INHIBITORY EFFECT OF UNSATURATED FATTY ACIDS ON LYMPHOCYTE-ANTIGEN INTERACTION WITH SPECIAL REFERENCE TO MULTIPLE SCLEROSIS

1975 ◽  
Vol 52 (2) ◽  
pp. 121-136 ◽  
Author(s):  
E. J. Field ◽  
B. K. Shenton
Keyword(s):  
Multiple Sclerosis ◽  
Fatty Acids ◽  
Special Reference ◽  
Unsaturated Fatty Acids ◽  
Inhibitory Effect ◽  
Lymphocyte Antigen ◽  
Antigen Interaction

Unsaturated fatty acids and cyclooxygenase inhibitors: effects on pial arterioles

1982 ◽  
Vol 242 (4) ◽  
pp. H629-H632
Author(s):  
W. I. Rosenblum
Keyword(s):  
Fatty Acids ◽  
Unsaturated Fatty Acids ◽  
Eicosatrienoic Acid ◽  
Inhibitory Effect ◽  
Cyclooxygenase Inhibitors ◽  
Dependent Manner ◽  
Double Bonds ◽  
Pial Arterioles ◽  
Dose Dependent

Cerebral surface arterioles of the mouse were constricted in a dose-dependent manner by three different unsaturated fatty acids each with one of its double bonds in the n-6 position: arachidonate, linoleic, and 11,14,17-eicosatrienoic acid (ETA) in doses of 10-200 micrograms/ml. The constriction was transient, and its magnitude was significantly reduced by pretreatment of the mice with intraperitoneal injections of indomethacin (5 mg/kg), aspirin (100 mg/kg), or sodium 2-amino-3-(4 chlorobenzyl)-phenylacetate (AHR-6293, 100 mg/kg). The inhibitory effect of these cyclooxygenase inhibitors suggests that this enzyme is involved in the response to these fatty acids and is in keeping with suggestions in the literature stating that such unsaturated fatty acids may interact with cyclooxygenase even when they cannot form prostaglandin (PG) endoperoxides, The PG endoperoxide formed by arachidonate or the analogous hydroperoxy compounds formed by linoleic or 11,14,17 ETA, may then alter cerebrovascular tone by production of reactive, O2-containing species. Alternate explanations for the data are also proposed.

scholarly journals Inhibitory effects of some long-chain unsaturated fatty acids on mitochondrial β-oxidation. Effects of streptozotocin-induced diabetes on mitochondrial β-oxidation of polyunsaturated fatty acids

1985 ◽  
Vol 230 (2) ◽  
pp. 329-337 ◽  
Author(s):  
H Osmundsen ◽  
K Bjørnstad
Keyword(s):  
Fatty Acids ◽  
Unsaturated Fatty Acids ◽  
Reductase Activity ◽  
Liver Mitochondria ◽  
Inhibitory Effect ◽  
Diabetic Rats ◽  
Inhibitory Property ◽  
Streptozotocin Induced Diabetes ◽  
Streptozotocin Diabetic Rats ◽  
Coa Reductase

Evidence showing that some unsaturated fatty acids, and in particular docosahexaenoic acid, can be powerful inhibitors of mitochondrial β-oxidation is presented. This inhibitory property is, however, also observed with the cis- and trans-isomers of the C18:1(16) acid. Hence it is probably the position of the double bond(s), and not the degree of unsaturation, which confers the inhibitory property. It is suggested that the inhibitory effect is caused by accumulation of 2,4-di- or 2,4,7-tri-enoyl-CoA esters in the mitochondrial matrix. This has previously been shown to occur with these fatty acids, in particular when the supply of NADPH was limiting 2,4-dienoyl-CoA reductase (EC 1.3.1.-) activity [Hiltunen, Osmundsen & Bremer (1983) Biochim. Biophys. Acta 752, 223-232]. Liver mitochondria from streptozotocin-diabetic rats showed an increased ability to β-oxidize 2,4-dienoyl-CoA-requiring acylcarnitines. Docosahexaenoylcarnitine was also found to be less inhibitory at lower concentrations with incubation under coupled conditions. With uncoupling conditions there was little difference between mitochondria from normal and diabetic rats in these respects. This correlates with a 5-fold stimulation of 2,4-dienoyl-CoA reductase activity found in mitochondria from streptozotocin-diabetic rats.

scholarly journals The inhibitory effect of reduced glutathione on the lipid peroxidation of the microsomal fraction and mitochondria

1968 ◽  
Vol 106 (2) ◽  
pp. 515-522 ◽  
Author(s):  
B. O. Christophersen
Keyword(s):  
Lipid Peroxidation ◽  
Fatty Acids ◽  
Protective Effect ◽  
Rat Liver ◽  
Microsomal Fraction ◽  
Unsaturated Fatty Acids ◽  
Reduced Glutathione ◽  
Inhibitory Effect ◽  
Inhibiting Effect ◽  
Heat Labile

1. GSH efficiently inhibited the ascorbate-stimulated lipid peroxidation of the unsaturated fatty acids in the fresh microsomal fraction and mitochondria of rat liver, whereas the peroxidation in heat-denatured particles was little inhibited. 2. Cysteamine and diethyldithiocarbamate inhibited the peroxidation in both fresh and boiled particles. Thioglycollate and 2-mercaptoethanol had no inhibiting effect. Cysteine and homocysteine both stimulated the lipid peroxidation even in the absence of ascorbate. 3. The added GSH disappeared at nearly the same rate in the presence of fresh and of boiled particles to which ascorbate had been added, although considerably more malonaldehyde was formed in the boiled particles. In the absence of ascorbate little GSH disappeared. 4. It is suggested that the protective effect of GSH against lipid peroxidation depends on the preservation of heat-labile structures in the microsomal fraction and mitochondria.

scholarly journals Unsaturated fatty acids in multiple sclerosis.

BMJ ◽  
1973 ◽  
Vol 2 (5869) ◽  
pp. 777-778 ◽  
Author(s):  
J Mertin ◽  
B K Shenton ◽  
E J Field
Keyword(s):  
Multiple Sclerosis ◽  
Fatty Acids ◽  
Unsaturated Fatty Acids

Unsaturated fatty acids inhibit ADP- arachidonate-induced platelet aggregation without affecting thromboxane synthesis

1986 ◽  
Vol 64 (9) ◽  
pp. 906-913 ◽  
Author(s):  
Ella Dratewka-Kos ◽  
D. O. Tinker ◽  
Brigitte Kindl
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Platelet Aggregation ◽  
Unsaturated Fatty Acids ◽  
Inhibitory Effect ◽  
Inhibitory Effects ◽  
Low Concentrations ◽  
Fatty Acid Inhibition ◽  
Induced Aggregation ◽  
Protein Free Medium

The inhibitory effects of three cis-unsaturated C18 fatty acids (oleic, linoleic, and linolenic acids, sodium salts) on ADP- and sodium-arachidonate-induced aggregation of washed rabbit platelets were investigated. When the platelets were suspended in protein-free medium containing dextran, it was found that these fatty acids at very low concentrations (2–45 μM) were potent inhibitors of platelet responsiveness and the inhibitory effect occurred within seconds. The inhibition of ADP-induced aggregation was not affected by abolishing the activity of platelet cyclooxygenase using aspirin. Human serum albumin relieved the inhibition caused by fatty acids for both ADP- and arachidonate-induced aggregation. The inhibitory effect of fatty acids does not seem to be due to decreased thromboxane formation (except possibly in the case of linolenate), and the relief of fatty acid inhibition by albumin does not potentiate thromboxane B2 formation from exogenous arachidonate. It is suggested that the inhibitory effect of polyunsaturated fatty acids on platelet aggregation is specific and not related to a general surfactant effect, since inhibition occurs far below the critical micelle concentration of fatty acid soaps.

scholarly journals Inhibitory Effect of Trehalose on the Autoxidation of Unsaturated Fatty Acids by Water/Ethanol System.

2003 ◽  
Vol 50 (3) ◽  
pp. 133-137 ◽  
Author(s):  
Kazuyuki Oku ◽  
Mayumi Kurose ◽  
Michio Kubota ◽  
Shigeharu Fukuda ◽  
Masashi Kurimoto ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Unsaturated Fatty Acids ◽  
Inhibitory Effect ◽  
Ethanol System

scholarly journals Arachidonic acid inhibits glycine transport in cultured glial cells

1990 ◽  
Vol 271 (1) ◽  
pp. 237-242 ◽  
Author(s):  
F Zafra ◽  
R Alcantara ◽  
J Gomeza ◽  
C Aragon ◽  
C Gimenez
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Unsaturated Fatty Acids ◽  
Membrane Vesicle ◽  
Selective Inhibition ◽  
Inhibitory Effect ◽  
C6 Glioma Cells ◽  
Plasma Membrane Vesicle ◽  
Glycine Uptake ◽  
Glycine Transport

The effects of arachidonic acid on glycine uptake, exchange and efflux in C6 glioma cells were investigated. Arachidonic acid produced a dose-dependent inhibition of high-affinity glycine uptake. This effect was not due to a simple detergent-like action on membranes, as the inhibition of glycine transport was most pronounced with cis-unsaturated long-chain fatty acids, whereas saturated and trans-unsaturated fatty acids had relatively little or no effect. Endogenous unsaturated non-esterified fatty acids may exert a similar inhibitory effect on the transport of glycine. The mechanism for this inhibitory effect has been examined in a plasma membrane vesicle preparation derived from C6 cells, which avoids metabolic or compartmentation interferences. The results suggest that part of the selective inhibition of glycine transport by arachidonic acid could be due to the effects of the arachidonic acid on the lipid domain surrounding the carrier.

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