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PubMed2005

Lipid peroxidation of a human hepatoma cell line (HepG2) after incorporation of linoleic acid, arachidonic acid, and docosahexaenoic acid.

Lipid peroxidation of human heptoma cell line, HepG2, after incorporation of linoleic acid (LA), arachidonic acid (AA), and docosahexaenoic acid (DHA) was measured with a fluorescent probe and gas chromatography-mass spectrometry (GC-MS) analysis. The analysis with a fluorescent probe showed that incorporation of each polyunsaturated fatty acid (PUFA) enhanced the cellular lipid peroxidation level, but there was little difference in the effect of LA, AA, or DHA on the enhancement of cellular lipid peroxidation. The fluorescent analysis also showed that the addition of H(2)O(2) (0.5 mM) enhanced the cellular lipid peroxidation levels in LA and AA supplemented cells as compared with those without H(2)O(2). However, the enhancement of lipid peroxidation by H(2)O(2) was not observed in DHA-supplemented cells. The same result was obtained in the GC-MS analysis of total amounts of monohydroperoxides (MHP) formed in the cellular phospholipid oxidation. In this case, the main source for MHP was LA in LA-, AA-, and DHA-supplemented cells. A significant amount of AA-MHP and a small amount of DHA-MHP were observed in AA- and DHA-supplemented cells respectively. GC-MS analysis also indicated the specific positional distribution of DHA-MHP isomers. The isomers were formed only by hydrogen abstraction at the C-18 (16-MHP + 20-MHP; 46.5%), C-6 (4-MHP + 8-MHP; 38.5%), and C-12 (10-MHP + 14-MHP; 15.1%) positions, but not at the C-9 or C-15 positions.

Arachidonic Acid↗
PubMed2000

A role for linoleic acid in erythrocytes infected with Plasmodium berghei.

Unesterified fatty acids were measured in mouse erythrocytes infected either with chloroquine-susceptible (CS) or with chloroquine-resistant (CR) lines of Plasmodium berghei. This work was undertaken to identify candidates for the lipid involved in ferriprotoporphyrin IX (FP) polymerization. Linoleic, oleic, palmitic, and stearic acids were quantified by gas chromatography/mass spectrometry. In total, they increased 4-fold with CS infections and 6-fold with CR infections. Treating infected mice with chloroquine did not affect the amounts of unesterified fatty acids in erythrocytes. Of the four fatty acids, only linoleic acid increased disproportionately to the total. It increased 16-fold for the CS line and 35-fold for the CR line. The method could detect monoglycerides but they were below the limit of detection. It could not detect diglycerides, triglycerides or phospholipids. Triglycerides and phospholipids have been tested previously, however, and found to be ineffective at promoting FP polymerization. Therefore, other than linoleic acid, the lipids most likely to be involved in FP polymerization are diglycerides. We tested dilinoleolyglycerol in the present work and found it to be an effective promoter of FP polymerization. These results suggest that linoleic acid or a diglyceride containing it has the critical role of promoting FP polymerization in malaria parasites.

Animals↗
PubMed1987

[Effects of equal amounts of linoleic acid in orally administered, polyunsaturated phospholipids or in safflower oil on blood lipoproteins].

The effects of polyenylphosphatidylcholine in a dosage of 10 g per day were compared with an equimolar amount of linoleic acid in 7 g safloroil per day in 8 healthy subjects for 3 weeks. The concentrations of cholesterol, triglycerides, phospholipids, apolipoproteins A-I, A-II and B were measured in serum, as well in VLDL, LDL, HDL, HDL2, HDL3 on the day before, after 2 and 3 weeks of application and 6 months after the experiment. The diet was controlled 10 days before and during the experiment using the dietary recall method. According to the dietary records there was an increase of fat supply during application of polyenylphosphatidylcholine inhibiting decrease of LDL cholesterol, which was observed with safloroil. Phospholipid concentrations increased significantly with polyenylphosphatidylcholine in VLDL. Apolipoprotein B in LDL was significantly decreased by both substances. Apolipoprotein A-I and A-II in HDL increased significantly with polyenylphosphatidylcholine. With safloroil this effect was limited to apolipoprotein A-I, but less impressive. The effects of both substances are comparable in the decrease of apolipoprotein B and probably cholesterol. A special effect of polyenylphosphatidylcholine was observed on phospholipids in VLDL and on apolipoprotein A-I and A-II in HDL.

Administration, Oral↗
PubMed1999

[Inhibitory effect of conjugated linoleic acid on human gastric carcinoma cell line].

The effects of conjugated linoleic acid (CLA) on human gastric carcinoma cell line (SGC-7901) were studied in cell culture. The four levels of CLA in medium were designed as 25, 50, 100 and 200 mumol/L, and the dissolvent control being ethane. The result displayed that CLA could inhibit the cell proliferation, cellular mitosis, cell clone formation and DNA synthesis and induce cellular differentiation of SGC-7901 cells.

Adenocarcinoma↗
PubMed1989

Heparin inhibits the "quasi-lipoxygenase" activity of hemoglobin toward linoleic acid by oxidant scavenging.

Previous studies have shown heparin to have antiinflammatory properties. We have attempted to determine if the mechanism involves the inhibition of lipid oxidation by utilizing a model system where linoleic acid is oxidized in the presence of oxygen and methemoglobin. Heparin inhibits this "quasi-lipoxygenase" activity prolonging the lag phase and slowing the rate of lipid peroxidation. An oxidant scavenging mechanism is also inferred from the fact that heparin is capable of inhibiting luminol-dependent chemiluminescence resulting from the reduction of 15-HPETE by methemoglobin. It is concluded that heparin, in at least this model system, is capable of inhibiting lipoxygenation by an oxidant scavenging mechanism.

Heparin↗
PubMed2005

Dietary conjugated linoleic acid increases endurance capacity and fat oxidation in mice during exercise.

Ingestion of CLA activates beta-oxidation and causes loss of body fat in rodents. We investigated the effects of dietary CLA on endurance capacity and energy metabolism during exercise in mice. Five-week-old male BALB/c mice were fed a control diet containing 1.0% linoleic acid or a diet containing 0.5% CLA that replaced an equivalent amount of linoleic acid for 1 wk. The maximum swimming time until fatigue was significantly higher in the CLA-fed group than in the control group. During treadmill running, the respiratory exchange ratio was significantly lower in the CLA-fed group, but oxygen consumption did not differ significantly between groups, suggesting that FA contributed more as an energy substrate in the CLA-fed mice. The muscle lipoprotein lipase activity was significantly higher in the CLA-fed group than in the control group. These results suggest that CLA ingestion increases endurance exercise capacity by promoting fat oxidation during exercise.

Animals↗
PubMed1986

Poison ivy/oak dermatitis. Use of polyamine salts of a linoleic acid dimer for topical prophylaxis.

Closed patch tests were used to evaluate the ability of 156 different preparations (based on 22 different chemicals) to prevent poison ivy dermatitis. Several polyamine salts of a linoleic acid dimer were identified that were totally able to prevent the usual dermatitis in approximately 70% of subjects. The effectiveness of the preparations improved when the antigen and the protectant were washed off within eight to 12 hours, instead of remaining on the skin for 48 hours. When washed off, and depending on the protectant, concentration, and vehicle used, several of the preparations were totally able to prevent a dermatitis in a range of 56% to 100% of subjects tested. Further work with these compounds may greatly benefit the many people currently plagued by their allergy to poison ivy and poison oak.

Adult↗
PubMed1989

Depletion of hepatic coenzyme A derivatives is one of the markers of the toxicity of orally administered secondary autoxidation products of linoleic acid in rat.

When 400 mg/rat/day of secondary autoxidation products of linoleic acid was orally administered 3 times to rats, they died at 30-40 h after the third dose. To search the markers of the toxicity of secondary products in vivo, the rats were killed at 24h after the third dose, and conditions of their digestive tracts and liver were analyzed. In the stomach, macroscopically, inflation, retention of undigested food, and edema were seen. Slight congestions were detected in the small intestines. It was considered that these injuries led to reduction in food consumption and then depression of the growth, but did not lead to the death of the animals. The lipid peroxide levels in the liver and the activities of its detoxifying enzymes were increased as compared to those in the control groups. The hepatic lipid contents and unsaturated fatty acid compositions were also not changed. The endogenous lipid peroxidation, therefore, did not give the rats a severe stress. The activities of hepatic acetyl-CoA carboxylase and carnitine palmitoyltransferase were 20 and 35% lower than those of control, respectively. The levels of CoASH, acetyl-CoA, and long-chain acyl-CoA were 1/9, 1/2, and 1/4 of those in control, respectively. Thus, one of the markers of the toxicity of secondary products was the depletion of hepatic CoA derivatives. In rat, bio-energy was reduced by the decrease in the intestinal absorption of nutrients, and the depletion of hepatic CoA derivatives also failed to supply energy with beta-oxidation.

Animals↗
PubMed2001

Trans-10,cis-12 conjugated linoleic acid reduces triglyceride content while differentially affecting peroxisome proliferator activated receptor gamma2 and aP2 expression in 3T3-L1 preadipocytes.

A series of experiments was conducted using 3T3-L1 preadipocytes as the cell model to determine: (i) whether the triglyceride (TG)-lowering effects of a crude mixture of conjugated linoleic acid (CLA) isomers were due to a specific isomer of CLA and the timing of treatment, (ii) if CLA reduced TG content by inhibiting a key regulator of adipogenesis, (iii) if CLA incorporated into either neutral lipid or phospholipid cell fractions, and (iv) whether the effects of CLA treatment were reversible. Trans-10,cis-12 CLA reduced TG content, whereas the cis-9,trans-11 isomer increased TG content compared to vehicle [bovine serum albumin (BSA)] controls. Treatment with 50 microM trans-10,cis-12 CLA during the entire 6 d of differentiation reduced TG content to a greater extent than treatment during either the first 3 d or last 3 d of differentiation. Trans-10,cis-12 CLA treatment of preadipocyte cultures for 48 h increased peroxisome proliferator activated receptor gamma2 (PPARgamma2) protein expression compared to cultures treated with linoleic acid (LA) or the BSA controls. CLA had no effect on adipose P2 (aP2), a fatty acid-binding protein regulated by PPARgamma2. Both the cis-9,trans-11 and the trans-10,cis-12 isomers of CLA were incorporated into neutral lipids and phospholipids. However, cis-9,trans-11 CLA levels were one- to twofold higher than trans-10,cis-12 CLA levels. Moreover, trans-10,cis-12 CLA treatment reduced cis-11 18:1 concentrations in both neutral lipids and phospholipids while increasing cis-9 18:1 and 18:2 concentrations. Palmitoleic acid (16:1) levels were also lower in the neutral lipid fraction of cultures treated with trans-10,cis-12 CLA. Supplementing trans-10,cis-12 CLA-treated cultures (50 microM) with increasing levels of LA resulted in a dose-dependent increase in TG content compared to cultures treated with 50 microM CLA alone. LA supplementation also prevented some of the morphological changes associated with trans-10,cis-12 CLA treatment as seen with scanning electron microscopy. Treatment with 50 microM trans-10,cis-12 CLA for 6 d decreased PPARgamma2 levels, and supplementation of CLA-treated cultures with LA increased PPARgamma2 levels compared with cultures treated with CLA alone. Taken together, these data indicate that in cultures of 3T3-L1 preadipocytes: (i) trans-10,cis-12 CLA is the TG-lowering isomer of CLA, and its effects are dependent on dose, duration of treatment, and the amount of LA in the cultures; (ii) trans-10,cis-12 CLA treatment alters the monounsaturated fatty acid profile of neutral- and phospholipids of the cultures; and (iii) although acute (2-d) trans-10,cis-12 CLA treatment increased PPARgamma2 protein levels, chronic (6-d) treatment decreased PPARgamma2 levels.

3T3 Cells↗
PubMed1999

Protective effect of flavonoids on endothelial cells against linoleic acid hydroperoxide-induced toxicity.

The protective effect of flavonoids against linoleic acid hydroperoxide (LOOH)-induced cytotoxicity was examined by using cultured endothelial cells. When the cells were incubated with both LOOH and flavonoids, most flavonols protected the cells from injury by LOOH. Flavones bearing an ortho-dihydroxy structure also showed a protective effect against the cytotoxicity of LOOH. However, flavanones had no effect. The structure-activity relationship revealed the presence of either the ortho-di-hydroxy structure in the B ring of the flavonoids or 3-hydroxyl and 4-oxo groups in the C ring to be important for the protective activities. The interaction between flavonoids and a-tocopherol was also examined in this system. Flavonoids that were protective against LOOH-induced cytotoxicity had at least an additive effect on the action of alpha-tocopherol against LOOH-induced damage.

Antioxidants↗
PubMed2003

Effect of separate conjugated linoleic acid isomers on murine mammary tumorigenesis.

Recent studies have linked conjugated linoleic acid (CLA) to altered tumorigenesis of several sites. We showed recently that a mixture of CLA isomers was able to significantly decrease mammary tumor metastasis in mice. That effect was seen with as little as 0.1% CLA in the diet. Other studies with dietary CLA have shown that various isomers may have differential effects. The purpose of this work was to assess which individual CLA isomers had similar effects in alteration of mouse mammary tumor metastasis. For that, we fed six 20% (w/w) total fat diets which contained either no CLA, low (0.1%, w/w) or high (0.25%, w/w) levels of cis9,trans11-CLA (c9,t11), trans10,cis12-CLA (t10,c12) or a mixture of the 2 isomers (0.125% of each, w/w) as free fatty acids. Neither the separate isomers nor the mixture had an effect on the latency or growth of primary line 4526 tumors when compared to the group without CLA. However, all diets containing CLA significantly decreased the total tumor burden (volume of tumor, mm(3)) in lungs of mice from both spontaneous metastasis (reduced by 42-73%) as well as implantation and survival of the metastatic cell (reduced by 46-61%) when compared with diets containing no CLA. Diets containing a greater concentration of either c9,t11 or t10,c12 had a significantly greater effect compared to the lower concentrations of the respective isomers when metastatic nodule size and total tumor burden were assessed. The diet containing both isomers decreased total tumor burden similarly to the diets containing the lower concentration of each of the isomers. Thus, the effects of c9,t11 and t10,c12 may not be additive and possibly share similar mechanisms for decreasing metastatic tumor burden in mice transplanted with mammary tumor cells.

Animals↗
PubMed2004

Dietary conjugated linoleic acid and insulin sensitivity and resistance in rodent models.

Dietary conjugated linoleic acid (CLA) is being investigated for beneficial effects for disease prevention and treatment in a variety of experimental models, including obesity and type 2 diabetes. To date, rodent studies suggest that trans-10,cis-12 (t10,c12) CLA is associated with greater insulin resistance, despite lower body fat, and that a CLA mixture (and perhaps c9,t11) could be beneficial for the management of insulin resistance. Studies investigating the mechanisms by which CLA operates at the cellular level show that the primary targets for CLA are members of the nuclear receptor family, particularly the lipostat transcription factors peroxisome proliferator-activated receptor alpha (PPARalpha), PPARgamma, sterol regulatory element-binding protein 1c, and liver X receptor alpha. Consequently, the effects of CLA on glucose metabolism are likely secondary effects mediated through factors such as PPARgamma coactivator 1 that are controlled by these nuclear receptors. The different responses of normal compared with insulin-resistant obese rodents suggest that interactions of CLA isomers with the cellular components that contribute to development of metabolic syndrome require further investigation.

Animals↗
PubMed2004

[Can linoleic acids in conjugated CLA products reduce overweight problems?].

BACKGROUND: CLA (conjugated linoleic acid) supplements are advertised as a way to reduce weight and to obtain a "better balance between fat and muscle". What evidence is there for these health claims, and is CLA supplementation safe and without adverse effects? MATERIAL AND METHODS: This review is based on peer-reviewed scientific publications. RESULTS: Large doses of CLA supplements in rodents reduce fat mass and increases muscle mass, but the results from 13 randomised, placebo-controlled clinical studies do not support these findings with regard to humans. However, results from both animal and human studies indicate that the CLA isomer 10-trans,12-cis may have a negative impact on carbohydrate and lipid metabolism by inducing insulin resistance and hyperlipidaemia. Studies of CLA supplementation to lactating women have revealed lower fat content in their milk. Furthermore, the cordial blood concentration of CLA in women has been shown to correlate negatively with both gestational length and birth weight. CONCLUSION: Even if reduced weight and fat mass has been observed in animal models following CLA supplementation, the basis is, at best, weak for such claims in humans. Provided that the fat mass reducing effect of CLA is mediated through PPARgamma, this may result in adverse metabolic effects.

Adipose Tissue↗
PubMed2003

Effects of conjugated linoleic acid on growth and cytokine expression in Jurkat T cells.

Conjugated linoleic acid (CLA) has shown beneficial properties in animal models including anti-cancer, anti-atherogenic and anti-diabetic effects, while contrasting immunological effects were reported. While its anti-inflammatory activity has been associated to inhibition of arachidonic acid biosynthesis and to peroxisome proliferator-activated receptors (PPARs) activity, the molecular pathways underlying its immunoenhancing activity are essentially unknown. The aim of our study was to examine whether CLA showed specific effects in vitro on a T cell model, represented by the Jurkat cell line. CLA was found non toxic for Jurkat in the range 50-200 microM, as assessed by LDH release; however, incubation with 50 microM CLA was associated to a significant inhibitory effect on cell proliferation. The analysis of IL-2 and IFN-gamma transcript levels, produced in stimulated Jurkat cells, showed an increased expression of both cytokines in CLA-treated cells. Interestingly, the increased induction of IL-2 but not of IFN-gamma mRNA, could be suppressed by co-incubation with Gö 6976, a protein kinase C (PKC) inhibitor. Co-incubation with superoxide dismutase (SOD) or N-acetyl-L-cysteine (NAC) restored the basal levels of RNA synthesis for both cytokines. Taken together, these results suggest a specific role for dietary CLA in the modulation of the immune response in a T cell line model that is mediated, at least in part, by PKC and through the production of oxidative molecules.

Antioxidants↗
PubMed2004

Conjugated linoleic acid isomer effects in atherosclerosis: growth and regression of lesions.

Conjugated linoleic acid (CLA), a mixture of positional and geometric isomers of octadecadienoic acid, has been shown to inhibit experimentally induced atherosclerosis in rabbits and also to cause significant regression of pre-established atheromatous lesions in rabbits. The two major CLA isomers (cis9,trans11 and trans10,cis12), now available at 90% purity, have been tested individually for their anti-atherogenic or lesion regression potency. The two major isomers and the mixture were fed for 90 d to rabbits fed 0.2% cholesterol. Atherosclerosis was inhibited significantly by all three preparations. The two CLA isomers and the isomer mix were also fed (1.0%) as part of a cholesterol-free diet for 90 d to rabbits bearing atheromatous lesions produced by feeding an atherogenic diet. A fourth group was maintained on a cholesterol-free diet. On the CLA-free diet atherosclerosis was exacerbated by 35%. Reduction of severity of atheromatous lesions was observed to the same extent in all three CLA-fed groups. The average reduction of severity in the three CLA-fed groups was 26 +/- 2% compared with the first control (atherogenic diet) and 46 +/- 1% compared with the regression diet. Insofar as individual effects on atherosclerosis were concerned, there was no difference between the CLA mix and the cis9,trans11 and trans10,cis12 isomers. They inhibit atherogenesis by 50% when fed as a component of a semipurified diet containing 0.2% cholesterol; and when fed as part of a cholesterol-free diet, they reduce established lesions by 26%. Reduction of atheromata to the observed extent by dietary means alone is noteworthy.

Animals↗
PubMed2002

Adipose depletion and apoptosis induced by trans-10, cis-12 conjugated linoleic Acid in mice.

OBJECTIVE: To compare the effectiveness of a conjugated linoleic acid (CLA) isomer mixture (mCLA) with each main isomer [trans-10,cis-12 CLA (CLA10,12) and cis-9,trans-11 CLA (CLA9,11)] in causing body lipid loss and adipose tissue apoptosis. RESEARCH METHODS AND PROCEDURES: Mice selected over 16 generations for high (MH) or low (ML) energy expenditure and a control group (MC) were fed diets containing either soy oil or soy oil plus mCLA, CLA10,12, or CLA9,11 for 5 days in one study and 14 days in a second study. RESULTS: Mice fed mCLA or CLA10,12 had less body lipid (p < 0.05), smaller retroperitoneal fat pads (p < 0.05), and ate less (p < 0.01) than mice fed no CLA or CLA9,11 for 5 days. Mice consuming 1% mCLA or 0.5% CLA10,12 gained less weight (p < 0.01) and had less body lipid (p < 0.05) and smaller epididymal (p < 0.05) and retroperitoneal fat pads (p < 0.01) than mice consuming either control or 0.5% CLA9,11-containing diets for 14 days. Only mCLA and CLA10,12 increased apoptosis in retroperitoneal fat pads (p < 0.01). The effects of mCLA and CLA10,12 were independent of genetic line except for the effect on adipocyte apoptosis. Mice of the MH line were slightly less sensitive than MC or ML mice to CLA-induced adipose tissue apoptosis. DISCUSSION: CLA10,12, but not CLA9,11, can induce both body fat loss and adipose apoptosis. Although mice of a genotype with less body fat and greater metabolic rate and feed intake appear less sensitive, these CLA effects are robust for mice of varying metabolic background.

Adipocytes↗