Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “LINOLEIC ACID”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,027 records · Page 57Linked to original sources
PubMed2002

Optimizing DHA levels in piglets by lowering the linoleic acid to alpha-linolenic acid ratio.

We examined the effect of altering the linoleic acid (LA, 18:2n-6) to alpha-linolenic acid (ALA, 18:3n-3) ratio in the dietary fats of 3 day old piglets fed formula for 3 weeks. The LA-ALA ratios of the experimental formulas were 0.5:1, 1:1, 2:1, 4:1, and 10:1. The level of LA was held constant at 13% of total fats while the level of ALA varied from 1.3% (10:1 group) to 26.8% (0.5:1 group). Incorporation of the n-3 long chain PUFA EPA and 22:5n-3 into erythrocytes, plasma, liver, and brain tissues was linearly related to dietary ALA. Conversely, incorporation of DHA into all tissues was related to dietary ALA in a curvilinear manner, with the maximum incorporation of DHA appearing to be between the LA-ALA ratios of 4:1 and 2:1. Feeding LA-ALA ratios of 10:1 and 0.5:1 resulted in lower and similar proportions of DHA in tissues despite the very different levels of dietary ALA (1.3 vs. 26.8% of total fats, respectively). These results are relevant to term infant studies in that they confirm our earlier findings of the positive effect on DHA status by lowering the LA-ALA ratio from 10:1 to 3:1 or 4:1, and they predict that ratios of LA-ALA below 4:1 would have little further beneficial effect on DHA status.

Animals↗
PubMed2002

Analysis of variation in cis-9, trans-11 conjugated linoleic acid (CLA) in milk fat of dairy cows.

Conjugated linoleic acid (CLA) is a fatty acid with numerous putative health benefits and is a natural component of ruminant-derived food products. An intermediate in rumen biohydrogenation is cis-9, trans-11 CLA, the major CLA isomer in milk fat. However, the major source of cis-9, trans-11 CLA in milk is endogenous synthesis by delta 9-desaturase conversion of trans-11 C18:1, another rumen biohydrogenation intermediate. The desaturase indices serve as a proxy for delta 9-desaturase activity and are calculated from the ratios of fatty acid pairs that represent product/substrate for this enzyme. This study analyzed individual animal variation in milk fat content of cis-9, trans-11 CLA and in desaturase indices in milk fat. Thirty lactating Holstein cows were allocated to one of three treatment groups: one received a standard total mixed ration, one received a diet that produced an elevated milk fat content of CLA, and a third treatment group was alternated between these diets at 3-wk intervals over the 12-wk study. There was a two- to threefold variation among individuals on the same diet for both milk fat content of CLA and desaturase indices in milk fat. This hierarchy was maintained to a large extent over the 12-wk study even in the variable treatment group that alternated between the two diets. Within the variable diet treatment, some animals consistently had a substantial response in milk fat content of CLA to dietary shifts, whereas other cows had little or no response. We conclude that while diet is a major determinant of the CLA content in milk fat, individual animal differences also have a substantial effect. The variation among individuals includes differences related to both rumen biohydrogenation and delta 9-desaturase activity in the mammary gland.

Analysis of Variance↗
PubMedDate not supplied

Cytotoxity of the trans10,cis12 isomer of conjugated linoleic acid on rat hepatoma and its modulation by other fatty acids, tocopherol, and tocotrienol.

This study was performed to evaluate the isomer-specific cytotoxic effects of conjugated linoleic acid (CLA) on rat hepatoma dRLh-84 cells in vitro. A 10trans,12cis (10t,12c)-CLA showed a strong cytotoxic effect on dRLh-84 cells in culture, whereas no such effect was observed with 9cis,11trans (9c,11t)-CLA or linoleic acid. The optimum concentration for induction of cytotoxicity by 10t,12c-CLA was 5 to 10 microM, but the effect was alleviated at higher concentrations. Coincubation with oleic or palmitoleic acid and 10t,12c-CLA cancelled the cytotoxic effect, but other major saturated or polyunsaturated fatty acids and eraidic acid did not interfere with 10t,12c-CLA-induced cytotoxity. The cytotoxic effect was also alleviated by alpha-tocopherol (alpha-toc) and alpha-tocotrienol but not by any other antioxidant reagent examined. Significant cytotoxicity of 10t,12c-CLA was detected after only a 15-min incubation, and the most noticeable effect was seen after 3 h. After incubation with 10t,12c-CLA at 10 microM, an additional 90 microM of 10t,12c-CLA or 100 microM of alpha-toc was also able to alleviate the cytotoxicity. When cells were treated with 10 microM 10t,12c-CLA for more than 48 h, treatment with additional CLA or alpha-toc could not prevent cell death.

Animals↗
PubMed1994

Comparison of linoleic acid and eicosapentaenoic acid incorporation into human breast cancer cells.

To gain some insight into the mechanisms involved in the opposing effects of linoleic acid (LA) and eicosapentaenoic acid (EPA) on the growth and invasiveness of MDA-MB-435 human breast cancer cells, the dynamics of the uptake by cells and the incorporation of [14C]LA and [14C]EPA into major lipid and phospholipid pools, as well as the effects of unlabeled EPA or LA on the uptake and distribution of [14C]LA or [14C]EPA, respectively, were examined. Cells were exposed to [14C]LA (1.28 micrograms/mL) or [14C]EPA (1.0 micrograms/mL) and unlabeled EPA or LA, respectively, at 0, 1, 4 and 16 micrograms/mL for 24 h in serum-free media. The uptake of each fatty acid (FA) was linear over time and was not affected by the presence of the opposing FA. For both FA, 80-90% was incorporated into the phospholipid fraction with the remaining 10-20% in neutral lipids. The relative distribution profile of [14C]LA among the phospholipid classes indicated a preferential incorporation into phosphatidylcholine (65%), whereas [14C]EPA was mostly found in phosphatidylethanolamine (58%). In the presence of unlabeled EPA or LA at various concentrations, corresponding dose-dependent shifts of [14C]LA or [14C]EPA from the phospholipid to the neutral lipid pool were noted, which did not alter the relative distribution of the FA among the phospholipid classes. Exogenous exposure to EPA or LA increased its content in membrane phospholipids while concurrently decreasing LA or EPA content, respectively, in a dose-dependent manner. Arachidonic acid content of membrane phospholipids remained constant.(ABSTRACT TRUNCATED AT 250 WORDS)

Arachidonic Acid↗
PubMed2001

Aldehydic lipid peroxidation products derived from linoleic acid.

Lipid peroxidation (LPO) processes observed in diseases connected with inflammation involve mainly linoleic acid. Its primary LPO products, 9-hydroperoxy-10,12-octadecadienoic acid (9-HPODE) and 13-hydroperoxy-9,11-octadecadienoic acid (13-HPODE), decompose in multistep degradation reactions. These reactions were investigated in model studies: decomposition of either 9-HPODE or 13-HPODE by Fe(2+) catalyzed air oxidation generates (with the exception of corresponding hydroxy and oxo derivatives) identical products in often nearly equal amounts, pointing to a common intermediate. Pairs of carbonyl compounds were recognized by reacting the oxidation mixtures with pentafluorobenzylhydroxylamine. Even if a pure lipid hydroperoxide is subjected to decomposition a great variety of products is generated, since primary products suffer further transformations. Therefore pure primarily decomposition products of HPODEs were exposed to stirring in air with or without addition of iron ions. Thus we observed that primary products containing the structural element R-CH=CH-CH=CH-CH=O add water and then they are cleaved by retroaldol reactions. 2,4-Decadienal is degraded in the absence of iron ions to 2-butenal, hexanal and 5-oxodecanal. Small amounts of buten-1,4-dial were also detected. Addition of m-chloroperbenzoic acid transforms 2,4-decadienal to 4-hydroxy-2-nonenal. 4,5-Epoxy-2-decenal, synthetically available by treatment of 2,4-decadienal with dimethyldioxirane, is hydrolyzed to 4,5-dihydroxy-2-decenal.

Air↗
PubMed2006

[Conjugated linoleic acid (CLA) and its relationship with cardiovascular disease and associated risk factors].

The term CLA (conjugated linoleic acid) corresponds to a mixture of positional and geometric isomers of linoleic acid, of which two (9/c/, 11/t/ and 10/t/, 12/c/) have biological activity. This review covers aspects related to CLA (sources, synthesis, distribution in human tissues, physiological activity), as well as its relationship with cardiovascular diseases. Most studies attribute the beneficial effects associated to the consumption of CLA to the reduction of risk factors for the development of cardiovascular diseases, such as the reduction of plasmatic triacylglycerols and cholesterol. Other research demonstrates the reduction of atherosclerotic processes. However, many studies indicate that CLA does not present beneficial effects or may even present negative effects. Thus, although there are a great number of studies related to CLA, we consider it premature to make any recommendation for the ingestion of these compounds, apart from those naturally present in a healthy diet.

Animals↗
PubMed2006

Conjugated linoleic acid inhibits Caco-2 cell growth via ERK-MAPK signaling pathway.

Conjugated linoleic acid (CLA) is a naturally occurring compound found in dairy and beef products. In recent years, it has received considerable attention because several studies showed a lower incidence of certain cancers in animals fed CLA-supplemented diets. In vitro studies further showed growth inhibitory activity on tumor cell proliferation, the CLA being effective above all against colon cancer cells. The aim of the present work was to investigate the growth inhibitory effect of CLA on Caco-2 cell line. Under our experimental conditions, CLA repressed Caco-2 cell proliferation, and the growth-inhibitory action increased by repeating treatments. However, in Caco-2 cells, CLA was unable to induce apoptosis, as revealed by cell-cycle analysis and Western blot studies. To determine the mechanism by which CLA inhibits cell growth, we studied its effect on extracellular-regulated kinase signaling. Conjugated linoleic acid reduced expression levels of Raf-1 and phosphorylation of ERK1/2, which was accompanied by a decrease in the expression of the downstream transcription factor c-myc. Our data suggest that CLA is dependent, at least in part, on the ERK kinase pathway for its ability to inhibit the growth of Caco-2 cancer cells.

Apoptosis↗
PubMed2006

trans-10,cis-12 conjugated linoleic acid inhibits the G1-S cell cycle progression in DU145 human prostate carcinoma cells.

Conjugated linoleic acid (CLA) is a group of positional and geometric isomers of linoleic acid, and has evidenced anti-cancer activities in experimental animal cancer models and in vitro studies. The two predominant isomers of CLA are cis-9,trans-11 CLA (c9t11) and trans-10,cis-12 CLA (t10c12). The present study was performed to study the effect of the individual CLA isomers on DU145 cell growth. The cells were incubated in serum-free medium with different concentrations of the fatty acids. Treatment of cells with t10c12 (at 2.5-10 micromol/L) resulted in a dose-dependent reduction in the numbers of viable cells, whereas c9t11 CLA at a concentration of 5 micromol/L slightly increased viable cell numbers at 3 days (P < .05). DNA flow cytometric analysis revealed that the treatment of DU145 cells with t10c12 for 24 hours induced a small but significant increase in the number of cells in the G1 phase, accompanied by a complementary decrease in cells in the S phase. c9t, however, had no effect on cell cycle progression. To determine the molecular mechanisms underlying t10c12-induced G1 arrest, the levels of cell cycle regulatory proteins were estimated by western blot analyses. t10c12 induced a marked increase in p21(CIP1/WAF1) protein levels in a dose-dependent manner. p27(KIP1) was not affected by t10c12. t10c12 moderately decreased cyclin A and cyclin D1 protein levels (P > .05). However, t10c12 did not affect the expression of cyclin-dependent kinase (CDK) 2, CDK4, or cyclin E. t10c12 increased p21(CIP1/WAF1) bound to CDK2 and attenuated CDK2 activity. These results indicate that t10c12-induced p21(CIP1/WAF1) binds to CDK, and inhibits the activity of this enzyme, which results in the observed decrease in the G1-S progression in DU145 cells.

Blotting, Western↗
PubMedDate not supplied

[Influence of rations with various linoleic acid contents on the fatty acid composition of phospholipids in blood platelets of rats].

Gas-liquid chromatography was used to study the fatty-acid composition of phospholipids in platelets of Wistar-Kioto rats which received semisynthetic rations with varying content of linoleic acid, 1 week prenatally and 18 weeks postnatally. In ration I the level of 18:2n6 was lower than 0.1 cal%, ration II contained 9.0 cal%, and ration III -- 16.0 cal%. Ration III, as compared to ration II, induced an increase in the content of linoleic fatty acids, arachidonic fatty acid content being unchanged. Ration I, as compared to ration II induced a decrease in linoleic fatty acid content, and an increase in the content of oleic and linolenic fatty acids attended by the appearance of appreciable amounts of 20:3n9 and 20:5n3. Long-term linoleic acid deficiency induced no changes in the unsaturation degree of fatty acids in platelet phospholipids of rats given ration I. This is an evidence of high reserve possibilities of the mechanisms regulating fatty acid metabolism in the mammals.

Animals↗
PubMed2003

Antioxidant effect of conjugated linoleic acid and vitamin A during non enzymatic lipid peroxidation of rat liver microsomes and mitochondria.

In the study reported here the effect of conjugated linoleic acid (CLA) and vitamin A on the polyunsaturated fatty acid composition, chemiluminescence and peroxidizability index of microsomes and mitochondria isolated from rat liver was analyzed. The effect of CLA on the polyunsaturated fatty acid composition of native microsomes was evidenced by an statistically significant p < 0.007 decrease of linoleic acid C18:2 n6, whereas in mitochondria it was observed a decrease p < 0.0001 of arachidonic acid C20:4 n6 when compared with vitamin A and control groups. Docosahexaenoic acid C22:6 n3 in mitochondria was reduced p < 0.04 in CLA and vitamin A groups when compared with control. After incubation of microsomes or mitochondria in an ascorbate (0.4 mM)-Fe++ (2.15 microM) system (120 min at 37 degrees C) it was observed that the total cpm/mg protein originated from light emission: chemiluminescence was lower in liver microsomes or mitochondria obtained from CLA group (received orally: 12.5 mg/daily during 10 days) than in the vitamin A group (received intraperitoneal injection: daily 0.195 g/ kg during 10 days). CLA reduced significantly maximal induced chemiluminescence in microsomes relative to vitamin A and control groups, whereas in mitochondria the effect was observed relative to control group. The polyunsaturated fatty acid composition of liver microsomes or mitochondria changed by CLA and vitamin A treatment. The polyunsaturated fatty acids mainly affected when microsomes native and peroxidized from control group were compared were linoleic, linolenic and arachidonic acids, while in vitamin A group linoleic and arachidonic acid were mainly peroxidized, whereas in CLA group only arachidonic acid was altered. In mitochondria obtained from the three groups arachidonic acid and docosahexaenoic acid showed a significant decrease when native and peroxidized groups were compared. As a consequence the peroxidizability index, a parameter based on the maximal rate of oxidation of fatty acids, show significant changes in the CLA group compare vitamin A and control groups. The simultaneous analysis of peroxidizability index, chemiluminescence and fatty acid composition demonstrated that CLA is more effective than vitamin A protecting microsomes or mitochondria from peroxidative damage.

Animals↗
PubMed2002

Isomer-dependent metabolic effects of conjugated linoleic acid: insights from molecular markers sterol regulatory element-binding protein-1c and LXRalpha.

Conjugated linoleic acid (CLA) is a heterogeneous group of positional and geometric isomers of linoleic acid. This study demonstrates the divergent effects of the cis-9 trans-11 (c9,t11-CLA) and trans-10 cis-12 (t10,c12-CLA) isomers of CLA on lipid metabolism and nutrient regulation of gene expression in ob/ob mice. The c9, t11-CLA diet decreased serum triacylglycerol (P = 0.01) and nonesterified fatty acid (NEFA) (P = 0.05) concentrations, and this was associated with reduced hepatic sterol regulatory element-binding protein-1c (SREBP-1c; P = 0.0045) mRNA expression, coupled with reduced levels of both the membrane-bound precursor and the nuclear forms of the SREBP-1 protein. C9,t11-CLA significantly reduced hepatic LXRalpha (P = 0.019) mRNA expression, a novel regulator of SREBP-1c. In contrast, c9,t11-CLA increased adipose tissue SREBP-1c mRNA expression (P = 0.0162) proportionally to the degree of reduction of tumor necrosis factor alpha (TNF-alpha) mRNA (P = 0.012). Recombinant TNF-alpha almost completely abolished adipose tissue SREBP-1c mRNA expression in vivo. The t10,c12-CLA diet promoted insulin resistance and increased serum glucose (P = 0.025) and insulin (P = 0.01) concentrations. T10, c12-CLA induced profound weight loss (P = 0.0001) and increased brown and white adipose tissue UCP-2 (P = 0.001) and skeletal muscle UCP-3 (P = 0.008) mRNA expression. This study highlights the contrasting molecular and metabolic effect of two isomers of the same fatty acids. The ameliorative effect of c9,t11-CLA on lipid metabolism may be ascribed to reduced synthesis and cleavage of hepatic SREBP-1, which in turn may be regulated by hepatic LXRalpha expression.

Animals↗
PubMed2001

Dietary manipulations of body fat-reducing potential of conjugated linoleic acid in rats.

To study whether the body fat-reducing potential of conjugated linoleic acid (CLA) could be increased through dietary manipulations, the effects of the combination of CLA with different proteins, fats, and sesamin were examined in rats. Male rats were fed diets containing 1% CLA or linoleic acid (LA) in combination with different proteins (20% of casein or soybean protein), fats (7% perilla oil or soybean oil) and 0.2% sesamin (SES) for 3 or 4 weeks. When the dietary fat source was soybean oil, CLA, as compared with LA, significantly reduced weights of epididymal and perirenal adipose tissues, irrespective of the dietary protein sources. However, the highest reducing effect was shown when soybean protein was given as a protein source. SES stimulated the reduction of epididymal and perirenal adipose tissue weights in both protein diets. In contrast, CLA increased the weight of brown adipose tissue, and SES further increased it in combination with soybean oil but not with perilla oil. No effect of dietary manipulation was observed on serum leptin and TNF-alpha levels. Thus, the body fat-reducing potential of CLA can be increased by an appropriate combination with food factors that may stimulate fatty acid beta-oxidation.

Adipose Tissue↗
PubMed1998

Formation of keto and hydroxy compounds of linoleic acid in submitochondrial particles of bovine heart.

To observe lipid peroxidation of additive-free submitochondrial particles, we incubated submitochondrial particles in the absence of exogenous irons and t-butyl hydroperoxide. After the incubation, the phospholipids were hydrolyzed by phopholipase A2, and the fatty acid constituents were analyzed by high-performance liquid chromatography, gas chromatography-mass spectrometry, and liquid chromatography-mass spectrometry. Contrary to a commonly accepted theory, lipid peroxidation in the submitochondrial particles did not need the addition of NADH. In the phospholipid constituent fatty acids of the oxidized submitochondrial particles, derivatives of hydroperoxides of linoleic acid such as keto, hydroxy, trihydroxy, and hydroxyepoxy compounds were generated. Lipid peroxidation in the submitochondrial particles was not inhibited by the addition of catalase, superoxide dismutase, hydroxyl radical scavengers, or ethylenediaminetetraacetic acid, but was inhibited by the addition of KCN, antimycin-A, NADH, ubiquinol, deferoxamine mesylate, ascorbic acid, and alpha-tocopherol. The cardiolipin-cytochrome c lipid peroxidation system could mimic the lipid peroxidation of the submitochondrial particles, in terms of linoleic acid products and the inhibitory patterns of radical scavengers and electron transfer chain inhibitors. Thus, lipid peroxidation in the submitochondrial particles seems to be due to phospholipid-hemoprotein lipid peroxidation systems such as the cardiolipin-cytochrome c system.

Animals↗
PubMedDate not supplied

Conjugated linoleic acid suppresses the growth of human breast adenocarcinoma cells in SCID mice.

Conjugated linoleic acid (CLA), which is mainly derived from dairy products, has been shown both in vitro and in animal models to have strong anti-tumor activity. Particular effects were observed on the growth and metastatic spread of transplantable mammary tumors. In this study, we examined the effect of dietary CLA on the growth of human breast adenocarcinoma cells in severe combined immunodeficient (SCID) mice. Mice were fed 1% CLA for two weeks prior to subcutaneous inoculation of 10(7) MDA-MB468 cells and throughout the study. Dietary CLA inhibited local tumor growth by 73% and 30% at 9 and 14 weeks post-inoculation, respectively. Moreover, CLA completely abrogated the spread of breast cancer cells to lungs, peripheral blood, and bone marrow. These results indicate the ability of dietary CLA to block both the local growth and systemic spread of human breast cancer via mechanisms independent of the host immune system.

Adenocarcinoma↗
PubMed2002

Characterization of factors that transform linoleic acid into di- and trihydroxyoctadecenoic acids in mash.

The qualities of beer are deteriorated by the presence of either di- or trihydroxyoctadecenoic acids, which reduce the beer 'head' and produce an astringent flavor. In this study we found that native extracts of malt mash transformed linoleic acid into di- and trihydroxyoctadecenoic acids, but this transforming activity and lipoxygenase activity were inactivated by heating the mash at 70 degrees C for 30 min. Recombinant barley lipoxygenase 1 was not able to transform linoleic acid into di- and trihydroxyoctadecenoic acids. The transforming activity of mash extract heated at 70 degrees C for 30 min could be restored by the addition of recombinant barley lipoxygenase 1; in contrast, the activity of boiled mash extract was not substantially restored by the recombinant enzyme. These results indicate that di- and trihydroxyoctadecenoic acids are generated from linoleic acid by both lipoxygenase and a heat-stable enzymatic factor present in the mash.

Journal Article↗
PubMed1987

Influence of dietary lipids and linoleic acid amounts on fatty acid content and composition of pig serum lipoproteins.

The effects of hyperlipidic polyunsaturated fat diets (PF) and saturated fat diets (SF) versus control diet (CO) on total lipid, phospholipid (PL) and cholesteryl ester (CE) content and composition of pig serum lipoproteins were studied in Large White pigs who first underwent a PF period for 14 days followed by a CO period and third a SF feeding during a fortnight. PF and SF diets induced an increase of linoleic acid in serum total lipids, especially in HDL fraction; this increase in CE and PL involved a reverse change of oleic acid. The modifications induced by the amounts of dietary linoleic acid could be explained by an alteration of LCAT activity. The fatty acid pattern of PL which constitute the LCAT substrate lead to an enrichment of cholesterol linoleate.

Animals↗
PubMed2003

Influence of conjugated and conventional linoleic acid on tumor growth and lipid peroxidation in pancreatic adenocarcinoma in hamster.

Conventional linoleic acid (LA) is regarded as a promotor of carcinogenesis. However, the effect of its conjugated derivative on cancer is still unknown. Therefore we investigated the influence of conventional and conjugated LA on tumor growth and lipid peroxidation in a solid model of pancreatic adenocarcinoma in Syrian hamsters. 60 male hamsters were randomized in 4 groups (Gr.) (n=15). Gr. 1 and 2 received 0.5 ml 0.9% sodium chloride subcutaneously (s.c.) once a week while Gr. 3 and 4 were injected 10 mg N-nitrosobis-2-oxopropylamine (BOP)/kg body weight weekly for 12 weeks to induce pancreatic cancer. Gr. 1 and 3 received a diet containing conventional LA, Gr. 2 and 4 were fed a diet of conjugated LA. After 29 weeks all animals were sacrificed, pancreas was weighed and examined macroscopically and histologically. The level of lipid peroxidation and activities of glutathion peroxidase and superoxide dismutase were determined in tumor-free as well as in pancreatic carcinoma tissue. Different diets did not influence the incidence of pancreatic carcinoma, however, pancreas weight was increased by conjugated LA compared to conventional LA. Furthermore both diets decreased the activity of glutathion peroxidase and increased the level of lipid peroxidation in pancreatic intratumoral tissue. The content of conjugated LA in dietary did not influence pancreatic tumor growth in a solid model of pancreatic adenocarcinoma in Syrian hamsters.

Adenocarcinoma↗
PubMed2000

Impact of dietary conjugated linoleic acid on the oxidative stability of rat liver microsomes and skeletal muscle homogenates.

Dietary conjugated linoleic acid (CLA; 0-2.0%) increased CLA concentrations in liver microsomes and skeletal muscle homogenates from rats. Dietary CLA decreased oleic and arachadonic acid concentrations in both liver microsomes and skeletal muscle. The presence of CLA in liver microsomes had no impact on linoleic acid, arachadonic acid, and alpha-tocopherol oxidation rates. Dietary CLA (2.0%) also did not alter alpha-tocopherol oxidation rates in liver microsomes or muscle homogenates. Formation of malonaldehyde (MDA) in oxidizing liver microsomes decreased with increasing CLA concentration as determined by measurement of thiobarbituric acid-MDA complexes by HPLC. The ability of CLA to decrease MDA formation without impacting other lipid oxidation markers such as the disappearance of fatty acid and alpha-tocopherol suggests that decreased MDA concentration was the result of CLA's ability to lower polyenoic fatty acids such as arachadonic acid. While CLA does not appear to act as an antioxidant, its ability to decrease polyenoic fatty acid concentrations could decrease the formation of highly cytotoxic lipid oxidation products such as MDA.

Animals↗