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PubMed1986

Inhibition of human colonic (Na+ + K+)-ATPase by arachidonic and linoleic acid.

The sodium pump, (Na+ + K+)-ATPase, which is involved in the transport of cations and water movement by the colonic mucosa, may be decreased in various diarrhoeal states. In this study, we have measured 3H-ouabain binding and (Na+ + K+)-ATPase activity in human colonic biopsy homogenates and the influence of various inflammatory and antiinflammatory compounds on these parameters. 3H-ouabain binds to one site of high affinity (KD 1.9 +/- 0.2 X 10(-9) mol/l) with a maximal binding capacity of 7.5 +/- 0.8 X 10(14) binding sites/g protein. Both arachidonic and linoleic acid inhibited (Na+ + K+)-ATPase activity (IC50 arachidonic acid: 7.5 X 10(-5) mol/l, linoleic acid: 6.5 X 10(-5) mol/l) and Mg2+-ATPase activity (IC50 arachidonic acid: 9 X 10(-5) mol/l, linoleic acid: 4 X 10(-5) mol/l). Arachidonic acid inhibited 3H-ouabain binding, (IC50 3.2 X 10(-5) mol/l). The following antiinflammatory compounds, at concentrations up to 1 X 10(-3) mol/l, did not influence ATPase activity directly nor reverse the arachidonic acid-induced inhibition: indomethacin (cyclooxygenase inhibitor), nordihydroguaiaretic acid (lipoxygenase inhibitor), sulphasalazine and its metabolites: 5-aminosalicylic acid, N-acetylaminosalicylic acid and sulphapyridine. These results indicate that human colonic (Na+ + K+)-ATPase is inhibited by the prostanoid precursors, arachidonic and linoleic acid. From a therapeutic point of view (effect on colonic (Na+ + K+)-ATPase and perhaps diarrhoea), the suppression of the production of these prostanoid precursors by drugs may, therefore, be beneficial in the treatment of inflammatory bowel disease.

Anti-Inflammatory Agents↗
PubMed2005

Reduction in voltage-gated K+ currents in primary cultured rat pancreatic beta-cells by linoleic acids.

Free fatty acids (FFAs), in addition to glucose, have been shown to stimulate insulin release through the G protein-coupled receptor (GPCR)40 receptor in pancreatic beta-cells. Intracellular free calcium concentration ([Ca(2+)](i)) in beta-cells is elevated by FFAs, although the mechanism underlying the [Ca(2+)](i) increase is still unknown. In this study, we investigated the action of linoleic acid on voltage-gated K(+) currents. Nystatin-perforated recordings were performed on identified rat beta-cells. In the presence of nifedipine, tetrodotoxin, and tolbutamide, voltage-gated K(+) currents were observed. The transient current represents less than 5%, whereas the delayed rectifier current comprises more than 95%, of the total K(+) currents. A long-chain unsaturated FFA, linoleic acid (10 microm), reversibly decreased the amplitude of K(+) currents (to less than 10%). This reduction was abolished by the cAMP/protein kinase A system inhibitors H89 (1 microm) and Rp-cAMP (10 microm) but was not affected by protein kinase C inhibitor. In addition, forskolin and 8'-bromo-cAMP induced a similar reduction in the K(+) current as that evoked by linoleic acid. Insulin secretion and cAMP accumulation in beta-cells were also increased by linoleic acid. Methyl linoleate, which has a similar structure to linoleic acid but no binding affinity to GPR40, did not change K(+) currents. Treatment of cultured cells with GPR40-specific small interfering RNA significantly reduced the decrease in K(+) current induced by linoleic acid, whereas the cAMP-induced reduction of K(+) current was not affected. We conclude that linoleic acid reduces the voltage-gated K(+) current in rat beta-cells through GPR40 and the cAMP-protein kinase A system, leading to an increase in [Ca(2+)](i) and insulin secretion.

Animals↗
PubMed1990

Metabolism of linoleic acid in porcine epidermis.

The time course of linoleic acid metabolism in porcine epidermis has been studied in order to better evaluate the lipid transformations that accompany differentiation in this tissue. One day after intradermal injection of [U-14C]linoleic acid, most of the radioactivity in the epidermis was associated with phospholipids, triglycerides, and free fatty acids. Within 3-7 days, a portion of the radiolabel was selectively transferred to acylglucosylceramide and acylceramide fractions, after which the specific activities of all lipids fractions decreased. The results suggest that neither the lipoxygenation of linoleate nor the hydrolysis of acylceramide to form acylacid and free sphingosine are major routes of linoleate metabolism in normal epidermis. The principal pathway of linoleate metabolism in normal epidermis appears to be transfer from phospholipids to acylglucosylceramide to acylceramide. The triglyceride fraction, although minor in amount, attains an initially high specific activity, and may serve as an intermediate in linoleate transfer.

Animals↗
PubMed1988

Prostacyclin biosynthesis by cultured human myometrial smooth muscle cells: dependency on arachidonic or linoleic acid in the culture medium.

Myometrial smooth muscle cells in culture were incubated for 18 hours in medium that contained serum (10%); under these conditions, there was a six to 26-fold increase in the amount of 6-keto-prostaglandin F1 alpha that accumulated in the medium (i.e., prostacyclin production) compared with that present after incubation in serum-free medium. In serum-free and serum-containing media, treatment of these cells with dexamethasone (10(-8) mol/L) or cortisol (10(-7) mol/L) suppressed the biosynthesis of prostacyclin by approximately 80% and 64%, respectively. Arachidonic acid (bound to fatty acid-free human serum albumin) added to serum-free medium caused a concentration-dependent increase in the production of prostacyclin by myometrial cells. Arachidonic acid was maximally effective at a concentration of 10(-5) mol/L and caused a five- to 28-fold increase in the biosynthesis and secretion of prostacyclin. Linoleic acid (bound to albumin) in serum-free medium also caused a concentration-dependent increase in the production of prostacyclin; however, the amount of prostacyclin produced in the presence of linoleic acid was lower than that produced in the presence of an equimolar concentration of arachidonic acid. In the presence of arachidonic (10(-5) mol/L) or linoleic acids (10(-4) mol/L) in serum-free medium, the addition of dexamethasone (10(-8) mol/L) or cortisol (10(-7) mol/L) suppressed but did not inhibit completely prostacyclin production. These findings are indicative that arachidonic and linoleic acids in the culture medium support prostacyclin biosynthesis by human myometrial smooth muscle cells. The inhibition of prostacyclin production by glucocorticosteroids in the absence or presence of extracellular arachidonic (or linoleic) acid may be caused by inhibition of phospholipase A2 activity.

6-Ketoprostaglandin F1 alpha↗
PubMed1981

A study of oxygen isotope scrambling in the enzymic and non-enzymic oxidation of linoleic acid.

Lipoxygenases-1 and -2 isolated from soybeans were incubated with linoleic acid in the presence of a mixture of 16O2 and 18O2. The formation of 16O/18O-molecules which is indicative for a head-to head reaction of peroxy radicals was determined and compared with that produced during autoxidation of a linoleic acid emulsion in the presence of ferric ions. Lipoxygenase-1 was much less active in scrambling than lipoxygenase-2 which was comparable to that found in the autoxidation reaction.

Isoenzymes↗
PubMed1975

The role of plant particles, bacteria and cell-free supernatant fractions of rumen contents in the hydrolysis of trilinolein and the subsequent hydrogenation of linoleic acid.

The role of different fractions of rumen contents in the hydrolysis of trilinolein and the subsequent hydrogenation of the linoleic acid has been investigated by a series of in vitro incubations. Hydrolysis of the trilinolein to free linoleic acid occurs almost wholly in the cell-free supernatant; the liberated linoleic acid in the supernatant can be rapidly adsorbed onto food particles where it is hydrogenated to stearic acid via the C18 trans-11 monoene. Some 25% of the trilinolein added as substrate was taken up by the bacteria and of this a small percentage appeared to be hydrolysed and the free linoleic acid hydrogenated to stearic acid intracellularly. No conclusive evidence was obtained to suggest that this intracellular hydrogenation proceeded by a route other than that which took place on the food particles.

Animals↗
PubMed1990

Effect of a vegetable oil formula rich in linoleic acid on tissue fatty acid accretion in the brain, liver, plasma, and erythrocytes of infant piglets.

The effect of feeding sow-milk formula (SMF) or a vegetable-oil infant formula (FF) with minimal n-6 and n-3 long-chain polyenoic fatty acids (LCPs) but high linoleic acid (18:2n-6) and a high ratio of 18:2n-6 to linolenic acid (18:3n-3) on the fatty acids of brain lipid and liver, plasma, and red cell phospholipids was studied in piglets fed from birth for 5, 10, 15, or 25 d. Compared with SMF, FF reduced the concentrations of 18:1 and n-3 LCPs, especially 22:6n-3, in all tissues and increased 22:4n-6 in brain, liver, plasma, and red cell phosphatidylethanolamine. FF also increased 22:5n-6 in brain lipid, liver, and plasma but not in red cell phospholipids. Thus, changes in tissues capable of in situ desaturation were not completely reflected in the red cell phospholipids. The increased liver and brain n-6 LCP accretion in the FF piglets may suggest competent desaturation and possible inhibition of n-3 desaturation and/or acylation by dietary n-6 fatty acids.

Animals↗
PubMed2003

Effects of abomasal infusion of conjugated linoleic acid on milk fat concentration and yield from pasture-fed dairy cows.

The aim of this study was to investigate the effects of conjugated linoleic acid supplementation on the synthesis of milk fat in pasture-fed Friesian cows. In four cows, a commercial mixture containing 62.3% (wt/vol) conjugated linoleic acid was infused intraabomasally to avoid rumen fermentation and biohydrogenation. The design was a 4 x 4 Latin square in which each cow received infusions of 0, 20, 40, and 80 g/d of conjugated linoleic acid mixture for 4 d. Cows were fed freshly cut ryegrass/white clover pasture ad libitum. Milk fat concentration was decreased by 36, 43, and 62% and milk fat yield was decreased by 32, 36, and 60% by the 20, 40, and 80 g of conjugated linoleic acid/d treatments. Dry matter intake, milk protein concentration, and protein yield were unaffected by treatments; however, milk yield was increased by 11% during the 40-g conjugated linoleic acid/d treatment. The effects of conjugated linoleic acid infusion were most pronounced in reducing de novo fatty acid synthesis and desaturation. Results show that the inhibitory effect of this conjugated linoleic acid mixture on milk fat synthesis occurs in pasture-fed cows, and demonstrate the potential to dramatically alter gross milk composition. This technology could offer a management tool to manipulate milk composition and energy demands of pasture-fed cows.

Abomasum↗
PubMed1975

Myocardial uptake of labeled oleic and linoleic acids.

Oleic acid labeled with 14C, (14C-OA) or 131I (131I-OA) and 131I-labeled linoleic acid (131I-LOA) were administered intravenously to rats and tissue distribution studies completed at various time intervals from 5 to 60 min. Tissue distribution of 131-I-labeled oleic acid or linoleic acid was also studied in dogs at 5- and 30-min time intervals after intravenous administration of the tracer dose. There were distinct differences in the patterns of tissue distribution between 14C-OA, 131I-OA, and 131I-LOA. Radioactivity concentration in the myocardium was the highest at all time intervals in the rats given 131I-OA only. In dogs, the myocardial uptake of 131I-OA was significantly higher than the radioactivity in the blood or other tissues at 30 min after injection. The disappearance rates of 131I-OA and 131I-LOA were almost identical but myocardial concentration of 131I-LOA at 30 min after the dose in the dog was half that of 131I-OA whereas 131I-LOA liver concentration was higher than that of 131I-OA. Since the concentrations of our formulated 131I-OA in the blood and in the myocardium are both highest at the earlier intervals, it should be difficult to detect myocardial ischemia or infarction with 131I-OA scanning.

Animals↗
PubMedDate not supplied

Aldrin epoxidation. Catalytic potential of lipoxygenase coupled with linoleic acid oxidation.

Epoxidation of aldrin was studied using highly purified soybean lipoxygenase in the presence of linoleic acid. Dieldrin, the primary stable reaction product, was quantified by electron-capture gas chromatography. The oxidation of aldrin to dieldrin was dependent on the concentration of linoleic acid, aldrin, and enzyme. The epoxidation was linear with time and exhibited a pH optimum of 7.4. The optimal conditions to observe maximum enzyme velocity included the presence of 0.25 mM linoleic acid, 200 microM aldrin, and 20 nM enzyme. Lipoxygenase inhibitors nordihydroguaiaretic acid, phenidone, 5,8,11-eicosatriynoic acid, and 5,8,11,14-eicosatetraynoic acid significantly inhibited epoxidation in a dose-dependent manner. Catalytic potential of lipoxygenase as expressed in terms of its turnover numbers was approximately 4.0 nmol/min/nmol of enzyme, and it appears that lipoxygenase is up to 20 times a better catalyst of aldrin epoxidation than cytochrome P-450. These results suggest that lipoxygenase, which is widely distributed in plants and animals, may represent yet another important pathway for epoxidation of aldrin.

Aldrin↗
PubMed1988

Effect of varying concentrations of linoleic acid on alpha-adrenoceptor responses in spontaneously hypertensive rats.

The effect of increased intake of linoleic acid on the alpha-adrenergic system was assessed by safflower oil supplementation to spontaneously hypertensive rats. Linoleic acid-enriched intake at 5%, 15% and 30% by weight of total food intake for 12 wk was associated with a reduction in resting arterial blood pressure, while heart rate and heart to body weight ratios were similar to control group values. A dose-response analysis to norepinephrine bitartrate administered intravenously indicated a significant reduction in the vascular reactivity to this alpha-adrenergic agonist in all groups given linoleic acid. Direct assessment of alpha-adrenoceptor number (Bmax) and affinity (KD) in cardiac sarcolemma with [3H]-prazosin indicated that receptor binding properties were not affected by linoleic acid intake. Our results suggest that short-term linoleic acid supplementation in the established hypertensive state may lower blood pressure through effects upon alpha-adrenergic reactivity in vascular tissue, without associated effects in cardiac tissue.

Animals↗
PubMed1992

Dietary arachidonic and linoleic acids: comparative effects on tissue lipids.

The effects of preformed dietary arachidonic acid (AA, 20:4n-6) on murine phospholipid fatty acid composition in tissues capable (liver) and incapable (peritoneal exudate cells, PEC) of desaturating and elongating linoleic acid (LA, 18:2n-6) to AA were investigated. The results were compared with those obtained on matched animals on LA diets by either substituting or supplementing dietary LA with AA. Modest amounts of AA ethyl ester (0.5 wt%) included in the diet significantly increased tissue phospholipid AA levels by 39% and 57% in the liver and in PEC, respectively. The changes were further enhanced when dietary LA and AA intakes were equivalent, i.e., 57% and 68% in liver and PEC, respectively. This enrichment was observed in all phospholipid classes analyzed, with the greatest impact on phosphatidylcholine. In addition, the doubling of dietary LA had little effect on tissue phospholipid AA levels. The data suggest that while the level of n-6 PUFA may have an important effect on tissue fatty acid composition, the type of n-6 PUFA in the diet could be of greater significance.

Animals↗
PubMedDate not supplied

[Effect of dietary linoleic acid on the platelet aggregation, fatty acid composition of platelet phospholipids and synthesis of platelet prostaglandins in rats].

Three groups of Wistar-Kyoto rats were kept on diets containing different quantity of linoleic acid (LA) in prenatal and postnatal periods up to 18 weeks age: I. less than 0.1 cal.% of LA, 2. 9.0 cal.% of LA and 3. 16 cal.% of LA. Aggregation of washed platelets with ADP and A23187, biosynthesis of prostaglandins from 14C-arachidonic acid in platelets and fatty acid composition of platelet phospholipids were studied using gas liquid chromatography. Modification of fatty acid composition of platelet phospholipids and changes in biosynthesis of platelet prostaglandins are the base for proaggregation effect of LA deficient and for antiaggregation effect of LA enriched diets. The effects of dietary LA were mediated not only via altered metabolism of fatty acids of linoleic family but also via metabolism of fatty acids of oleic and linolenic series.

Animals↗
PubMed1976

Co-oxydation of a carotenoid by the enzyme lipoxygenase: influence on the formation of linoleic acid hydroperoxides.

A partially purified soybean lipoxygenase (L-3) was incubated for 15 min at pH 6.5 with linoleic acid and oxygen. Systems with and without the polyene glycoside crocin were compared. The system with crocin reacted with higher velocity with oxygen than did the control experiment without polyene. From the crocin 40% was destroyed. In the presence of crocin about 40% more linoleic acid hydroperoxides was formed than without the polyene but the linoleic acid break-down was equal in both experiments. L-3 peroxidises linoleic acid to 13L:13D:9L:9D-hydroperoxides in the proportions 43:11:21:25. In the presence of crocin the ratio of the isomers changed to 64:11:11:14.

Carotenoids↗
PubMed2005

Development of conjugated linoleic acid (CLA)-mediated lipoatrophic syndrome in the mouse.

Conjugated linoleic acids (CLA) are positional and geometric dienoic isomers of linoleic acid. Dietary CLA supplementation leads to a drop in fat mass in various species, including in humans. The t10,c12-CLA isomer is responsible for this anti-obesity effect. The reduction of fat mass is especially dramatic in the mouse, in which it is associated with severe hyperinsulinemia, insulin resistance and massive liver steatosis. The origin of these adverse side effects and putative chronology of events leading to CLA-mediated lipoatrophic syndrome are presented and discussed in this review.

Adipose Tissue↗
PubMed1983

Formation of diacylglycerol and degradation of phosphatidylinositol induced in rat lymphocytes by non-esterified oleic or linoleic acid.

Rat spleen lymphocytes were incubated for 3 h with [14C]arachidonic acid in foetal calf serum. It was found that arachidonic acid distributed into phospholipids in the order phosphatidylcholine greater than phosphatidylethanolamine greater than phosphatidylinositol. After labelling with arachidonic acid the lymphocytes were washed, and incubated for up to 2 h with non-radioactive palmitic, oleic or linoleic acid dissolved in ethanol. The presence of ethanol or palmitic acid during a 2 h post-incubation had little effect on the amount of radioactivity found in different lipid fractions. Both oleic acid and linoleic acid, however, brought about an accumulation (up to 8-fold) of radioactivity in the diacylglycerol fraction. These fatty acids also brought about a change of radioactivity in several phospholipids, notably in phosphatidylinositol, which lost more than 50% of its counts during the 2 h incubation. Although maximum effects were seen at 2 h, diacylglycerol radioactivity was increased by 100% within 5 min after adding the fatty acids. The minimum concentration of fatty acids used (50 microM) gave an almost maximum response. The results indicate that unsaturated fatty acids may activate phosphatidylinositol phosphodiesterase in lymphocytes, as they do in brain. The possibility that a phospholipase A is activated is discussed. Possible implications for any experiments in which cells are incubated with fatty acids are pointed out.

Animals↗
PubMed2002

Linoleic acid metabolites act to increase contractility in isolated rat heart.

Previous in vivo studies in dogs suggest that the 9,10-monoepoxide of linoleic acid (9,10-cis-epoxyoctadecenoic acid [9,10-EOA]) has toxic cardiovascular effects that result in death at higher doses. More recent work with rabbit renal proximal tubule cells suggests that the 12,13-metabolites of linoleic acid are more toxic than the 9,10-isomers. Thus, in the current study, we tested the hypothesis that 12,13-EOA and 12,13-dihydroxyoctadecadienoic acid (12,13-DHOA) have direct adverse effects on the heart. Langendorff-perfused rat hearts were exposed to 30 microM linoleic acid, 30 microM 12,13-EOA, or 30 microM 12,13-DHOA for 60 min followed by a 30-min recovery period. As indicated by peak left intraventricular pressure and/or +dP/dt(max), all three of the agents elicited moderate increases in contractile function that peaked within 10 20 min. The effects of linoleic acid and 12,13-EOA returned to control values during the remainder of the 60-min exposure, whereas the positive inotropic response to 12,13-DHOA was maintained until washout. Sustained arrhythmias and negative inotropic actions were not observed with any of the three compounds. Subsequently, the monoepoxides were infused into conscious rats (35 mg/kg/h) while blood pressure, heart rate, and EKG were monitored for 24 h using biotelemetry techniques. The only effect observed was a slight decline in blood pressure. Thus, current data suggest that linoleic acid and its oxidative metabolites do not have direct cardiotoxic effects during acute exposure.

Animals↗
PubMed1976

[Investigations on the development of volatile substances during lipoxygenase-linolic-acid-reaction (author's transl)].

During incubation of soja-lipoxygenase with linolic acid, volatile compounds are formed the development of which can be seen in two possible ways:from preformed linolic-acid-hydroperoxides splitproducts arise or volatile substances of different chemical nature are built depending on the reaction conditions like temperature, O2-pressue, partner-concentration etc. By trials with hydroperoxyde-decomposing enzymes (peroxidase) and by means of radio-active labelled linolic-acid-hydroperoxides the pathways mentioned above were investigated. The results indicate that the volatile compounds are built from by-products; n-hexanal was formed from these by-products as well as from decomposed hydroperoxide. The previously proposed reaction-scheme has this been ascertained by experimental means.

Chemical Phenomena↗