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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↗
PubMed2001

Inhibitory effect of conjugated linoleic acid on linoleic acid elongation in transformed yeast with human elongase.

Conjugated linoleic acid (CLA; 18:2) refers to a group of positional and geometric isomers derived from linoleic acid (LA; delta9,12-18:2). Using a growing baker's yeast (Saccharomyces cerevisiae) transformed with human elongase gene, we examined the inhibitory effect of CLA at various concentrations (10, 25, 50, and 100 microM) on elongation of LA (25 microM) to eicosadienoic acid (EDA; delta11,14-20:2). Among four available individual CLA isomers, only c9,t11- and t10,c12-isomers inhibited elongation of LA to EDA. The extent of inhibition (ranging from 20 to 60%) was related to the concentration of CLA added to the medium. In the meantime, only these two isomers, when added at 50 microM to the media, were elongated to conjugated FDA (c11,t13- and t12,c14-20:2) by the same recombinant elongase at the rate of 28 and 24%, respectively. The inhibitory effect of CLA on LA elongation is possibly due to competition between CLA isomers and LA for the recombinant elongase. Thus, results from this study and a previous study suggest that the biological effect of CLA is exerted through its inhibitory effect on delta6-desaturation as well as elongation of LA which results in a decrease in long-chain n-6 fatty acids and consequently the eicosanoid synthesis.

Acetyltransferases↗
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↗
PubMed1996

Comparative effects of linoleic acid and linoleic acid hydroperoxide on growth and morphology of bovine retinal pigment epithelial cells in vitro.

PURPOSE: Outer segments of the photoreceptor rods that are phagocytized by the retinal pigment epithelial (RPE) cells contain a high proportion of polyunsaturated fatty acids (PUFA). PUFA are susceptible to lipid peroxidation. We hypothesized that the resulting peroxides could injure RPE cells leading to retinal degeneration. Accordingly, we compared the effects of linoleic acid (LA) and its hydroperoxide (LHP) on the growth and morphology of RPE cells using laser scanning microscopy and transmission microscopy. METHODS: We counted the number of RPE cells after incubation for 24 and 48 hrs with concentrations of LA or LHP of 0.035, 0.175, and 0.35 mM. To observe the actin filaments, cultured RPE cells were stained with rhodamine phalloidin. The cells were prefixed with 2% glutaraldehyde and postfixed in 1% osmium tetroxide. Specimens were embedded in Epon 812 after dehydration, and the ultrathin sections were doubly stained with 2% uranyl acetate and 2% lead acetate for examination by transmission electron microscopy. RESULTS: Exposure to LA or LHP produced dose-dependent damage to RPE cells with a significantly greater effects of LHP than LA. After incubation for 24 hrs with 0.35 mM LA, the number of vacuoles in RPE cells exceeded that observed in control RPE cells by 365 nm laser microscopy. Exposure to 0.35 mM LHP for 24 hrs produced a pycnotic nucleus, with diffuse and granular autofluorescences observed in and around it. Exposure of RPE cells to 0.35 mM LA for 24 hrs showed that the LA incorporated into the lysosomes was digested and released extracellularly from lysosomes via exocytotic vesicles. However, such exposure to LHP damaged the RPE cells, including the membranes in the pinocytotic vesicles. The packed membranes resembled myelin. CONCLUSIONS: While the LA incorporated into the lysosomes was released extracellularly, LHP persisted in the RPE cells, being observed as autofluorescent lipofuscin-like materials. LHP was cytotoxic, and caused damage to the membranes of pinocytotic vesicles and lysosomes.

Animals↗
PubMed1997

Myoglobin-catalyzed bis-allylic hydroxylation and epoxidation of linoleic acid.

Linoleic acid was treated with metmyoglobin and cumene hydroperoxide at 0 degrees C under anaerobic conditions. Five major compounds were identified, i.e., 11-hydroxylinoleic acid (29% yield), cis-9,10-epoxy-(12Z)-octadecenoic acid (16%), cis-12,13-epoxy-(9Z)-octadecenoic acid (8%), 9-hydroxy-(10E,12Z)-octadecadienoic acid (4%), and 13-hydroxy-(9Z,11E)-octadecadienoic acid (4%). Steric analysis showed that these compounds were all racemic. The steric course of the formation of the major metabolite, (11R,S)-hydroxylinoleic acid, was studied by incubation of linoleic acids stereospecifically deuterated at C-11. It was found that the (11R)-hydroxylinoleic acid lost most of the deuterium label when formed from [(11R)-2H]linoleic acid but retained the label when formed from [(11S)-2H]linoleic acid. Furthermore, the (11S)-hydroxylinoleic acid retained and lost most of the label when produced from [(11R)-2H]- and [(11S)-2H]linoleic acids, respectively. Thus, although the myoglobin-promoted hydroxylation of linoleic acid into 11-hydroxylinoleic acid lacked apparent stereospecificity and produced equal amounts of the R and S enantiomers, the course of the reaction was stereospecific and involved hydrogen abstraction and oxygen insertion occurring with retention of absolute configuration of the carbon atom hydroxylated.

Benzene Derivatives↗
PubMed1995

Do trans fatty acids impair linoleic acid metabolism in children?

Trans isomeric fatty acids disturb the metabolism of essential polyunsaturated fatty acids in animals and in premature infants. We assessed whether similar effects may also occur in healthy children. Plasma phospholipid fatty acid composition was analysed in 53 apparently healthy children aged 1-15 years (mean 7.5 years). Trans fatty acids were found in all samples and contributed 1.78 +/- 0.10% (w/w, mean +/- SEM). There was no relation of the major trans isomer octadecenoic acid and of total trans fatty acids to the precursor essential fatty acid linoleic acid. In contrast, we found significant inverse correlations of trans octadecenoic acid and total trans isomers to the principal n-6 metabolite arachidonic acid as well as to the sum of all n-6 metabolites. Furthermore, there was an inverse correlation of total trans fatty acids to the ratio of arachidonic to linoleic acid, an indirect indicator of linoleic acid conversion. These findings are compatible with inhibition of arachidonic acid biosynthesis by trans fatty acids. Since the availability of long-chain polyunsaturated fatty acids, including arachidonic acid, is of essential importance for tissue growth and development, these findings question the safety of high dietary trans fatty acid intakes in childhood.

Adolescent↗
PubMed1983

Inability of rabbit peritoneal polymorphonuclear leukocytes to synthesize arachidonic acid from linoleic acid.

In PMN leukocytes isolated from rabbit peritoneal exudate the major phospholipids were choline phosphoglycerides (40%), ethanolamine phosphoglycerides (26%) and sphingomyelin (20%) with lesser amounts (3-6%) of serine and inositol phosphoglycerides. The essential fatty acid, linoleic acid, predominated (greater than 35%) in each phospholipid except in inositol phosphoglycerides where it was slightly less than arachidonate and in sphingomyelin where saturated acids predominated. However, on a total mass basis there was more arachidonate in ethanolamine and choline phosphoglycerides than in inositol phosphoglycerides. The uptake, incorporation and metabolism of [1-14C] fatty acids of varying chain length and degrees of unsaturation were examined. All fatty acids were taken up but incorporation of saturated acids varied inversely with chain length. Arachidic acid and trans-isomers of 18:1 and 18:2 were esterified primarily to triacylglycerol whereas phospholipids contained a large portion of the other acids. Icosatrienoic and arachidonic acids were esterified to ethanolamine, serine and inositol phosphoglycerides to a comparatively greater extent, reflecting the normal distribution of these fatty acids. PMN leukocytes had a low capacity for delta 9 desaturation and chain elongation and no delta 6 or delta 5 desaturation could be detected. Thus, PMN leukocytes lack the ability to form arachidonate from 18:2 precursor molecules available in the cellular neutral lipids and phospholipids and arachidonate per se is an essential fatty acid for these cells.

Animals↗
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↗
PubMed1980

Inhibition of platelet phospholipase-A2 as a mechanism for the anti-aggregating effect of linoleic acid.

Linoleic acid was incorporated into platelet phospholipids and then released after activation of phospholipase A2 (PL-A2) with thrombin or ionophore A23187. The rate of this release was tenfold lower for linoleic than for arachidonic acid. This observation strongly suggests that incorporation of linoleic acid in platelet phospholipids might inhibit platelet PL-A2 and might explain the anti-aggregating effect of linoelic acid. In fact it has also been shown that linoleic acid inhibits PL-A2 activity at concentrations which antagonize platelet aggregation. Moreover, in experimental conditions where platelet cyclo-oxygenase is totally inhibited, aggregation does occur and can still be blocked by linoleic acid. This latter observation led to the conclusion that the anti-aggregating effect of linoleic acid is independent from prostaglandin pathway and is probably related to the phospholipid metabolism.

Animals↗
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↗
PubMed2000

Effects of dietary conjugated linoleic acid and linoleic:linolenic acid ratio on polyunsaturated fatty acid status in laying hens.

A study was conducted to determine the effects of dietary conjugated linoleic acid (CLA) and the ratio of linoleic:linolenic acid on long-chain polyunsaturated fatty acid status. Thirty-two 31-wk-old White Leghorn hens were randomly assigned to four diets containing 8.2% soy oil, 4.1% soy oil + 2.5% CLA (4.1% CLA source), 4.1% flax oil + 2.5% CLA, or 4.1% soy oil + 4.1% flax oil. Hens were fed the diets for 3 wk before eggs and tissues were collected for the study. Lipids were extracted from egg yolk and tissues, classes of egg yolk lipids were separated, and fatty acid concentrations of total lipids, triglyceride, phosphatidylethanolamine, and phosphatidylcholine were analyzed by gas chromatography. The concentrations of monounsaturated fatty acids and non-CLA polyunsaturated fatty acids were reduced after CLA feeding. The amount of arachidonic acid was decreased after CLA feeding in linoleic acid- and linolenic acid-rich diets, but amounts of eicosapentaenoic acid and docosahexaenoic acid were increased in the linolenic-rich diet, indicating that the synthesis or deposition of long-chain n-3 fatty acids was accelerated after CLA feeding. The increased docosahexaenoic acid and eicosapentaenoic acid contents in lipid may be compensation for the decreased arachidonic acid content. Dietary supplementation of linoleic acid increased n-6 fatty acid levels in lipids, whereas linolenic acid increased n-3 fatty acid levels. Results also suggest that CLA might not be elongated to synthesize long-chain fatty acids in significant amounts. The effect of CLA in reducing the level of n-6 fatty acids and promoting the level of n-3 fatty acids could be related to the biological effects of CLA.

Animal Nutritional Physiological Phenomena↗
PubMed2004

Comparative toxicity of oleic acid and linoleic acid on Jurkat cells.

BACKGROUND: Lipid emulsions for parenteral nutrition commercially available are mainly composed of long-chain triacylglycerol containing a high proportion of alpha-6 polyunsaturated fatty acids or alpha-9 monounsaturated fatty acids. The immunological impact of such therapy is particularly important because parenteral and enteral diets are often administered to critical ill patients. The comparative toxicity of oleic acid and linoleic acid on Jurkat cells, a human T lymphocyte cell line, and the type of cell death induced by these fatty acids were determined. METHODS: Cell death was investigated by cytometry: decrease in cell volume, increase of granularity, DNA fragmentation, phosphatidylserine externalization, mitochondrial depolarization, lipid accumulation; by fluorescence microscopy: chromatin condensation and acridine orange/ethidium bromide assay; and by RT-PCR: mRNA expression of apoptotic genes. RESULTS: Evidence is presented herein that oleic acid is much less toxic to Jurkat cells than linoleic acid. Both fatty acids promote apoptosis and necrosis of these cells. The mechanism of cell death induced by these fatty acids seem to involve with mitochondrial depolarization, lipid accumulation and the levels of C-MYC and P53 mRNA expression. CONCLUSION: Therefore, oleic acid may offer an immunological less harmful alternative to linoleic acid for parenteral and enteral diets preparation.

Apoptosis↗
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↗