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At least 19 recordsLinked to original sources
PubMed1989

Growth-inhibition effects of oleic acid, linoleic acid, and their methyl esters on transplanted tumors in mice.

We investigated the effects of oleic acid and linoleic acid on transplanted Ehrlich ascites carcinoma and Ehrlich solid carcinoma in ACR mice. Both acids significantly prolonged the life spans of Ehrlich ascites carcinoma-bearing mice and inhibited the growth of Ehrlich solid carcinoma in mice compared with the findings in untreated control mice. Methyl esters of these acids also prolonged the survival of Ehrlich ascites carcinoma-bearing mice, but they were less effective in lengthening the survival of mice given transplants of Ehrlich ascites carcinoma. In addition, gas-chromatography analysis of tumor cell lipids showed that appreciable changes occurred in the fatty acid composition of the tumor cell grown in mice treated with oleic acid or linoleic acid. Linoleic acid caused more pronounced alterations in fatty acid composition of tumor cell lipids than did oleic acid, a feature that parallels the intensity of the cytotoxicity potential of the two free fatty acids. These results suggest that (a) the free carboxyl group of free fatty acids plays a role in killing tumor cells and (b) the modification of the fatty acid composition of tumor cells also correlates with the antitumor effects of oleic and linoleic acids. In addition, these results indicate that free fatty acids may be of tumor-oriented distribution; as a consequence, free fatty acids selectively inhibit the growth of tumor cells.

Animals↗
PubMed1992

Formation of monohydroxy derivatives of arachidonic acid, linoleic acid, and oleic acid during oxidation of low density lipoprotein by copper ions and endothelial cells.

An important event in the formation of atherosclerotic lesions is the uptake of modified low density lipoprotein (LDL) by macrophages via scavenger receptors. Modification of LDL, which results in its recognition by these receptors, can be initiated by peroxidation of LDL lipids. The first step in this process is the formation of monohydroperoxy derivatives of fatty acids, which are subsequently degraded to the corresponding monohydroxy compounds, or to a variety of secondary oxidation products. In order to understand this process more completely, we have developed a mass spectrometric procedure to measure the amounts of specific hydroperoxy/hydroxy fatty acids formed by oxidation of the major unsaturated fatty acids in human LDL, oleic acid, linoleic acid, and arachidonic acid. Oxidation of human LDL in the presence of a relatively strong stimulus (20 microM CuSO4) resulted in very large increases in the amounts of the major monohydroxy derivatives of linoleic acid (9- and 13-hydroxy derivatives) and arachidonic acid (5-, 8-, 9-, 11-, 12-, and 15-hydroxy derivatives) in LDL lipids in the early stages of the reaction. After 20 h, the amounts of these products declined due to substrate depletion, but large amounts of monohydroxy derivatives of oleic acid (8-, 10-, and 11-hydroxy derivatives) were detected. Although thiobarbituric acid-reactive substances clearly increased under these conditions, the changes were not nearly so dramatic as those observed for monohydroxy fatty acids. Oxidation of LDL in the presence of endothelial cells, a much milder stimulus, resulted in 2.5- to 3-fold increases in the amounts of monohydroxy derivatives of linoleic and arachidonic acids, as well as thiobarbituric acid-reactive substances, with more modest increases in the amounts of hydroxylated derivatives of oleic acid. There was little positional specificity in the oxidation of the above fatty acids in the presence of either stimulus, suggesting that the formation of these products proceeds primarily by lipid peroxidation, rather than by catalysis by lipoxygenases. However, an important role for lipoxygenases in the initiation of these reactions cannot be excluded. In conclusion, oxidation of LDL in the presence of copper ions or endothelial cells results in the formation of a large number of monohydroxy derivatives of oleic, linoleic, and arachidonic acids. The relative amounts of products formed from each of these fatty acids depends on the strength of the stimulus as well as the incubation time.

Arachidonic Acids↗
PubMed1988

The use of gamma linolenic acid, linoleic acid and natural vitamin E for the treatment of multicentric lymphoma in two dogs.

The use of Gamma linolenic acid (GLA) and other essential fatty acid (EFA) metabolites in malignant cancer treatment in vitro and in vivo is briefly reviewed. Treatment of two dogs with multicentric lymphoma with large empirical daily doses of a combination of 40 mg gamma linolenic acid, 350 mg linoleic acid and 10 mg natural vitamin E per capsule resulted, after approximately one week, in slight to marked reduction in size of enlarged peripheral lymph nodes, spleen, skin nodules and tonsils. Both animals showed transient improved habitus and appetite, but deteriorated due to complications, apparently unrelated to therapy.

Animals↗
PubMed1990

Modification of prostacyclin-stimulatory activity in sera by glucose, insulin, low density lipoprotein, linoleic acid and linoleic acid hydroperoxide.

Reduced prostacyclin (PGI2) production by the vascular wall has been proposed as one of the possible causes of diabetic vascular complications. We found an activity which stimulated PGI2 production by cultured endothelial cells (PGI2-stimulatory activity, PSA) in human plasma-derived serum (PDS). The PSA was less in patients with diabetes mellitus. The present study was undertaken to evaluate how metabolic factors relevant to diabetic angiopathy modify the PSA. Pooled PDS was prepared from 10 healthy volunteers. The 6-keto-PGF1 alpha (6KF, a stable metabolite of PGI2) production by cultured bovine aortic endothelial cells was maximally stimulated by Dulbecco's modified Eagle's medium (DMEM) containing 10% pooled PDS after incubation for 60 min. The production of 6KF was reduced in a dose-dependent manner by the addition of 10% pooled PDS with glucose and linoleic acid hydroperoxide (lipid peroxide). In contrast, human low density lipoprotein (LDL) and linoleic acid (unsaturated fatty acid) enhanced the production of 6KF by 10% pooled PDS in a dose-dependent manner. Insulin, however, showed no effect on the production of 6KF by 10% pooled PDS. These results suggest that the reduced PSA in diabetics may be the result, in part, of a modification of the PSA by diabetic metabolic factors such as glucose and lipid peroxide.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

Stimulation of growth of human breast cancer cell lines in culture by linoleic acid.

Linoleic acid, an omega-6 unsaturated fatty acid, stimulated growth of the MDA-MB-231 and MCF-7 human breast cancer cell lines in culture. Responses of the estrogen-independent MDA-MB-231 cells both in serum-free medium and with 1% fetal bovine serum added were positively correlated with linoleic acid concentration over the entire range examined (5-750 ng/ml). Growth stimulation of the estrogen-responsive MCF-7 cell line was maximal at a LA concentration of 500 ng/ml when cultured in 1% fetal bovine serum-containing medium with added estradiol. Linoleic acid had no mitogenic effect on three human cancer cell lines derived from sites other than breast, or on untransformed 3T3 cells.

Breast Neoplasms↗
PubMed1991

Production of arachidonic acid and linoleic acid metabolites by human bronchoalveolar lavage cells.

Fatty acid-derived inflammatory mediators are considered to play an important role in airway hyperresponsiveness of asthmatic patients. The pulmonary macrophage may be an important source for these mediators in airway tissue. We investigated the metabolism of arachidonic acid and linoleic acid by human bronchoalveolar lavage cells, mainly comprising pulmonary macrophages. Arachidonic was mainly metabolized by 5-lipoxygenase, giving rise to the formation of leukotriene B4 and 5-hydroxy-eicosatetraenoic acid (5-HETE). Linoleic acid was converted to 5 major metabolites, including the 9-hydroxy and 13-hydroxy derivatives, 9- and 13-hydroxy-octadecadienoic acid (9- and 13-HODE). The formation of HODEs could be inhibited by cyclooxygenase inhibitors as well as lipoxygenase inhibitors, indicating that both enzymic species play a role in the generation of HODEs.

Arachidonate 5-Lipoxygenase↗
PubMed1991

Lymphatic absorption of structured glycerolipids containing medium-chain fatty acids and linoleic acid, and their effect on cholesterol absorption in rats.

The effects of various structured triglycerides containing medium-chain (caprylic or capric acids) and long-chain (linoleic acid) fatty acids on fatty acid and cholesterol absorption were studied in lymph-cannulated rats. A considerable portion of capric and caprylic acid was absorbed through the lymph duct, although to a lesser extent than was linoleic acid. Capric and linoleic acid located at the 2-position of 2-decanoyl-1,3-dilinoleoyl-glycerol (18:2/10:0/18:2) and 2-linoleoyl-1,3-didecanoyl-glycerol (10:0/18:2/10:0), respectively, tended to be absorbed more efficiently than those located at the 1- and 3-position or those from tricaprin (10:0/10:0/10:0) or trilinolein (18:2/18:2/18:2). A similar trend was observed when the medium-chain fatty acid was caprylic acid instead of capric acid. Caprylic acid absorption from 2-octanoyl-1,3-dilinoleoyl-glycerol (18:2/8:0/18:2) was significantly greater (p less than 0.05) than from 2-linoleoyl-1,3-dioctanoyl-glycerol (8:0/18:2/8:0) or tricaprylin (8:0/8:0/8:0). Preferential absorption of caprylic and linoleic acid was not observed when the 1 to 2 and the 2 to 1 mixtures of 8:0/8:0/8:0 and 18:2/18:2/18:2, respectively, were administered. The structured lipids did not affect the lymphatic absorption of cholesterol. The results suggest that structured triglycerides composed of medium-chain fatty acids and linoleic acid may be more useful for the treatment of lipid malabsorption than are mixtures of medium-chain triglyceride (MCT) and long-chain triglyceride (LCT).

Absorption↗
PubMed1992

Hydrogenation alternatives: effects of trans fatty acids and stearic acid versus linoleic acid on serum lipids and lipoproteins in humans.

The objective of this study was to compare the effects of linoleic acid (cis,cis-C18:2(n-6)) and its hydrogenation products elaidic (trans-C18:1(n-9)) and stearic acid (C18:0) on serum lipoprotein levels in humans. Twenty-six men and 30 women, all normolipemic and apparently healthy, completed the trial. Three experimental diets were supplied to every subject for 3 weeks each, in random order (multiple cross-over). The Linoleate-diet provided 12.0% of total energy intake as linoleic acid, 2.8% as stearic acid, and 0.1% as trans fatty acids. The Stearate-diet supplied 3.9 energy % as linoleic acid, 11.8% stearic acid, and 0.3% trans fatty acids. The Trans-diet provided 3.8 energy % as linoleic acid, 3.0% stearic acid, and 7.7% as monounsaturated trans fatty acids, largely elaidic acid (trans-C18:1(n-9)). Other nutrients were constant. Fasting blood was sampled at the end of each dietary period. Mean (+/- SD) serum LDL cholesterol was 109 +/- 24 mg/dl (2.83 +/- 0.63 mmol/l) on the Linoleate-diet. It rose to 116 +/- 27 mg/dl (3.00 +/- 0.71 mmol/l) on the Stearate-diet (change, 7 mg/dl or 0.17 mmol/l, P = 0.0008) and to 119 +/- 25 mg/dl (3.07 +/- 0.65 mmol/l) on the Trans-diet (change, 9 mg/dl or 0.24 mmol/l, P less than 0.0001). High density lipoprotein (HDL) cholesterol decreased by 2 mg/dl (0.06 mmol/l, P less than 0.0001) on the Stearate-diet and by 4 mg/dl (0.10 mmol/l, P less than 0.0001) on the Trans-diet, both relative to linoleic acid. Our findings show that 7.7% of energy (mean, 24 g/day) of trans fatty acids in the diet significantly lowered HDL cholesterol and raised LDL cholesterol relative to linoleic acid. Combination with earlier results (Mensink, R. P., and M. B. Katan. 1990. N. Engl. J. Med. 323: 439-445) suggests a linear dose-response relation. Replacement of linoleic acid by stearic acid also caused somewhat lower HDL cholesterol and higher LDL cholesterol levels. Hydrogenation of linoleic acid to either stearic or trans fatty acids produces fatty acids that may increase LDL and decrease HDL cholesterol relative to linoleic acid itself.

Adolescent↗
PubMed1991

Gas chromatographic analysis of malonaldehyde and 4-hydroxy-2-(E)-nonenal produced from arachidonic acid and linoleic acid in a lipid peroxidation model system.

Malonaldehyde (MA) and 4-hydroxynonenal (4-HN) formed upon oxidation with Fe2+/H2O2 from arachidonic acid and linoleic acid, and their ethyl esters were analyzed by gas chromatography (GC). The MA and 4-HN produced were reacted with N-methylhydrazine (NMH) to give 1-methylpyrazole and 5(1'-hydroxyhexyl)-1-methyl-2-pyrazoline, respectively. The derivatives were analyzed by GC on a fused silica capillary column using a nitrogen-phosphorus detector. With arachidonic acid, more MA and 4-HN were formed from the ester (88 nmol/mg and 23 nmol/mg, respectively) than from the free acid (25 nmol/mg and 9 nmol/mg, respectively). In contrast, with linoleic acid, more MA and 4-HN were produced from the free acid (53 nmol/mg and 13 nmol/mg, respectively) than from the ester (39 nm/mg and 8 nmol/mg, respectively).

Aldehydes↗
PubMed1991

The fate of arachidonic acid and linoleic acid in isolated working rat hearts containing normal or elevated levels of coenzyme A.

If myocardial levels of coenzyme A (CoA) are elevated, an increase in the rate of esterification of palmitate into myocardial triacylglycerols will occur. In this study, we determined the fate of linoleic acid and arachidonic acid in isolated working rat hearts containing normal or elevated levels of CoA. In hearts containing normal levels of CoA, oxidative rates (measured as 14CO2 production) of [14C]arachidonic acid were significantly lower than those of [14C]palmitic acid, whereas a significantly greater incorporation of [14C]arachidonic acid into myocardial neutral lipids (comprised predominantly of triacylglycerols) was seen when compared to hearts perfused with [14C]palmitic acid. In a second series of hearts, myocardial CoA levels were elevated by perfusing hearts with no carbon substrate, 15 microM pantothenate, 0.5 mM cysteine and 1 mM dithiothreitol, resulting in an increase in myocardial CoA levels from 553 +/- 2 to 918 +/- 63 nmol/g dry wt. Subsequent perfusion of hearts containing elevated CoA levels with 1.2 mM [3H]arachidonic acid or [14C]linoleic acid resulted in a significant increase in incorporation of both these fatty acids into myocardial neutral lipids compared to control hearts. Incorporation of these fatty acids into phospholipids was significantly lower than their incorporation into neutral lipids and was not affected by myocardial CoA levels. Linoleic acid oxidation was unaffected by increases in myocardial levels of CoA. If linoleic acid oxidation was inhibited by adding 5 mM pyruvate to the perfusate, no effect on the incorporation of [14C]linoleic acid into neutral lipids was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Formation of 9-hydroxyoctadecadienoic acid from linoleic acid in endothelial cells.

Human umbilical vein endothelial cells convert linoleic acid to two monohydroxyoctadecadienoic (HODE) acids, 9- and 13-HODE. More 9-HODE than 13-HODE is formed under most conditions. The production of these metabolites is reduced substantially by acetylsalicylic acid, ibuprofen, or arachidonic acid, suggesting that cyclooxygenase may be involved in endothelial HODE synthesis. Incubations lasting up to 4 h indicate that the endothelial cells can convert [U-14C] linoleic acid into at least four additional products, some of which may be derived from the HODE that is formed initially. Radioactive 9- and 13-HODE are produced when the endothelial cells are labeled with linoleic acid and then exposed to thrombin, suggesting that these metabolites also may be formed when the endothelium is activated. If endothelial monolayers grown on micropore filters are incubated with linoleic acid, a substantial amount of the HODE formed accumulates in the basolateral fluid. This suggests that HODE may have extracellular effects, especially within the vascular wall. Furthermore, when 9- or 13-HODE are added, endothelial cultures produce less prostaglandin I2 and convert less 12-hydroxyeicosatetraenoic acid to its main metabolite, 8-hydroxyhexadecatrienoic acid. Therefore, in addition to extracellular actions, HODE also may have functional effects within the endothelium.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1977

Enzymatic oxydation of linoleic acid: formation of bittertasting fatty acids.

Linoleic acid was oxidized with a protein fraction from soya beans (25 degrees C; 2h), in which lipoxygenase and peroxydase activities occurred. The fatty acids formed were isolated and, after emulsification with a sugar ester, were evaluated for bitter taste. The main components of the bitter-tasting fractions was a mixture of 9.12.13-trihydroxyoctadec-10- and 9.10.13-trihydroxyoctadec-11-enoic acids. The taste threshold lies in the range 0.6-0.9 mumol/ml. Two further trihydroxy-acids and two oxodihydroxy-acids were also identified in the bitter-tasting fraction.

Fatty Acids↗
PubMed1989

Synthesis of hydroxy fatty acids from linoleic acid by human blood platelets.

The metabolism of linoleic acid by washed human platelets was investigated. [1.14C] linoleic acid was converted to [1.14C] hydroxy octadecadienoic acids (HODEs) at about the same rate with which [1.14C] 12-HETE was produced from [1.14C] arachidonic acid. The total radioactivity in HODEs was distributed among two isomers: 13-HODE (85%) and 9-HODE (15%) as defined by CG-MS. The production of HODEs by intact washed platelets was inhibited by indomethacin (IC50:5 x 10(-7) M) which suggest that hydroxy fatty acids were produced by PGH-synthase. By contrast, the production of HODEs by platelet cytosolic fractions was not modified under indomethacin treatment but completely abolished by NDGA (10(-3) M) and inhibited by the platelet lipoxygenase inhibitors 15-HETE (2.10(-5) M) and baicalein (10(-5) M). Platelets thus contain two different active systems which may convert linoleic acid to hydroxy fatty acids. Since these compounds remained essentially associated with the platelets, their presence may significantly participate in the mechanisms of platelet activation.

Arachidonate 15-Lipoxygenase↗
PubMed1992

Effects of cytochalasin, colchicine, and ethylenediaminetetraacetic acid on linoleic acid transport across rat jejunal enterocytes.

The involvement and the site of interference of the cytoskeleton in the transport of linoleic acid across the rat jejunum was investigated by administration of microfilamentous and microtubular altering agents such as cytochalasin, colchicine, and ethylenediaminetetraacetic acid (EDTA). An isolated jejunal segment was perfused with a buffer containing labeled linoleic acid, and portal blood and perfusate samples were collected concomitantly at 5-min intervals and assayed for their radioactivity. At the end of the perfusion, the amount of radioactivity retained in the intestine was also determined. The results were analyzed by using a three-compartment physical model that allows the determination of mucosal and serosal permeability coefficients, from which changes in the permeability of the mucosal and serosal membranes were assessed. Cytochalasin decreased the permeability of the mucosal membrane to linoleic acid, but not that of the serosal membrane. The administration of colchicine, EDTA, or cytochalasin + colchicine increased the permeability of the serosal membrane but did not affect the mucosal membrane.

Animals↗
PubMedDate not supplied

Differential stimulatory and inhibitory responses of human MCF-7 breast cancer cells to linoleic acid and conjugated linoleic acid in culture.

Consumption of dietary fat has been linked to the high incidence of certain cancers. However, recent research has stimulated interest in conjugated linoleic acid (CLA), a newly recognized anticarcinogenic fatty acid. Human MCF-7 breast cancer cells were incubated for 12 d in culture medium supplemented with various concentrations (1.78-7.14 x 10(-5) M) of linoleic acid (LA) or CLA. Linoleic acid initially stimulated MCF-7 cell growth with an optimal effect at concentrations of 3.57-7.14 x 10(-5) M, but was inhibitory at similar concentrations after 8 and 12 d of incubation. In contrast, CLA was inhibitory to cancer cell growth at all concentrations and times tested. Cell growth inhibition by CLA was dose- and time-dependent. Growth retardation at the prescribed LA and CLA concentrations ranged, respectively, from 4 to 33% and 54 to 100% following 8 to 12 d of treatment. At similar LA and CLA concentrations, cytostatic and cytotoxic effects of CLA were more pronounced (8-81%) than LA. These in vitro results suggest that CLA is cytotoxic to MCF-7 cells.

Breast Neoplasms↗
PubMed1991

Dietary alpha-linolenic acid is as effective as oleic acid and linoleic acid in lowering blood cholesterol in normolipidemic men.

The effect of dietary oleic acid (OA), linoleic acid (LA), and linolenic acid (LNA) on plasma lipid metabolism was studied in eight normolipidemic men. A mixed-fat diet composed of conventional foods was fed during 6-d pre- and post-experimental periods. The same basic diet but with 75% of the fat (26% of total energy) provided by sunflower and olive; canola; soybean; and sunflower, olive, and flax oils was fed during four 18-d experimental periods. Mean plasma total cholesterol (-18%), low-density-lipoprotein-cholesterol, (-22%) and very-low-density-lipoprotein-cholesterol (-41%) concentrations were significantly (P less than 0.004) lower after the experimental diets than after the mixed-fat diet. Mean serum apolipoprotein B (-19%) and apolipoprotein A-I (-9%) concentrations were also significantly (P less than 0.0007) lower after the experimental diets. The experimental diets were equally effective in lowering total and lipoprotein cholesterol and apolipoprotein concentrations in plasma, indicating that dietary OA, LA, and LNA were equally hypocholesterolemic.

Adult↗
PubMed1989

Bidirectional control of membrane expression and/or activation of the tumor cell IRGpIIb/IIIa receptor and tumor cell adhesion by lipoxygenase products of arachidonic acid and linoleic acid.

Lewis lung carcinoma cells express a plasma membrane receptor (i.e., IRGpIIb/IIIa) which is immunologically and functionally related to the platelet aggregation receptor complex (i.e., GpIIb/IIIa). Both fluorescence microscopy and flow cytometric analysis reveal that surface expression and/or activation of this tumor cell receptor is enhanced by a phorbol ester [i.e., 12-O-tetradecanoylphorbol-13-acetate (TPA)] and a lipoxygenase metabolite of arachidonic acid; 12-hydroxyeicosatetraenoic acid (i.e., 12-HETE). TPA-enhanced expression appears to be mediated by a lipoxygenase metabolite, as this effect can be reversed by lipoxygenase inhibitors but not by cyclooxygenase inhibitors. In parallel with these results both TPA and 12(S)-HETE [but not 12(R)-HETE] enhance tumor cell adhesion to endothelial cells, subendothelial matrix and fibronectin, but not to type IV collagen. TPA-enhanced adhesion can be reduced by lipoxygenase inhibitors but not by cyclooxygenase inhibitors and in addition, stimulated adhesion can be blocked by pretreatment of tumor cells with specific polyclonal or monoclonal antibodies which react against IRGpIIb/IIIa. 12(S)-HETE-enhanced adhesion can also be inhibited by these same antibodies. In contrast, a lipoxygenase product of linoleic acid, 13(S)-hydroxyoctadecadienoic acid, inhibited TPA and 12(S)-HETE-enhanced tumor cell adhesion to endothelial cells, subendothelial matrix, and fibronectin. These results suggest that (a) IRGpIIb/IIIa is a multifunctional receptor which mediates tumor cell adhesion to a variety of biological substrata, (b) TPA enhances surface expression and/or activation of this receptor possibly via a lipoxygenase metabolite of arachidonic acid, and (c) these effects are opposed by a lipoxygenase metabolite of linoleic acid.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗