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PubMed1978

Tumor promoting phorbol diesters stimulate release of radioactivity from [3H]-arachidonic acid labeled- but not [14C]linoleic acid labeled-cells. Indomethacin inhibits the stimulated release from [3H] arachidonate labeled cells.

The tumor promoting phorbol diester, 12-O-tetradecanoyl-phorbol-13-acetate, stimulates MDCK cells to deacylate cellular phospholipids and to produce prostaglandins when measured as the release of arachidonic acid and its metabolites into the culture fluid. Indomethacin, at levels of 2.8 x 10(-8) to 2.8 x 10(-6) M, inhibits the release of radioactivity from [3H]arachidonate labeled cells stimulated by 12-O-tetradecanoyl-phorbol-13-acetate treatment in a concentration dependent manner. At these concentrations, the conversion of released [3H]arachidonic acid into prostaglandins E2 and F2alpha and the production of PGE2 measured serologically also is suppressed in a concentration dependent manner. Indomethacin, at these levels, has no effect on the acylation of [3H]arachidonic acid into cellular lipids. The tumor promoting phorbol diester does not stimulate the release of radioactive materials from MDCK cells labeled with [14C]linoleic acid, although prostaglandin production by these cells is stimulated.

Animals↗
PubMed1998

Low levels of linoleic acid in plasma total lipids of HIV-1 seropositive children.

OBJECTIVE: To assess the plasma fatty acid status of a group of well-nourished children with the human immunodeficiency virus type-1 (HIV-1) and how this relates to the blood total CD4+ lymphocyte count. SUBJECTS: Fourteen HIV-1 seropositive children at various stages of disease and with adequate growth indices were assessed and compared to a control group of 30 healthy children. RESULTS: The concentrations (mg/dL) of plasma total fatty acids were not different between the two groups. HIV-1 seropositive children presented lower levels of 18-C essential polyunsaturated fatty acids (PUFA: linoleic acid, LA, and alpha-linolenic acid) and higher levels of their 20-C long-chain derivatives (di-homo-gamma-linolenic acid, arachidonic acid, AA, and eicosapentaenoic acid) and docosahexaenoic acid in their plasma total lipids. The lowest plasma LA levels were observed in the subgroup of patients with more advanced stages of disease. In bivariate analyses the plasma LA levels related positively (Spearman r = 0.50, p = 0.06), while the LA/AA ratio related negatively (Spearman r = -0.51, p = 0.06), to the total CD4+ count. CONCLUSIONS: Childhood HIV-1 infection is associated with changes in plasma fatty acid profile suggestive of an increased PUFA turnover. Decreased levels of LA (together with higher plasma AA levels) appear to be associated with more advanced clinical and biochemical stages of disease.

8,11,14-Eicosatrienoic Acid↗
PubMed1990

Influence of dietary linoleic acid and trans fatty acids on the fatty acid profile of cardiolipins in rats.

Cardiolipins (CL) have unique fatty acid profiles with generally high levels of polyunsaturated fatty acids, primarily 18:2n-6, and low levels of saturated fatty acids. In order to study the effect of dietary fatty acid isomers on the fatty acid composition of cardiolipins, rats were fed partially hydrogenated marine oils (HMO), rich in 16:1, 18:1, 20:1, and 22:1 isomeric fatty acids, supplemented with linoleic acid at levels ranging from 1.9% to 14.5% of total fat. Although the dietary fats contained 33% trans fatty acids, the levels of trans fatty acids in CL were below 2.5% in all organs. The fatty acid profiles of cardiolipins of liver, heart, kidney and testes showed different responses to dietary linoleic acid level. In liver, the contents of 18:2 reflected the dietary levels. In heart and kidney, the levels of 18:2 also paralleled increasing dietary levels, but in all groups fed HMO, levels of 18:2 were considerably higher than in the reference group fed palm oil. In testes, the 18:2 levels were unaffected by the dietary level of 18:2 and HMO.

Animals↗
PubMed2003

Interactions of conjugated linoleic acid and lipoic acid on insulin action in the obese Zucker rat.

The fatty acid conjugated linoleic acid (CLA) and the antioxidant R-(+)-alpha-lipoic acid (R-ALA) individually enhance glucose tolerance and insulin action on skeletal muscle glucose transport in the insulin-resistant obese Zucker rat. To date, no study has assessed the potential interactions between these 2 interventions in treating insulin resistance. The present study was designed to determine whether chronic treatment with CLA and R-ALA in combination would enhance skeletal muscle glucose transport to a greater extent than either intervention individually. CLA, R-ALA, or a combination treatment of R-ALA and CLA were administered to female obese Zucker rats for 20 days at low or high doses. Whereas low-dose R-ALA (10 mg/kg body weight) alone did not alter muscle glucose transport, low-dose CLA (0.3 g/kg) induced a significant increase (38%, P <.05) in insulin-mediated glucose transport in epitrochlearis, but not in soleus. Low-dose combination therapy brought about the greatest enhancement of insulin-mediated glucose transport in epitrochlearis (77%) and soleus (54%), with the latter effect being associated with a 50% reduction in protein carbonyls (an index of tissue oxidative stress) and a 33% diminution in muscle triglycerides. High-dose treatments with CLA (1.5 g/kg), R-ALA (50 mg/kg), and the combination of CLA and R-ALA elicited increases in insulin-mediated glucose transport in epitrochlearis (57%, 58%, and 77%) and soleus (32%, 35%, and 54%). However, whereas the individual high-dose treatments with CLA and R-ALA reduced protein carbonyls (63% and 49%) and triglycerides (29% and 28%) in soleus, no further reductions were observed with the high-dose combination treatment groups. These findings support a significant interaction between low doses of CLA and R-ALA for enhancement of insulin action on skeletal muscle glucose transport, possibly via reductions in muscle oxidative stress and in lipid storage.

Animals↗
PubMed2003

Isomer-specific actions of conjugated linoleic acid on muscle glucose transport in the obese Zucker rat.

The fatty acid-conjugated linoleic acid (CLA) enhances glucose tolerance and insulin action on skeletal muscle glucose transport in rodent models of insulin resistance. However, no study has directly compared the metabolic effects of the two primary CLA isomers, cis-9,trans-11-CLA (c9,t11-CLA) and trans-10,cis-12-CLA (t10,c12-CLA). Therefore, we assessed the effects of a 50:50 mixture of these two CLA isomers (M-CLA) and of preparations enriched in either c9,t11-CLA (76% enriched) or t10,c12-CLA (90% enriched) on glucose tolerance and insulin-stimulated glucose transport in skeletal muscle of the insulin-resistant obese Zucker (fa/fa) rat. Animals were treated daily by gavage with either vehicle (corn oil), M-CLA, c9,t11-CLA, or t10,c12-CLA (all CLA treatments at 1.5 g total CLA/kg body wt) for 21 consecutive days. During an oral glucose tolerance test, glucose responses were reduced (P < 0.05) by 10 and 16%, respectively, in the M-CLA and t10,c12-CLA animals, respectively, whereas insulin responses were diminished by 21 and 19% in these same groups. There were no significant alterations in these responses in the c9,t11-CLA group. Insulin-mediated glucose transport activity was enhanced by M-CLA treatment in both type I soleus (32%) and type IIb epitrochlearis (58%) muscles and by 36 and 48%, respectively, with t10,c12-CLA. In the soleus, these increases were associated with decreases in protein carbonyls (index of oxidative stress, r = -0.616, P = 0.0038) and intramuscular triglycerides (r = -0.631, P = 0.0028). Treatment with c9,t11-CLA was without effect on these variables. These results suggest that the ability of CLA treatment to improve glucose tolerance and insulin-stimulated glucose transport activity in insulin-resistant skeletal muscle of the obese Zucker rat are associated with a reduction in oxidative stress and muscle lipid levels and can be specifically ascribed to the actions of the t10,c12 isomer. In the obese Zucker rat, the c9,t11 isomer of CLA is metabolically neutral.

Abdomen↗
PubMed2006

The yin and yang of 15-lipoxygenase-1 and delta-desaturases: dietary omega-6 linoleic acid metabolic pathway in prostate.

One of the major components in high-fat diets (Western diet) is the omega (omega, n)-6 polyunsaturated fatty acid (PUFA) called linoleic acid (LA). Linoleic acid is the precursor for arachidonic acid (AA). These fatty acids are metabolized to an array of eicosanoids and prostaglandins depending upon the enzymes in the pathway. Aberrant expression of the catabolic enzymes such as cyclooxygenases (COX-1 and/or -2) or lipoxygenases (5-LO, 12-LO, 15-LO-1, and 15-LO-2) that convert PUFA either AA and/or LA to bioactive lipid metabolites appear to significantly contribute to the development of PCa. However, PUFA and its cellular interactions in PCa are poorly understood. We therefore examined the mRNA levels of key enzymes involved in the LA and AA pathways in 18 human donor (normal) prostates compared to 60 prostate tumors using the Affymetrix U95Av2 chips. This comparative (normal donor versus prostate cancer) study showed that: 1) the level of 15-LO-1 expression (the key enzyme in the LA pathway) is low (P < 0.001), whereas the levels of delta-5 desaturase (P < 0.001, the key enzyme in the AA pathway), delta-6 desaturase (P = 0.001), elongase (P = 0.16) and 15-lipoxygenase-2 (15-LO-2, P = 0.74) are higher in donor (normal) prostates, and 2) Contrary to the observation in the normal tissues, significantly high levels of only 15-LO-1; whereas low levels of delta-6 desaturase, elongase, delta-5 desaturase and 15-LO-2 respectively, were observed in PCa tissues. Although the cyclooxygenase (COX)-1 and COX-2 mRNA levels were high in PCa, no significant differences were observed when compared in donor tissues. Our study underscores the importance of promising dietary intervention agents such as the omega-3 fatty acids as substrate competitors of LA/AA, aimed primarily at high 15-LO-1 and COX-2 as the molecular targets in PCa initiation and/or progression.

Journal Article↗
PubMed1990

Ferrylmyoglobin-catalyzed linoleic acid peroxidation.

The addition of linoleic acid (18:2) to a solution containing oxymyoglobin (MbIIO2), metmyoglobin (MbIII), or metmyoglobin-azide complex (MbIII-N3-) resulted in the formation of a common complex with identical absorption spectral properties. The addition of H2O2 to a MbIII/linoleic acid mixture revealed a spectral profile with lambda max at 530 nm and different from that observed in the reaction of MbIII with H2O2 and identical to that of ferrylmyoglobin. This was accompanied by a progressive decrease in the absorption in the visible region, indicating heme degradation during the lipid peroxidation process. The oxidation products of linoleic acid during the MbIII/18:2/H2O2 interaction were assessed by HPLC under anaerobic and aerobic conditions. In both instances, the chromatograms at lambda 234 nm revealed the formation of a main peak with a retention time of 11.1 min, which cochromatographed with a standard of 9-hydroperoxide of linoleic acid. The latter adduct was not degraded by the oxoferryl complex of myoglobin. The conclusions originating from this research are two-fold. On the one hand, the identical spectral properties exhibited by the product originating from the reaction of either MbIIO2 or MbIII with linoleic acid bridge the apparent discrepancy between the different reactivities of MbIIO2 and MbIII toward H2O2 and their ability to promote lipid peroxidation. On the other hand, the pattern of oxidation products of linoleic acid observed during the MbIII/H2O2 interaction, i.e., the formation of a 9-hydroperoxide adduct as a major product, points to a specific binding character and a regioselectivity of the oxoferryl complex in the oxidation of unsaturated fatty acids or a catalytic preference for decomposition of the various isomeric hydroperoxides over that of the 9-hydroperoxide.

Animals↗
PubMed1992

Effect of feeding palmitic, oleic, and linoleic acids to Japanese quail hens (Coturnix coturnix japonica). 2. Maternal diets and stage of incubation on the lipid metabolism of quail embryos.

An experiment was conducted to evaluate the effects of diets containing 3% of either palmitic acid (Diet PA), oleic acid (Diet OA), or linoleic acid (Diet LA) and three stages of development (Days 11, 13, and 15 of incubation) on 1) weights of yolk plus yolk sac membrane (TY), yolk sac membrane (YSM), yolk, liver, and extrahepatic tissue (ET); and 2) the fatty acid composition of phospholipid, triglyceride, and cholesterol ester fractions of YSM and ET of quail embryos. Embryos from birds fed Diet LA had the highest (P less than .05) weights of TY and yolk followed by those from birds fed Diet OA and Diet PA. The weight of ET was highest (P less than .05) in embryos from birds fed Diet PA followed by those from birds fed Diet LA and Diet OA. The weights of YSM and liver were not affected by the maternal diet (P greater than .05). The weight of TY decreased whereas the weights of liver and ET increased as incubation progressed (P less than .05). The weight of YSM was maximum at Day 13 of incubation. In the phospholipid, triglyceride, and cholesterol ester fractions of both YSM and ET of embryos, the fatty acid present at the highest level, except palmitic acid, was the one added to the maternal diet. In phospholipids of both YSM and ET the oleic acid content decreased and linoleic acid increased as incubation progressed. In triglycerides and cholesterol esters of both YSM and ET, the levels of palmitic acid increased, but oleic and linoleic acids decreased, with advancing embryonic development. The results of the present study indicate that embryos from birds fed Diet PA mobilize more yolk material and produce heavier ET than embryos from birds fed Diet OA and Diet LA. The fatty acid profiles of phospholipid, triglyceride, and cholesterol esters of embryonic tissues are consistently influenced by dietary fatty acid and the stage of development.

Animals↗
PubMedDate not supplied

Perturbation of lipid metabolism by linoleic acid hydroperoxide in CaCo-2 cells.

Dietary hydroperoxides are being discussed as potential health hazards contributing to oxidative stress-related diseases. However, how food-born hydroperoxides could exert systemic effects remains elusive in view of the limited chances to be absorbed. Therefore, the metabolic fate of 13-HPODE (13-hydroperoxy octadecadienoic acid), 13-HODE (13-hydroxy octadecadienoic acid) and linoleic acid (LA) was investigated in a CaCo-2 cell monolayer as a model of the intestinal epithelium. [1-14C]-13-HPODE, up to a non-cytotoxic concentration of 100 microM, did not cross the CaCo-2 cell monolayer unreduced if applied to the luminal side. The [1 -14C]-HPODE-derived radioactivity was preferentially recovered from intracellular and released diacylglycerols (DG), phospholipids (PL) and cholesterol esterified with oxidized fatty acids (oxCE). A similar distribution pattern was obtained with 13-HODE. In contrast, LA is preferentially incorporated into triacylglycerols (TG), cholesteryl esters (CE) and PL (but mainly released as TG). 13-HPODE dose-dependently decreased the incorporation of LA into released TG, while LA accumulated in cellular and released DGs, effects similarily exerted by 13-HODE. We concluded that food-born hydroperoxy fatty acids are instantly reduced by the gastrointestinal glutathione peroxidase, which was previously shown to persist in selenium deficiency. Accordingly, modulation of the glutathione peroxidases by selenium deprivation/repletion did not modify the disturbance of the lipid metabolism by 13-HPODE. Thus, hydroperoxy fatty acids disturb intestinal lipid metabolism by being esterified as hydroxy fatty acids into complex lipids, and may render lipoproteins synthesized thereof susceptible to further oxidative modifications.

Biological Transport↗
PubMedDate not supplied

Polyunsaturated but not conjugated linoleic acid supplementation of leukemic U937 cells can act as an amplification factor for photofrin-mediated photodynamic therapy.

Polyunsaturated fatty acids located in leukemia cell membranes are excellent targets for peroxidation. They can significantly enhance the effectiveness of Photofrin-mediated photodynamic therapy (PDT)-induced cell killing. In this study, the peroxidizability of conjugated fatty acid isomers (9c,11t-linoleic acid and 9c,11c-linoleic acid) and polyunsaturated fatty acids (PUFAs; linoleic acid, gamma-linolenic acid and arachidonic acid) with 2,2'-azo-bis(2-amidinpropane)dihydrochloride, soybean lipoxygenase and photomediated peroxidation are compared with each other. Peroxidation was determined using different methods: by means of gas chromatography to estimate the fatty acid (FA) consumption, by photometry for the level of FA peroxides or phospholipid peroxides and by definition of the content of malondialdehyde for thiobarbituric acid reactive substances (TBARS). The results suggest that the generation of oxidation products from individual FAs indicate a different formation rate of oxidation products. Radical FA peroxides were produced most by polyunsaturated arachidonic acid, followed by linoleic acid and gamma-linolenic acid, whereas conjugated FA isomers did not generate peroxides. Accordingly, the levels of lipid peroxides and TBARS were substantially increased after incorporation and oxidation of polyunsaturated FAs into U937 cells and could significantly enhance the effectiveness of Photofrin-PDT-induced cytotoxicity. The results showed that PUFA, but not conjugated FA supplementation of U937 cells, can act as a PDT amplification factor.

Cell Line↗
PubMed1979

A dual, concentration-dependent absorption mechanism of linoleic acid by rat jejunum in vitro.

Linoleic acid absorption was studied using everted rat jejunal sacs. At low concentrations (42-1260 microM), the relationship between linoleic acid concentration and its absorption rate fitted best to a rectangular hyperbola. At high concentrations (2.5-4.2 mM) the relationship between the two parameters was linear. The separate additions of 2,4-dinitrophenol, cyanide, or azide, or decrease in the incubation temperature from 37 to 20 degrees C did not change the absorption rate of linoleic acid. Absorption rate of linoleic acid at low concentrations increased as the hydrogen ion and taurocholate concentrations were increased or as the unstirred water layer thickness was decreased. Linoleic acid absorption rate was decreased after the additions of lecithin, oleic, linolenic, and arachidonic acids or the substitution of taurocholate with the nonionic surfactant Pluronic F 68. These observations indicate that a concentration-dependent, dual mechanism of transport is operative in linoleic acid absorption. Facilitated diffusion is the predominant mechanism of absorption at low concentrations, while at high concentrations, simple diffusion is predominant. At low concentrations, the absorption rate of linoleic acid is influenced by the pH, surfactant type and concentration, the simultaneous presence of other polyunsaturated fatty acids, and the thickness of the unstirred water layer.

Animals↗
PubMed1970

Sequential enzymes of linoleic acid oxidation in corn germ: lipoxygenase and linoleate hydroperoxide isomerase.

Linoleic acid oxidation catalyzed by lipoxygenase (lipoxidase) activity in extracts of defatted corn germ does not terminate in the product, linoleic acid hydroperoxide, unless the lipoxygenase is first partially purified. If purification is not attempted, the hydroperoxide product exists only as a barely detectable intermediate in the synthesis of three products. One of these was identified as 9-hydroxy-10-oxo-cis-12-octadecenoic acid formed from the hydroperoxide by the enzyme, linoleate hydroperoxide isomerase. Another product, 13-hydroxy-10-oxo-trans-11-octadecenoic acid, is believed to be formed by an isomerase also. The third product was the linoleate ester of one of the hydroxy-oxo-fatty acids, 9-(cis-9,cis-12-octadecadienoyl)-10-oxo-cis-12-octadecenoic acid. It is not known if the synthesis of the ester is enzyme-catalyzed. When a mixture of 13-hydroperoxy-cis-9,trans-11-octa-decadienoic acid and 9-hydroperoxy-trans-10,cis-12-octa-decadienoic acid from soybean lipoxygenase oxidation of linoleic acid was used as a substrate, 13-hydroxy-12-oxo-cis-9-octadecenoic acid and 9-hydroxy-12-oxo-trans-10-octadecenoic acid were formed as the major products of catalysis by linoleate hydroperoxide isomerase(s) from corn. Smaller quantities of 9-hydroxy-10-oxo-cis-12-octadecenoic acid and 13-hydroxy-10-oxo-trans-11-octadecenoic acid were also formed.

Chromatography↗
PubMed1991

Metabolites of cis,trans, and trans,cis isomers of linoleic acid in mice and incorporation into tissue lipids.

Metabolism of octadecadienoic acid isomers in weanling mice was studied by feeding fat-free diets supplemented with 2% by weight of cis-9,trans-12-octadecadienoic acid (c,t-18:2-d0), tetradeuterated trans-9,cis-12-octadecadienoic acid (t,c-18:2-d4) or dideuterated cis-9,cis-12-octadecadienoic acid (c,c-18:2-d2). Rates for conversion of c,t-18:2-d0 and c,c-18:2-d2 to c,t-20:4-d0 and c,c-20:4-d2 were identical and both were 5-times higher than conversion of t,c-18:2-d4 to t,c-20:4-d4. Accumulation of t,c-18:2-d4 in liver lipids was 2-4-times higher than for c,t-18:2-d0 or c,c-18:2-d2. The t,c-18:2 diet significantly increased with the 20:3(n-9) and total lipid concentrations in liver but not in heart, plasma or brain. The 20:3(n-9)/20:4(n-6) ratio in the liver lipids was 2-4-times higher for t,c-18:2-d4 than c,c-18:2-d2 fed mice. The position of the trans bond had a marked influence on the distribution of the various intermediate desaturation and elongation products. Intermediate metabolite data for the liver lipids indicated t,c-18:2-d4 was preferentially converted to 5c,11c,14t-20:3 ('dead end' product) rather than to t,c-20:4. Concentration of the 18:3(n-6) metabolite of c,t-18:2-d0 was about 10-times greater than the 18:3(n-6) metabolite of c,c-18:2-d2. Conversely, the concentration of the normal 20:3(n-6) metabolite from c,c-18:2-d2 was 4-times higher than the 20:3(n-6) metabolite of c,t-18:2-d0. Compared to the c,c-18:2 diet, the t,c- and c,t-18:2 diets significantly increased the total n-3, but not the total n-6 fatty acid content of heart lipids. These results illustrate that the position of the trans double-bond influences a variety of enzyme activities and the isomers differ in their physiological effects.

Animals↗