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Results for “LINOLEIC ACID”

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At least 19 recordsLinked to original sources
PubMed1997

Effect of linoleic acid, linoleic acid anilide, and arachidonic acid on the expression of adhesion molecules on human neutrophils.

The effects of linoleic acid, linoleic acid anilide, and arachidonic acid on the expression of CD11b/ CD18, CD11c/CD18 integrins and L-selectin on human neutrophils were studied by flow cytometry in a whole blood assay. None of these compounds had any effect on the basal expression of CD11b, CD11c, or L-selectin in the concentration range of 20-100 microM. However, linoleic acid at a concentration of 1000 microM slightly up-regulated CD11b and CD11c by a factor of 2.1 and 1.7, respectively. Linoleic acid, linoleic acid anilide, and arachidonic acid did not affect the formyl-methionyl-leucyl-phenylalanine induced up-regulation of CD11b or CD11c. However, linoleic acid and linoleic acid anilide slightly inhibited the phorbol myristate acetate (PMA)-induced expression of CD11b, which was decreased by 27 and 21% at concentrations of 100 and 1000 microM, respectively. Likewise, arachidonic acid at 40 microM inhibited the PMA-induced expression of CD11b by 19%. Our results suggest that linoleic acid, linoleic acid anilide, and arachidonic acid do not dramatically affect the expression of leukocyte adhesion molecules in a whole blood assay.

Anilides↗
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↗
PubMed1984

Some effects of the essential fatty acids linoleic acid and alpha-linolenic acid and of their metabolites gamma-linolenic acid, arachidonic acid, eicosapentaenoic acid, docosahexaenoic acid, and of prostaglandins A1 and E1 on the proliferation of human osteogenic sarcoma cells in culture.

Gamma-linolenic acid has been shown to suppress the rate of proliferation of a number of malignant cell lines in culture. To test the proposal that this was a specific prostaglandin 1- or 2-series effect, 379 batches of MG63 human osteogenic sarcoma cells were seeded in Greiner flasks and cultured in media supplemented with a range of unsaturated fatty acids and prostaglandins. The monounsaturated fatty acid oleic acid enhanced the rate of cancer cell proliferation. The polyunsaturated fatty acids linoleic acid, gamma-linolenic acid, arachidonic acid, alpha-linolenic acid, eicosapentaenoic acid and docosahexaenoic acid, as well as prostaglandins E1 and A1 suppressed the rate of cell proliferation. Total suppression of colony forming and cell proliferation occurred at high levels of polyunsaturated fatty acid supplementation. In addition gamma-linolenic in the form of evening primrose seed oil and vitamin C has been given to 6 patients with histologically diagnosed primary liver cell cancer. Some clinical improvement and reduction in tumor size occurred in 3 cases. One patient has shown remarkable improvement in reduction of liver and tumor size on the CAT scan and reduction of the serum alkaline phosphatase from 2830 to 295 units and gamma-glutamyl transaminase from 274 to 82 units. Thus preliminary clinical results suggest that gamma-linolenic acid may be effective in the management of human cancer patients and further trials should be conducted. However, the cell culture results suggest that although the essential fatty acids suppress proliferation, eicosanoids of all 3 series may be involved. The proliferation suppressive effect of docosahexaenoic acid suggests that other aspects than only eicosanoid activity may also be important in the suppression of cancer cell proliferation.

Alprostadil↗
PubMed1998

Pathophysiologic studies of experimental chronic pancreatitis in rats induced by injection of zein-oleic acid-linoleic acid solution into the pancreatic duct.

An experimental model of chronic pancreatitis was induced by a retrograde injection of a viscous solution consisting of zein-oleic acid-linoleic acid (0.05 ml/100 g body weight) into the rat pancreatic duct. Histologic and biochemical changes were investigated over a period of 6 months after induction of this model. The treated rats gained weight, but pancreatic weight decreased with time. Histologically, the widening of acinar lumen and cellular vacuolization occurred within 24 h at the parenchyma neighboring the small ducts filled with the injected solution. Degenerative parenchyma, interstitial edema, and inflammatory cell infiltration were pronounced 1 week later. Thereafter, duct-like tubular complex formation progressed, and the exocrine tissue exhibited marked atrophy of the gland with irregular fibrosis and fat replacement over a period of 6 months. Pancreatic contents of protein, amylase, DNA, and RNA markedly decreased, as did pancreatic weight, whereas hydroxyproline content increased. Oral administration of camostat did not affect pancreatic weight and contents of enzyme in this model. Urinary para-aminobenzoic acid (PABA) excretion in the BT-PABA test decreased to 54% at 6 weeks and 22% at 6 months. Although three quarters of pancreatic immunoreactive insulin (IRI) content was lost after 6 months, overt diabetes did not occur. The results suggest that an obstructive mechanism in the small ducts plays an important role in the genesis and development of chronic pancreatitis.

Amylases↗
PubMed2000

Effect of omega-6 polyunsaturated fatty acid (linoleic acid) on BRCA1 gene expression in MCF-7 cell line.

Dietary unsaturated fatty acids have been implicated in breast cancer. Since mutations in BRCA1 gene are known to predispose to breast cancers, and BRCA1 gene is known to be regulated by estradiol, the effect of linoleic acid, an omega-6-polyunsaturated fatty acid, with and without estradiol was studied for the expression of BRCA1 gene, in MCF-7 cell line, which has only one wild type allele. MCF-7 cells exposed to either linoleic acid or estradiol showed relatively greater number of colonies on soft agar, extent of proliferation and BRCA1 mRNA expression compared with controls. However, cells treated with both linoleic acid and estradiol showed significantly higher number of colonies, proliferation index and appreciably decreased expression of BRCA1 mRNA compared with controls or cells treated with linoleic acid or estradiol alone. The synergistic effects of these two agents were abrogated when indomethacin, an inhibitor of prostaglandin pathway, was added to the culture. From these observations it appears that diet rich in omega-6-polyunsaturated fatty acid like linoleic acid and endogenous estrogen may modulate BRCA1 gene expression thereby promoting breast cancer.

Agar↗
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↗
PubMed1996

Effects of superoxide dismutase and catalase on growth of retinal pigment epithelial cells in vitro following addition of linoleic acid or linoleic acid hydroperoxide.

The rod outer segments of the retina that are phagocytized by retinal pigment epithelial (RPE) cells are susceptible to lipid peroxidation because of their high content of polyunsaturated fatty acids. Linoleic hydroperoxides (LHP), synthesized by peroxidation of linoleic acids (LA), produce greater damage to retinal function than does LA. We compared the effects of LHP and LA on the growth of cultured chick embryonic RPE cells and analyzed a model of data sets using multiple linear regression for the number of cells as a function of time. The spectrum of LA had a sharp peak at 205 nm and a broad spectrum at 235 nm, while LHP had only a broad spectrum at 235 nm. Exposure to LA and LHP caused dose-dependent damage of chick embryonic RPE cells: they were significantly more affected by the addition of LHP than LA. The antioxidative enzymes catalase and superoxide dismutase minimized damage to the RPE cells caused by LHP in proportion to the enzyme concentration. However, RPE cells incubated with LA were more affected by the enzymes than when no enzymes were added.

Animals↗
PubMed1997

Conjugated linoleic acid and linoleic acid are distinctive modulators of mammary carcinogenesis.

Previous work by Ip and co-workers showed that mammary cancer prevention by conjugated linoleic acid (CLA) is independent of the level of fat in the diet. Because CLA is an isomer of linoleic acid, there is the question regarding whether the effect of CLA is due to a displacement of linoleic acid in cells. To further evaluate whether there might be an interaction between linoleic acid and CLA, the present study was designed to examine the dose response to CLA (at 0.5%, 1%, 1.5%, and 2%) in rats fed a 2% or a 12% linoleate diet (both basal diets contained 20% total fat by weight). The end points of investigation included the bioassay of mammary tumorigenesis in the rat dimethylbenz[a]anthracene model as well as the incorporation of CLA, linoleic acid, and arachidonic acid in mammary glands. The mammary carcinogenesis results showed that the efficacy of tumor suppression by CLA was not affected by linoleate intake. With either linoleate diet, no further protection was evident with levels of CLA > 1%. Analysis of neutral lipids and phospholipids of the mammary tissue indicated that 1) the accumulation of CLA in mammary tissue was dose dependent from 0.5% to 2%, 2) CLA concentration was 10 times higher in neutral lipids than in phospholipids, 3) the incorporation of CLA in either fraction was not affected by the availability of linoleic acid, and 4) CLA did not appear to displace linoleic acid or arachidonic acid in the mammary tissue. The above findings suggest that there may be distinctive mechanisms in the modulation of tumor development by linoleic acid and CLA.

9,10-Dimethyl-1,2-benzanthracene↗
PubMedDate not supplied

Proliferative responses of normal human mammary and MCF-7 breast cancer cells to linoleic acid, conjugated linoleic acid and eicosanoid synthesis inhibitors in culture.

Potential mechanisms for the stimulation or inhibition of cell growth by linoleic acid (LA) and conjugated linoleic acid (CLA) were investigated by using eicosanoid synthesis inhibitors. Normal human mammary epithelial cells (HMEC) and MCF-7 breast cancer cells were incubated in serum-free medium supplemented with LA or CLA and cyclooxygenase (indomethacin; INDO) or lipoxygenase (nordihydroguaiaretic acid; NDGA) inhibitors. Linoleic acid stimulated the growth and [3H]thymidine incorporation of normal HMEC and MCF-7 cancer cells, while CLA was inhibitory. Supplementation with LA increased intracellular lipid peroxide concentrations in normal HMEC and MCF-7 cancer cells, whereas CLA did not affect lipid peroxide formation. Normal HMEC and MCF-7 cells supplemented with LA and INDO or NDGA resulted in growth inhibition. The treatment of normal HMEC with CLA and INDO or NDGA, and MCF-7 cells with CLA and INDO stimulated cell growth. However, the addition of CLA and NDGA to MCF-7 cells resulted in synergistic growth suppression suggesting that CLA effects were mediated through lipoxygenase inhibition. Although NDGA was more inhibitory of cell growth in the presence of LA or CLA than INDO, growth was associated with both prostaglandin and leukotriene production. Additional studies are warranted to elucidate the mechanism(s) whereby LA or CLA affect breast cell growth.

Breast Neoplasms↗
PubMed1999

Effects of fluorescent light on growth of bovine retinal pigment epithelial cells in vitro incubated with linoleic acid or linoleic acid hydroperoxide.

Light-induced peroxidation of polyunsaturated fatty acids (PUFA) may generate lipid hydroperoxides, which may have toxic effects on retinal pigment epithelial (RPE) cells in vitro. We investigated the effects of cool-white fluorescent light on the RPE cells incubated with linoleic acids (LA) or linoleic acid hydroperoxides (LHP) and the influence of antioxidative enzymes. We measured the bovine RPE cell number after exposure to fluorescent light (610 and 1,200 lux) in the presence of LA or LHP. Furthermore, the effects of superoxide dismutase (SOD) and catalase on LA- or LHP-treated RPE cells were also examined. Both LA and LHP treatment increased RPE cell number under weak illumination (610 lux), but dose-dependently decreased the number of cells exposed to strong illumination (1,200 lux). With exposure to strong illumination, LA caused a greater reduction in RPE cell number than LHP. Multiple linear regression analysis showed that the number of RPE cells was significantly decreased in a manner dependent on the interactions of the illuminance of light and the concentrations of LA or LHP. The antioxidative enzymes significantly ameliorated the damage to RPE cells from LA or LHP and exposure to light. Therefore, the exposure to fluorescent light augmented the cytotoxic effects of LA and LHP on RPE cells, and this effect is likely to be mediated by reactive oxygen species.

Animals↗
PubMed1998

Changes in lipid peroxide level in retinal pigment epithelial cells in vitro upon addition of linoleic acids or linoleic acid hydroperoxides under varying concentrations of oxygen.

We previously observed the presence of autofluorescent lipofuscin or its like in retinal pigment epithelial (RPE) cells, which were incubated with linoleic acid hydroperoxides (LHP). We studied the effect of oxygen on the level of lipid peroxides in RPE cells in the presence of linoleic acids (LA) or LHP. The level of lipid peroxides in these cells was determined by use of the thiobarbituric acid-reactive substance (TBARS), which responded to oxygen concentrations qualitatively, and a linear regression analysis. Multiple linear regression analysis disclosed that treatment with LA for 24 hr resulted in detectable increase in the level of TBARS in the cells, whereas treatment with LA or LHP for 48 hr caused detectable decrease. Stepwise linear regression analysis showed that the level of TBARS decreased in an oxygen-tension dependent manner in the cells incubated with LA for 48 hr. Thus, it was shown that short-term incubation with LA increased the level of TBARS in the cells and that LA decreased its level in an oxygen-tension dependent manner. For these results, the postulation was made that the prolonged auto-oxidation of LA caused production of lipofuscin-like materials, a complex of lipid peroxides and proteins that were insoluble in SDS and acetic acid solution.

Animals↗