a fatty-acid profile of the affected rats showed serum linoleic acid levels of 931 to 1566 micromol/liter, whereas those for control (SS/Jr) samples ranged from 2711 to 3145 micromol/liter. Dietary analysis of the specially formulated diet showed that it contained only 0.225% linoleic acid, which is below the recommended level of 0.3 to 0.6%. In light of the clinical and dietary findings, a diagnosis of linoleic acid deficiency was made. The food manufacturer revised its dietary formulation to increase the linoleic acid content to 1.05%, and no further cases of dermatitis developed in any subsequent groups of rats maintained under the same study protocol.

Animals↗
PubMed1996

The effect of linoleic acid on pH inside sodium bis(2-ethylhexyl)sulfosuccinate reverse micelles in isooctane and on the enzymic activity of soybean lipoxygenase.

The effective pH of sodium bis(2-ethylhexyl)sulfosuccinate (AOT) reverse micelles (pHrm), containing buffers of different pH (pHst) and various amounts of linoleic acid, was studied within the range of compositions used to study the activity of soybean lipoxygenase in reverse micelles. Significant shifts of pHrm versus pHst were observed for the solutions of relatively higher pHst, dependent on linoleic acid and buffer concentrations. The effect diminished as pHst became closer to 7. When low-ionic-strength buffers were added to AOT solutions in isooctane, a significant buffering effect of linoleic acid in reverse micelles was observed. Solubilization of > 3 mM linoleic acid in micellar solutions containing 25 mM buffers gave the observed pHrm values almost independent of pHst. This effect diminished with the ionic strength of the buffering solution, but did not vanish even at 200 mM buffer. The observed effects result from the balance between ionization of linoleic acid and its partition between the water pool and the micellar interface. The enzymic activity of soybean lipoxygenase in the AOT reverse micellar solutions of the determined pHrm values was also studied. A significant reduction of the kinetics of the enzymic activity was observed, for all studied reverse micellar solutions. Changes of pHrm, caused by the presence of acidic substrate (linoleic acid) do not explain the observed reduction of activity directly through the effect on the enzyme. Due to unfavourable partition of the substrate between the microphases present in the systems, enhanced by reduction of pH at higher total concentrations of linoleic acid, the saturation of the enzyme with the substrate was not observed in the system and is difficult to attain experimentally in reverse micelles. A shift of the lipoxygenase activity/pHrm profile but negligible shift of the activity/pHst profile, with respect to aqueous buffer solutions, were observed. This indicates that either the information given by pH indicators used does not reveal the true pH of the enzyme in these reverse micelles, or that the sample of the enzyme is pH-insensitive over a broader pH range than results from the relationship observed for linoleic acid in aqueous solutions. The latter conclusion is consistent with the data on lipoxygenase activity towards linoleyl sulfate in aqueous solutions [Bild, G. S., Ramadoss, C. S. & Axelrod, B. (1977) Lipids 12, 732-735]. Conditions for measuring pH-independent lipoxygenase activity in reverse micelles are discussed.

Dioctyl Sulfosuccinic Acid↗
PubMed1988

Effect of high/low dietary linoleic acid levels on the function and fatty acid composition of T-lymphocytes of normal and diabetic rats.

T-lymphocytes play a central role in the initiation, regulation and effector functions of immune responses. Changes in membrane composition can alter the membrane fluidity, receptor distribution and consequently function of these cells. Altered immune response in the diabetic state may be attributed partly to diabetes induced alterations in the metabolism of essential fatty acids. We have investigated the effect of dietary linoleic acid on T cell membrane composition and T cell mediated immune responses in normal and diabetic rats. Streptozotocin induced diabetes was found to produce lower T cell proliferative responses in mixed lymphocyte reactions and upon mitogen stimulation. Feeding of a diet rich in linoleic acid did not improve these responses. Feeding a diet low in linoleic acid further lowered the T cell dependent immune responses. We also found lower levels of 18:2 omega 6 fatty acids in the membrane phospholipids of these T cells. Levels of 20:4 omega 6 fatty acids were altered as a result of diabetes and diet composition. These fatty acids are the precursors of prostaglandins which are known to influence immune responses. It is concluded that diabetes results in significant alterations in T cell membrane composition and function in a manner that can be manipulated by modifications of the fatty acid composition of the diet. The present study suggests that diet fat modification may be important in regulating T cell-mediated immunity in insulin dependent diabetes mellitus.

Animals↗