Sodium Linoleate Research Articles

The effect of fatty acid addition in vitro on direct migration inhibition with paramyxoviral antigens

Sodium linoleate was found to significantly decrease direct migration inhibition (DMI) of leukocytes taken from healthy subjects that displayed a vigorous DMI response to paramyxoviral antigens (measles and parainfluenza Type 1) and to increase reactivity of leukocytes from subjects with poor response to these antigens. Similar effects were found with sodium arachidonate, PGE 1, and PGE 2, but not with sodium oleate. Linoleate was found to exert its effects through its conversion to prostaglandins by a nonglass-adherent mononuclear subpopulation of the white blood cells.

A possible role for elastin ligands in the proteolytic degradation of arterial elastic lamellae in the rabbit.

Thoracic aortae of normal rabbits were perfused with pancreatic elastase in vitro at 37 degrees C and 70 mm Hg pressure in the presence or absence of elastin ligands previously shown to stimulate or inhibit the enzymatic degradation of elastin. Perfusion with elastase results in an average of 3.6 lamellae degraded, whereas addition of sodium linoleate before and during the perfusion with elastase increases this value to 7.9 (P less than 0.001). Conversely, perfusion with the cationic detergent, dodecyltrimethylammonium chloride, completely prevents the degradation of elastic lamellae by elastase. These effects do not reflect alterations of the intrinsic catalytic activity of elastase, but apparently indicate the formation of complexes between the elastin ligands and arterial elastic lamellae, as is consistent with prior studies indicating such interactions between fatty acids or detergents and purified elastin. These studies suggest that agents such as fatty acids may significantly alter the metabolic susceptibility of elastin in vivo and possibly contribute to the degradation of elastic lamellae seen in arteries with advanced atherosclerosis.

Pulse Radiolysis Studies in Model Lipid Systems. The Influence of Aggregation on Kinetic Behavior of OH Induced Radicals in Aqueous Sodium Linoleate

AbstractThe kinetic and spectral behavior of radicals formed by hydroxyl radical attack on linoleate anions has been studied by pulse radiolysis. Reactivity of ·OH toward this surfactant is an order of magnitude greater in monomeric form [k·OH+linoleate= 8.0 ± 109M−1sec−1] than in micellar form [k·OH+lin(micelle)= 1.0 ± 109M−1sec−1]. Abstraction of a hydrogen atom from the doubly allylic position gives rise to an intense absorption in the UV region (δmax= 282–286 nm, ε 3·104M−1cm−1) which may be used as a probe of radical activity at that site. This abstraction may occur, to a small extent, directly via ·OH attack. However, greater than 90% of initial attack occurs at other sites. Subsequent secondary abstraction of doubly allylic H atoms appears to occur predominantly by: (1) intramolecular processes in monomers, (2) intermolecular processes in micelles. Disappearance of radicals by secondary processes is slower in the micellar pseudo phase than in monomeric solution.

Brain edema: induction in cortical slices by polyunsaturated fatty acids.

The presence of polyunsaturated and saturated fatty acids in leukocytic membranes prompted study of their possible role in the induction of brain edema. Polyunsaturated fatty acids including sodium arachidonate, sodium linoleate, sodium linolenate, and docasahexaenoic acids induced edma in slices of rat brain cortex. This cellular edema was specific, since neither saturated fatty acids nor a fatty acid containing a single double bond had such effect.

Vascular actinos of arachidonic acid and its metabolites in perfused mesenteric and femoral beds of the dog

The effects of arachidonate and its major metabolites were examined in vascular beds perfused via the femoral and mesenteric arteries of chloralose-anaesthetised dogs. Close intra-arterial injection of prostacyclin (PGI 2, 0.02–2 μg), PGE 2 (0.05–1 μg) and their precursors, the endoperoxide PGH 2 (0.5–2 μg) and sodium arachidonate (100–550 μg), all induced vasodilatation. Sodium linoleate (500 μg) was inactive. Prostacyclin was equally active in both vascular beds, but PGE 2 was more potent in the femoral and less so in the mesenteric bed. PGH 2 was of similar potency to prostacyclin in both beds, but 6-oxo-PGF 1α (10–100 μg) was inactive. Thromboxane A 2 (TXA 2, 1–2 μg) was a potent vasoconstrictor of the mesenteric bed, but not the femoral bed, but not the femoral bed, although the endoperoxide analogue U46619 was vasoconstrictor in both vasculatures. Fatty acid hydroperoxides did not specifically modify the vasodilator effects of PGH 2 or arachidonate, presumably because these inhibitors are rapidly reduced in vivo. Indomethacin and meclofenamate potentiated vasodilatation induced by prostacyclin or endoperoxide, but reduced or abolished that caused by arachidonate. The rise in perfusion pressure induced by TXA 2 was potentiated and prolonged by indomethacin. Inhibition of synthesis of endogenous prostacyclin, by exacerbating the vasoconstrictor action of TXA 2, may have contributed to this effect.

Prostacyclin (PGI 2) is a weak contractor of coronary arteries of the pig

The actions of prostacyclin (PGI 2), prostaglandin E 2 (PGE 2), prostaglandin H 2 (PGH 2) and arachidonic acid have been examined on isolated coronary arteries from pigs. Arachidonate metabolites contracted this tissue, the order of potency being PGH 2 > PGE 2 > PGI 2 suggesting that the coronary vasoconstrictor effects of PGH 2 are limited by metabolism to PGI 2. Sodium arachidonate and linoleate weakly relaxed porcine coronary arteries, but the former induced a secondary prolonged contraction: only the contraction was abolished by indomethacin. Thus the relaxation induced by fatty acids does not depend on metabolism to prostaglandin-like substances.

L'effet préventif de l'acide pyruvique et d'autres acides cétoniques sur la dénaturation des protéines dans le poisson congelé

Fish muscles were treated with sodium pyruvate (by dipping or adding pyruvate solution to ground muscles to the final concentration of about 0.5%) and stored at 10°F for up to 16 weeks. By use of the extract release volume (ERV) method, the hydration capacities of the treated muscles were found to have greatly increased as compared to untreated samples or to samples which were similarly treated with sodium acetate, EDTA, chloride, citrate, phosphate, polyphosphate and glutamate. Sodium pyruvate (up to 0.9%) as well as sodium glyoxylate and α-ketoglutarate were also added to fish muscle homogenates which were then stored at 10°F for 1 week and 4 weeks, and the total salt extractable protein (TEF) in the homogenates was determined. It was found that the TEP values in homogenates containing pyruvate or α-ketoglutarate were higher, and the TEP values in homogenates containing glyoxylate were lower, than the TEP values in the homogenates which did not contain the keto acids. The anidenaturant effects of pyruvates and a-ketoglutarate were observed throughout the normal pH range of fish muscle, being stronger at pH 7.1 than at pH 6.3. The effects were also observed in the presence of KC1 (0.6M), malonaldehyde (1100ppm) formaldehyde (100ppm) and sodium linoleate (0.08%). Sodium pyruvate and sodium α-ketoglutarate appeared to prevent portein denaturation in frozen fish more effectively than sodium glutamate or polyphosphate. The anti-denaturation mechanims of keto acids could have arisen from their formation of Schiff bases with free amino groups of muscle proteins.

Reaction of autoxidizing linoleate with Coho salmon myosin.

AbstractReactions that contribute to denaturation, destruction and quality changes of fish muscle lipids and protein were studied. Compounds with characteristic fluorescence spectra were isolated by extraction and thin layer chromatography from an autoxidizing system consisting of sodium linoleate, Coho salmon myosin and buffer. Similar compounds were also present in extracts from freeze‐dried salmon steaks and salmon kept frozen at −20 C for 1 year. TBA values and oxygen uptake of the autoxidizing system showed initial rapid increases with time followed by a significant decrease in TBA values and gradual leveling off of oxygen uptake upon prolonged oxidation. IR spectra before and after borohydride reduction and UV, visible and fluorescence spectra indicated the presence of C=N functional groups in extracts from the various samples. These compounds were not extractable from the control myosin solutions allowed to oxidize without addition of linoleate. Amino acid analyses of the myosin from the autoxidizing system, when compared with nonoxidized myosin‐linoleate systems, indicated significant decreases in the amounts of histidine, lysine and methionine following oxidation. These reactions apparently contribute to the denaturation and destruction of the lipids and protein in the model system, as well as in a frozen or freeze‐dried product.

The Polymerization of Styrene in the Presence of Sodium Salts of Higher Aliphatic Carboxylic Acids

The polymerization of styrene (St) in the presence of sodium oleate was investigated in an aqueous system without any ordinary radical initiators. The reaction proceeded at 800C to give a stable emulsion of poly(St) which has an unusually high molecular weights.St also pelymerized in the presence of sodium salts of saturated higher aliphatic carboxylic acids in the concentration range above their CMC. The polymerization rate ef St was independent on the carbon number of sodium salts of saturated carboxylic acids.St polymerized remarkably in the presence of surfactants such as sodium linolate or sodium linolenate having internal double bond with cis configuration or sodium undecylenate having external double bond, but scarcely polymerized in the presence of sodium elaidate containing internal double bond with trans configuration.In the presence of sodium linolate or linolenate, the polymerization of St would be initiated by the peroxide contained in surfactants, but the initiation mechanism of polymerization of St in the presence of sodium oleate was not clarified yet.

Effect of Sodium Linoleate Infusion on Plasma Free Fatty Acids, Glucose, Insulin, and Ketones in Unanesthetized Dogs

By using a continuous-flow centrifuge to separate carotid artery blood into cells and plasma, sodium linoleate was infused into the jugular vein of five conscious dogs at a mean rate of 41.9 μEq. · kg.−1 · min−1 for ninety minutes without adverse side effects. Linoleate infusion quickly elevated plasma free fatty acid (FFA) levels to approximately 1.50 μEq./ml. and was accompanied by a rapid four- to sixfold increase in plasma immunoreactive insulin (IRI) which was sustained throughout the infusion. After thirty minutes of infusion, plasma glucose began to fall, ultimately declining 35 per cent from control levels. Plasma ketone levels rose to twice their control levels during linoleate infusion but were always less than 20 per cent of the ketone levels shown to be insulinogenic in dogs. Upon termination of the infusion, plasma FFA, IRI, and ketones fell quickly to control levels, while plasma glucose rose toward normal. The half-life of plasma linoleate, estimated from the infusion rate and the increment in plasma FFA during steady-state infusion, was 0.76 minute. This result, based on net flux, validates estimates based on tracer experiments. The similarity between the metabolic responses to linoleate infusion and those previously found to oleate suggests that these effects may be common to most physiologic long-chain FFA. Stimulation of insulin secretion by high levels of FFA could thus play a role in modulating lipolytic responses and changes in glucose metabolism accompanying such responses.

Autoxidation of Sodium Linoleate in the Protein Solution

Journal Article Autoxidation of Sodium Linoleate in the Protein Solution Get access Susumu Yukami Susumu Yukami Research Laboratory, The Lion Dentifrice Co., Ltd. Search for other works by this author on: Oxford Academic Google Scholar Agricultural and Biological Chemistry, Volume 36, Issue 5, 1 May 1972, Pages 871–874, https://doi.org/10.1080/00021369.1972.10860334 Published: 01 May 1972 Article history Received: 17 September 1971 Published: 01 May 1972

17O Nuclear Magnetic Resonance Spectrum of H 217O in Frog Striated Muscle

Whole striated muscles from the frog Rana esculenta were bathed in Ringer's solution enriched with H(2) (17)O; the muscle water was subsequently collected by vacuum distillation. The integrated intensity of the nuclear magnetic resonance (NMR) signal of (17)O in the muscle was measured to be approximately (3/4) of the signal observed in the distilled water. The phenomenon may arise either from immobilization of a population of the water molecules which may be a very small fraction or as much as (1/4) of the total, or may reflect tumbling of (1/3) of the water molecules in a compartment containing an anisotropic medium. Such an effect was demonstrated for H(2) (17)O using the model system of sodium linoleate in water.

Nuclear Magnetic Resonance of Sodium-23 Linoleate-Water: Basis for an Alternative Interpretation of Sodium-23 Spectra within Cells

The (23)Na spectrum from liquid crystals of sodium linoleate in water has been studied by nuclear magnetic resonance (NMR) techniques. The integrated intensity of the visible central spectral line was 34-39% of the intensity of a reference sample containing an equal quantity and concentration of (23)Na nuclei. Since satellite signals were clearly demonstrable, the effect reflected a nuclear quadrupolar interaction rather than a splitting of the (23)Na into two populations of bound and free nuclei. It is proposed that a similar quadrupolar effect may be the basis for the apparent binding of the (23)Na observed in biological systems.

Autoxidation of Sodium Linoleate in the Protein Solution

Autoxidation of Sodium Linoleate in the Protein Solution

Effect of essential fatty acid deficiency on release of triglycerides by the perfused rat liver

Studies are reported on release of triglycerides during perfusion of livers of male Sprague-Dawley rats fed a fat-free diet or diets containing hydrogenated coconut oil or corn oil. Perfusions were carried out with Krebs-Ringer bicarbonate buffer containing albumin with and without infusion of oleate or linoleate. Infusion with sodium oleate or linoleate caused an accumulation of triglycerides in the livers of the corn oil-fed animals and stimulated the release of triglycerides into the perfusing medium. In similar experiments with essential fatty acid-deficient animals, which were fed fat-free diets or diets containing hydrogenated coconut oil, there was no increase in secretion of triglycerides into the perfusate, and the amount of triglyceride which accumulated in the liver was greater than in the livers of the control (corn oil-fed) animals. Tracer experiments with oleate-1-(14)C or linoleate-1-(14)C also showed that with livers of essential fatty acid-deficient animals, secretion of triglyceride into the perfusate was not stimulated by infusion of fatty acids into the perfusing medium. It is concluded that impairment of the secretion of triglycerides is a factor in the accumulation of fat in the livers of essential fatty acid-deficient animals.

Relationship between critical micelle concentration and rate of radiolysis of aqueous sodium linoleate

Relationship between critical micelle concentration and rate of radiolysis of aqueous sodium linoleate

Inhibition of gastric secretion in the rat with sodium oleate

The effect on gastric secretion in the rat by small quantities of sodium oleate (7.5 and 15.0 mg.) has been investigated. It was found that intravenous or intraperitoneal administration of small amounts (0.25 cc. of 0.1 N solutions) decreased gastric secretion by one-third over a 4-hour period. Sodium propionate, sodium stearate, sodium linoleate, other fatty acids, and normal saline did not inhibit gastric secretion under identical conditions. We conclude, therefore, that Na oleate may have a specific pharmacologic effect on gastric secretion in the rat. Furthermore, this action is not predicated upon contact with the duodenal mucosa but rather a function of its presence in the bloodstream.

コロイド水溶液におけるリノール酸ナトリウムの自動酸化およびその生成物を開始剤兼乳化剤とするスチレンの新型乳化重合

コロイド水溶液におけるリノール酸ナトリウムの自動酸化およびその生成物を開始剤兼乳化剤とするスチレンの新型乳化重合

Antioxidative abilities of some porphyrins on the oxidation of sodium linoleate

Antioxidative abilities of some porphyrins on the oxidation of sodium linoleate

Effect of Lipid Content on Protein‐Sodium Linolenate Interaction in Fish Muscle Homogenates

SUMMARYA species difference in reactivity of fish muscle proteins toward sodium linolenate in muscle homogenates is demonstrated. The proteins of muscle having higher lipid content show greater stability. Sodium linolenate uptake by natural lipids, resulting in competition between lipids and protein for added sodium linolenate, is suggested. The significance of these findings in terms of a possible in situ relationship of lipid hydrolysis to protein denaturation in frozen stored fish muscle is discussed.