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PubMed1988

Regulation of the metabolism of linoleic acid to arachidonic acid in rat hepatocytes.

When 5 X 10(6) hepatocytes were incubated for 40 min with from 0.15 to 0.60 mM [1-14C]linoleic acid, [1-14C]6,9,12-octadecatrienoic acid, or [1-14C]8,11,14-eicosatrienoic acid, there was a concentration-dependent acylation of radioactive metabolites into both triglycerides and phospholipids. When the concentration of either [1-14C]linoleic acid or [1-14C]8,11,14-eicosatrienoic acid exceeded 0.3 mM, there was no further increase in the metabolism of either fatty acid to other (n-6) metabolites. When the concentration of [1-14C]6,9,12-octadecatrienoic acid exceeded 0.15 mM, there was an apparent substrate-induced inhibition in its metabolism to 8,11,14-eicosatrienoic acid. With all three substrates (0.3 mM), there was time-dependent metabolism to other (n-6) acids. Cells then were incubated simultaneously with 0.3 mM [1-14C]linoleic acid along with 0.15 to 0.45 mM 6,9,12-octadecatrienoic acid or 8,11,14-eicosatrienoic acid. These exogenous nonradioactive (n-6) acids suppressed but did not abolish the conversion of [1-14C]linoleate to radioactive arachidonate. These findings suggest that some linoleate is converted to arachidonate without intracellular mixing of 6,8,12-octadecatrienoic or 8,11,14-eicosatrienoic acids. This hypothesis is supported by the finding that exogenous linoleate did not markedly affect the metabolism of [1-14C]6,9,12-octadecatrienoic or [1-14C]8,11,14-eicosatrienoic acid by microsomal chain elongating or desaturating enzymes.

Animals↗
PubMed1981

The effect of a virtually cholesterol-free, high-linoleic-acid vegetarian diet on serum lipoproteins of children with familial hypercholesterolemia (type II-A).

The effect of a virtually cholesterol-free, high-linoleic-acid vegetarian diet and a high-linoleic-acid "normal" diet with a moderate cholesterol content was tested in 39 children heterozygote for hypercholesterolemia type II-A. The diets were administered in an outpatient cross-over design of two periods of 10 weeks each and the serum lipoproteins were analyzed at the end of the two 10-week periods. The vegetarian diet induced a decrease in serum concentrations of LDL-II total and free cholesterol and of apo-B, by an average of 10%, whereas HDL cholesterol and apo-A-I decreased by 4%. The disproportionately large change in LDL compared to the small change in HDL was interpreted as an antiatherogenic effect of the vegetarian diet.

Adolescent↗
PubMed1985

Metabolic profile of linoleic acid in porcine leukocytes through the lipoxygenase pathway.

Porcine neutrophilic leukocytes were found to contain a lipoxygenase which converted linoleic acid into 13-hydroxy-9,11-octadecadienoic acid (n-6 specificity), arachidonic acid into 12-hydroxy-5,8,10,14-eicosatetraenoic acid (n - 9 specificity) and 5-hydroxy-6,8,11,14-eicosatetraenoic acid into 5,12-dihydroxy-6,8,10,14-eicosatetraenoic acid. This lipoxygenase was partially purified and it appeared that its substrate specificity and other properties were quite different from the 12-lipoxygenase of blood platelets. Incubations of intact or broken porcine leukocytes with added linoleic acid revealed the formation of not only 13-hydroxy-9,11-octadecadienoic acid but also of substantial amounts of epoxyhydroxy and trihydroxy isomers. These products from linoleate, collectively described by the name 'octadecanoids' were characterized in detail by a combination of chemical, chromatographic and mass spectrometric techniques. The phospholipids of porcine leukocytes contain more than twice as much linoleate than arachidonate (22 vs. 8%). In accordance with this fatty acid composition we found that in the stimulated neutrophil the endogenous production of octadecanoids often surpassed that of the eicosanoids. Lipoxygenation of endogenously liberated linoleic acid was especially pronounced when a suspension of leukocytes in citrated plasma was recalcified and allowed to clot.

Animals↗
PubMed1988

The effects of orally administered linoleic acid and its autoxidation products on intestinal mucosa in rat.

Linoleic acid and its autoxidation products, hydroperoxides and their secondary products, were orally administered to rats (350 mg each/rat). Hemorrhage was seen in the alimentary canal at 6 h after the dose of hydroperoxides. To examine their toxicities on intestinal mucosa, the activities of mucous enzymes (sucrase, maltase, and alkaline phosphatase) were measured. Hydroperoxides and their secondary products decreased the enzyme activities in jejunum at 6 h after the doses and increased them in both jejunum and ileum at 15 h, as compared to linoleic acid or saline solution. The decrease of enzyme activity was marked in the hydroperoxide group and the increase was marked in the secondary product group. Then, in in vitro experiments, the effects of autoxidation products on these enzymes were determined. Autoxidation products inactivated only alkaline phosphatase. Thus, the results in vivo disagreed with those in vitro. It was assumed that autoxidation products orally administered attacked a membrane of intestinal microvilli whereas in vitro they directly affected the enzymes.

Administration, Oral↗
PubMed1990

Stereochemical nature of the products of linoleic acid oxidation catalyzed by lipoxygenases from potato and soybean.

When linoleic acid was incubated with the purified potato lipoxygenase under O2 atmosphere, a mixture of 9 and 13-hydroperoxyoctadecadienoic acids was formed. Stereochemical analysis of the respective methyl-hydroxyoctadecadienoic acids revealed that the 9-isomer was in S-configuration whereas 13-hydroxyoctadecadienoic acid was a mixture of S (39%) and R (61%). Exactly the opposite was the case with the soybean lipoxygenase products, where the 13-isomer was found to be in S-configuration and 9-hydroxyoctadecadienoic acid - a mixture of S (73%) and R (27%). A general scheme is proposed for the stereochemical nature of oxidation products of enzymes which are predominantly either [+2] or [-2] lipoxygenases.

Chromatography, High Pressure Liquid↗
PubMedDate not supplied

Conjugated linoleic acids: all the same or to everyone its own function?

Conjugated linoleic acid (CLA) is a generic term referring to a mixture of geometrical and positional isomers of linoleic acid in which up to 16 members have been identified. Many potentially beneficial health effects have been ascribed to these fatty acids when consumed as a mixture, and where generally 2 isomers dominate, e.g. the 9c, 11t-isomer, the so-called rumenic acid, and the 10t, 12c-isomer: anti-carcinogenic, immune modulator, anti-atherosclerotic, and anti-obesity among the most spectacular. The question arises as to whether the pleiotropic biological activity is supported by one or several of the isomers. Recent studies using pure individual isomers have started to elucidate this issue, but many others are required to ascribe a respective role to each CLA isomer (the main ones as well as the minor ones), such as those occurring in some complex mixtures already commercially available, or even in foodstuff. The aim of the present study was to focus on the CLA-isomer specific effects depicted in the literature up to now.

Animals↗
PubMed2003

Effects of lipid-esterified conjugated linoleic acid isomers on platelet function: evidence for stimulation of platelet phospholipase activity.

The effects of four conjugated linoleic acid (CLA) isomers on in vitro collagen-induced human platelet aggregation and thromboxane (TXB(2), the inactive metabolite of the proaggregatory TXA(2)) production were examined. As the free fatty acid (FFA), 9t, 11t-CLA was the most effective inhibitor of these two processes (I(50)s of 2.2 and 4 microM, respectively) and the 9c, 11c-CLA was the least effective (I(50)s of 8.3 and 37 microM) of the isomers tested. When platelets were preesterified with either 25 microM 9t, 11t-CLA or 9c, 11c-CLA, CLA incorporation in total platelet lipids increased from 0.24% to 0.31% and 0.38%, and most of this increase was found to be in the phosphatidyl choline and phosphatidyl ethanolamine subclasses. The decrease in arachidonic acid (AA) content in total fatty acids or phospholipids was an order of magnitude greater. Furthermore, no significant differences between platelets prelabeled with either 9t, 11t- or 9c, 11c-CLA in the inhibition of collagen-induced aggregation and TXB(2) formation were observed. However, platelets prelabeled with 9c, 11c-CLA stimulated basal TXB(2) production (4-fold) which was not observed with platelets pretreated with either 9t, 11t-CLA, linoleic acid or stearic acid. This enhancement was associated with a 2.4-5-fold increase in the release of endogenous AA. Our results suggest that the presence of a conjugated cis, cis double bond appears to change the lipid environment sufficiently to stimulate the basal platelet phospholipase activity, which in turn increases the formation of TXB(2).

Arachidonic Acid↗
PubMed1993

Enhancement of aortic cholesterol deposition by dietary linoleic acid in cholesterol-fed mice: an animal model for primary screening of antiatherosclerotic agents.

We tried to develop an experimental model using mice for the primary screening of antiatherosclerotic agents. Male ICR strain mice were given a high-cholesterol diet supplemented with 10% linoleic acid for 14 weeks. Throughout the experimental period, weight gain of these mice was significantly inhibited as compared to that of control mice given a basal diet, but displayed a steady increase comparable to that of the high-cholesterol diet without linoleic acid. The cholesterol and linoleic acid-fed mice showed increased serum cholesterol and phospholipid levels, and decreased serum triglyceride and high-density lipoprotein-(HDL) cholesterol levels and lecithin/cholesterol acyltransferase (LCAT) activity, as well as a markedly increased lipid peroxide level which was a characteristic appearance in the serum of this mouse model. At the end of the experiment, uniform and significant increases in cholesterol, notably cholesteryl ester, were observed in the aorta. Also found were marked decreases in the aorta contents of desmosine and isodesmosine, which are cross-linking amino acids present only in the elastin. Histological observations showed accumulations of fatty droplets in the intima. These changes were much less in mice receiving a high-cholesterol diet without linoleic acid. In this mouse model, probucol prevented elevation of serum cholesterol, phospholipid, and cholesterol accumulation in the aorta. Increases in lipid peroxide level and decreases in LCAT activity were also prevented. These findings indicate that this mouse model is useful for primary screening of antiatherosclerotic agents with antioxidative activity.

Animals↗
PubMed1999

Effects of linoleic acid metabolites on electrical activity in adult rat ventricular myocytes.

Leukotoxin (Lx), an epoxide derivative of linoleic acid, has been suggested to be a toxic mediator of multiple organ failure in burn patients and of acute respiratory distress syndrome. Lx production was recently shown during myocardial ischemia/reperfusion. However, a recent study suggested that to be toxic Lx must be metabolized to Lx-diol. In the present study, isolated adult rat ventricular myocytes were studied with the whole-cell patch-clamp technique to determine the effects of these compounds on cardiac electrical activity. Measurements of action potentials showed that neither linoleic acid nor Lx (100 microM) caused any significant changes in action potential properties. However, Lx-diol in the range of 10-100 microM produced a dose dependent increase in duration and a decrease in overshoot of the action potential. Subsequent voltage clamp experiments isolating Na current (INa) and transient outward K current (Ito) revealed that Lx-diol inhibited INa and Ito by about 80% at 100 microM, while linoleic acid and Lx had no effect on these currents at the same concentration. While Lx-diol produced the same inhibition of INa and Ito at 100 microM, its effects were more potent on Ito with significant inhibition at 10 microM. Lx-diol also hastened the activation kinetics of Ito but not INa. The action of Lx-diol was rapid (reaching steady state in 3-5 min) and was reversible in 5-10 min following washout. Thus, Lx-diol could favor arrhythmias or cardiac arrest in intact heart and may be responsible for the cardiac problems seen in systemic inflammatory response syndrome. These results further support the suggestion that Lx is not toxic in the heart but rather must be metabolized to Lx-diol to produce toxic effects on cardiac muscle.

Action Potentials↗
PubMed1999

Effects of conjugated linoleic acid (CLA) isomers on lipid levels and peroxisome proliferation in the hamster.

Effects of the conjugated linoleic acid (CLA) isomers cis-9, trans-11 (c9,t11 CLA) and trans-10, cis-12 (t10,c12 CLA) on lipid metabolism and markers of peroxisome proliferation were investigated in hamsters fed on purified diets containing 30% energy as fat and 0.1 g cholesterol/kg for 8 weeks. Four groups (n 32 each) received diets without CLA (control), with a mixture of equal amounts of c9,t11 and t10,c12 CLA (CLA mix), with c9,t11 CLA, and with t10,c12 CLA. The total amount of CLA isomers was 1.5% energy of 6.6g/ kg diet. CLA was incorporated into glycerides and exchanged for linoleic acid in the diet. Compared with the control, the CLA mix and t10,c12 CLA decreased fasting values of LDL- (21 and 18% respectively) and HDL-cholesterol (8 and 11%), increased VLDL-triacylglycerol (80 and 61%, and decreased epididymal fat pad weights (9 and 16%), whereas c9,t11 CLA had no significant effects. All CLA preparations increased liver weight, but not liver lipids. However, the increase in liver weight was much less in the c9,t11 CLA group (8%) than in the other two groups (25%) and might have been caused by the small amount of t10,c12 CLA present in the c9,t11 CLA preparation. Liver histology revealed that increased weight was due to hypertrophy. Markers of peroxisome proliferation, such as cyanide-insensitive palmitoyl CoA oxidase (EC 1.3.3.6) and carnitine acetyl transferase (EC 2.3.1.7) activities, were not increased by CLA. Both c9,t11 CLA and t10,c12 CLA were incorporated into phospholipids and triacylglycerols, but t10,c12 CLA only about half as much as c9,t11 CLA. In addition, linoleic acid and linolenic acid concentrations were lower in lipids of the t10,c12 CLA group compared with the c9,t11 CLA group. These data suggest that t10,c12 CLA stimulated the oxidation of all C18 polyunsaturated fatty acids. The results indicate that the t10,c12 CLA isomer, and not the so-called natural CLA isomer (c9,t11), is the active isomer affecting lipid levels in hamsters.

Adipose Tissue↗
PubMed1994

4-hydroxy-2-nonenal levels increase in the plasma of patients with adult respiratory distress syndrome as linoleic acid appears to fall.

Gas chromatograph-mass spectrometry has been applied to the analysis of plasma linoleic acid and one of its oxidation products, 4-hydroxy-2-nonenal (HNE), in adult patients with the acute respiratory distress syndrome (ARDS). Peak areas of total ion chromatograms showed there to be negative correlations between loss of linoleic acid and formation of HNE (measured by selective ion monitoring) in 7 out 10 patients studied. When HNE was quantitated by selective ion monitoring, with reference to a pure standard of HNE and an internal standard of nonanoic acid, ARDS patients showed significantly increased levels of HNE (0.412 +/- 0.023 nmol/ml) compared with normal healthy controls (0.205 +/- 0.018 nmol/ml).

Adult↗
PubMed2006

Conjugated linolenic acid is slowly absorbed in rat intestine, but quickly converted to conjugated linoleic acid.

We showed previously that alpha-eleostearic acid (alpha-ESA; 9Z11E13E-18:3) is converted to 9Z11E-conjugated linoleic acid (CLA) in rats through a Delta13-saturation reaction. To investigate this further, we examined the absorption and metabolism of alpha-ESA in rat intestine using a lipid absorption assay in lymph from the thoracic duct. In this study, we used 4 test oils [tung oil, perilla oil, CLA-triacylglycerol (TG), and pomegranate seed oil, containing alpha-ESA, alpha-linolenic acid (LnA; 9Z12Z15Z-18:3), CLA, and punicic acid (PA; 9Z11E13Z-18:3), respectively]. Emulsions containing the test oils were administered to rats, and lymph from the thoracic duct was collected over 24 h. The positional and geometrical isomerism of CLA produced by PA metabolism was determined using GC-electron impact (EI)-MS and (13)C-NMR, respectively; the product was confirmed to be 9Z11E-CLA. A part of alpha-ESA and PA was converted to 9Z11E-CLA 1 h after administration; therefore the lymphatic recoveries of alpha-ESA and PA were modified by the amount of recovered CLA. Cumulative recovery of CLA, alpha-ESA, and PA was lower than that of LnA only during h 1 (P < 0.05), and cumulative recovery of alpha-ESA and PA was significantly lower than that of LnA and CLA for 8 h (P < 0.05). Therefore, the absorption rate was LnA > CLA > alpha-ESA = PA. The conversion ratio of alpha-ESA to 9Z11E-CLA was higher than that of PA to 9Z11E-CLA over 24 h (P < 0.05). These results indicated that alpha-ESA and PA are slowly absorbed in rat intestine, and a portion of these fatty acids is quickly converted to 9Z11E-CLA.

Animals↗
PubMed1988

Effect of dietary linoleic acid and essential fatty acid deficiency on resting metabolism, nonshivering thermogenesis and brown adipose tissue in the rat.

Rats were fed a diet either deficient (0.05%) in essential fatty acids (EFA), or providing 4% (control) and 10% (surplus) of the total energy intake in the form of linoleic acid. All diets were isoenergetic and provided 13.9% of the energy as fat. The rats were kept at 29 or 5 degrees C. Growth and food intake of rats fed linoleic acid surplus at either temperature for 10 wk were not different from that of controls; basal metabolism, norepinephrine-induced nonshivering thermogenesis (NST) and thermogenic variables in the brown adipose tissue (amount of mitochondria and mitochondrial uncoupling protein) also were not different. The effects of EFA deficiency were drastically enhanced in the cold: After 10 wk of consuming a diet low in EFA at 5 degrees C, the body weight of rats was 75% of that of controls (87% at 29 degrees C); the food intake was 135% of controls at 5 degrees C (120% at 29 degrees C). The resting respiration in deficient rats was 125% of controls at 5 degrees C (110% at 29 degrees C); body temperatures as low as 35.1 degrees C were measured in deficient rats after 3 wk at 5 degrees C; the cold tolerance of the rats was significantly diminished (30% died within 3 wk at 5 degrees C), thus emphasizing the essential role of dietary EFA during cold stress. Norepinephrine-induced NST and the thermogenic parameters in brown fat were not influenced by EFA deficiency.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue, Brown↗
PubMed2005

Enhancing alpha-tocopherol and linoleic acid in ewe's milk by feeding emulsified sunflower oil and DL-alpha-tocopheryl acetate in a chemically treated protein matrix.

Chemically treated dietary supplements (CTDS) were prepared with defatted soy flour, sunflower oil, dl-alpha-tocopheryl acetate (TA), and 2,3-butanedione (a generally recognized as safe chemical), and the effects on alpha-tocopherol (VE) concentration and fatty acid profile in ewe's milk were estimated. Ewes fed control diet (CD) had the lowest levels of milk VE (0.66 microg/mL) and serum VE (1.59 microg/mL). Feeding ewes the CD plus 500 IU of TA increased milk and serum VE by 30 and 70%, respectively, compared to ewes fed the CD. The CTDS-fed ewes showed further increased milk and serum VE levels by 40 and 32%, respectively, over those in ewes fed the CD plus 500 IU of TA. Feeding ewes CTDS did not affect milk fat content (3.13%) but altered the fatty acid composition by decreasing the levels of hypercholesteremic fatty acids, while increasing the content of linoleic acid (8.5%). Inclusion of CTDS in ruminant diets might produce nutritionally enhanced milk products.

Animals↗
PubMed1993

Influence of linoleic acid on desaturation and uptake of deuterium-labeled palmitic and stearic acids in humans.

Objectives of this study were to investigate the desaturation of stearic acid (18:0) and palmitic acid (16:0), to determine if differences in their metabolism provide a reasonable explantation for differences in their effect on serum cholesterol levels, and to investigate the affect of linoleic acid on delta 9-desaturase products in man. Deuterium-labeled 16:0 and 18:0 were used to follow the metabolism of these fatty acids in young adult male subjects that were pre-fed diets containing two different levels of linoleic acid. Results indicate that absorption of 16:0 and 18:0 was similar when all components of the mixture used to formulate the deuterated fat mixture were kept above the melting point of tristearin. The percent of 18:0 desaturated to 9c-18:1 was higher than the percent of 16:0 desaturated to 9c-16:1 (9.2% vs. 3.9%). The subject-to-subject variability suggests that differences in ability to desaturate saturated fatty acids may be related to the variability observed in response of serum cholesterol levels to dietary saturated fatty acids. Data for the distribution of 16:0 and 18:0 between triacylglycerol and phosphatidylcholine (PC) was markedly different. Based on PC data, phospholipid acyltransferase selectivity was about 2-fold higher for 18:0 than for 16:0. A 2-fold difference in the linoleic acid content of the pre-fed diets had little influence on desaturation or distribution of 16:0 and 18:0 between plasma lipid classes. A deuterium isotope effect was estimated to reduce delta 9-desaturase enzyme activity by 30-50%.

Adult↗
PubMed1994

Linoleic acid hydroperoxide-induced peroxidation of endothelial cell phospholipids and cytotoxicity.

Peroxidation of endothelial cell phospholipids was examined following treatments with linoleic acid hydroperoxide. The treatment effects were analyzed over a range of toxicities and exposure intervals as determined by cell plating efficiencies and survival. Over the concentration ranges where lipid peroxidation was evident (20-40 microM treatments in complete medium), significant cytotoxicity was apparent after 1 h of exposure. The extent of toxicity was dependent on the time interval between the end of peroxide treatment and replating of cells. Maximum toxicity was found when cells were replated 1-3 h after treatment. When cells were replated 4 h after treatment a linear increase in cell survival was found as a function of replating time following peroxide exposure. Analysis of cell phospholipids by HPLC after 1 h of exposure to linoleic acid hydroperoxide revealed that peroxidation (evidenced by conjugated diene content) had taken place among a number of phospholipid species with the most marked increases in phosphatidylcholine. Analysis of the fatty acyl composition of phospholipids also showed that the proportions of polyunsaturated fatty acids were reduced relative to saturated fatty acids, indicating peroxidative damage to phospholipids. Pretreatment of cells with vitamin E prevented the peroxidation of all phospholipids and blocked the cytotoxic action of linoleic acid hydroperoxide. These findings indicate that an immediate cytotoxic action of lipid hydroperoxide is associated with peroxidation of membrane phospholipids. This cytotoxicity is a transient effect, and cells surviving the acute injury display a time-dependent increase in plating efficiency representing a period of repair.

Animals↗
PubMed2001

Effects of conjugated linoleic acid on the belly firmness and fatty acid composition of genetically lean pigs.

A study of the effects of conjugated linoleic acid (CLA) on the belly firmness and fatty acid composition of genetically lean pigs was conducted. From 75 to 120 kg live weight, 30 gilts were allowed ad libitum access to a corn-soybean meal diet supplemented with either 1% CLA oil (CLA-60) or 1% sunflower oil (SFO) or were fed the sunflower oil-supplemented diet restricted to the amount consumed by pigs fed the CLA-60 diet (RSFO). Conjugated linoleic acid oil consists of 60% positional and geometric isomers of CLA. Pigs fed SFO exhibited higher average daily gains (0.98 vs 0.80 kg/d, P < 0.01) than RSFO-fed pigs, but there were no effects of dietary treatment on feed intake or feed efficiency. Dietary treatment did not affect (P > 0.05) backfat thickness or longissimus muscle area. Bellies of gilts fed CLA-60 were subjectively evaluated to be firmer (2.91 vs 2.43 or 2.07 +/- 0.13, P < 0.01) than those of SFO- or RSFO-fed gilts, respectively. The longissimus muscle of gilts fed CLA-60 contained more saturated fatty acids (39.77 vs. 36.04 or 36.73 +/- 0.74%, P < 0.001) and less unsaturated fatty acids (60.23 vs 63.96 or 63.27 +/- 0.74%, P < 0.001) than that of gilts fed SFO or RSFO, respectively. The belly fat of gilts fed CLA-60 contained more saturated fatty acids (44.45 vs. 37.50 or 36.60 +/- 0.46%, P < 0.001) and less unsaturated fatty acids (54.78 vs. 61.75 or 62.47 +/- 0.46%, P < 0.001), resulting in lower iodine values (57.69 vs 66.37 or 65.62 +/- 0.91, P < 0.001) than that of gilts fed SFO or RSFO, respectively. Gilts fed CLA-60 accumulated more CLA in the longissimus muscle (0.55 vs 0.09 or 0.09 +/- 0.03%, P < 0.01) and belly fat (1.56 vs. 0.13 or 0.13 +/- 0.15%, P < 0.001) than did gilts fed SFO or RSFO, respectively. Dietary treatment did not affect (P > 0.05) 24-h pH, drip loss or subjective quality evaluations of the longissimus muscle. The effect of supplemental CLA to improve belly firmness is of practical significance and may provide a nutritional solution to carcass fat and belly firmness problems, thereby enhancing the overall value of extremely lean carcasses.

Adipose Tissue↗
PubMed1990

Conjugated dienoic derivatives of linoleic acid: a new class of anticarcinogens.

Evidence establishing the anticarcinogenic activity of the conjugated dienoic derivatives of linoleic acid (CLA) is reviewed. Our findings demonstrate that CLA is a potent antioxidant and that the c-9,t-11 CLA isomer is selectively incorporated into cellular phospholipid, which may at least in part explain the anticarcinogenic activity of CLA. Dietary sources of CLA include grilled beef, cheese, and related foods. Another source of CLA is its endogenous generation via the carbon centered free radical oxidation of linoleic acid. We propose that the formation and action of CLA represents a previously unrecognized in situ defense mechanism against membrane attack by oxygen radicals.

Animals↗