PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “ANILIDES”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1998

Single step thin-layer chromatographic method for quantitation of enzymatic formation of fatty acid anilides.

The activity of the enzyme involved in catalyzing the formation of fatty acid anilides can be measured by quantitating the fatty acid anilides formed. We have shown earlier that oleic acid is the most preferred substrate among other fatty acids studied for the conjugation with aniline. The reaction product (oleyl anilide) could be separated by thin-layer chromatography (TLC) and then quantified by reversed-phase high-performance liquid chromatography (HPLC). Using [1-(14)C]oleic acid as substrate, the fatty acid anilide forming activity can be determined in a single step by TLC analysis. The conventional TLC methods used for the separation of the fatty acid esters, however, could not resolve oleyl anilide from the residual [1-(14)C]oleic acid. Therefore, a simple and reliable TLC method was developed for the separation of oleyl anilide from oleic acid using a freshly prepared solvent consisting of petroleum ether-ethyl acetate-ammonium hydroxide (80:20:1, v/v). Using this solvent system the relative flow (Rf) values were found to be 0.54 for oleyl anilide and 0.34 for aniline, whereas oleic acid remained at the origin. The TLC procedure developed in the present study could be used to determine the fatty acid anilide forming activity using [1-(14)C]oleic or other fatty acids as substrate and was also found suitable for the analysis of fatty acid anilides from the biological samples.

Acyltransferases↗
PubMed1995

Interactions of cis-fatty acids and their anilides with formyl-methionyl-leucyl-phenylalanine, phorbol myristate acetate and dioctanoyl-s,n-glycerol in human leukocytes.

Aniline-denaturated rape-seed food oils that contained anilides of linoleic and oleic acids caused a poisoning epidemic, known as Toxic Oil Syndrome, in Spain in 1981. Toxic Oil Syndrome affected mainly the lungs and the immune system of exposed individuals. Linoleic and oleic acids, and linoleic and oleic anilides increased the production of reactive oxygen metabolites in human polymorphonuclear leukocytes. Both cis-fatty acids inhibited a chemotactic peptide-, fMLP-induced production of reactive oxygen metabolites without affecting fMLP-induced elevation of intracellular calcium levels. Linoleic acid anilide slightly amplified fMLP-induced respiratory burst, whereas oleic acid anilide was without an effect. However, both fatty acid anilides decreased fMLP-induced elevation of levels of free intracellular calcium. Moreover, both cis-fatty acids and their anilides inhibited phorbol myristate acetate (PMA)- and dioctanoyl-s,n-glycerol (DiC8)-induced production of reactive oxygen metabolites. Thus, both cis-fatty acids and their anilides inhibited agonist-stimulated production of reactive oxygen metabolites; this is most likely due to interactions with cell signalling events. These results suggest that both linoleic and oleic acids and their anilides may inhibit immunological responses of leukocytes.

Analysis of Variance↗
PubMed1995

Decrease of 12-hydroxyeicosatetraenoic acid production in mouse lungs following dietary oleic anilide consumption: implications for the toxic oil syndrome.

A study was performed to examine the ability of dietary oleic anilide to alter 12-hydroxyeicosatetraenoic acid (12-HETE) production. The structure of oleic anilide, synthesized by reacting oleic acid with aniline, was confirmed by mass spectrometry. The purity of oleic anilide, 75%, was measured by gas chromatography. Oleic acid, which constituted the remaining 25%, is a major component of the rapeseed oil vehicle. Balb/c mice were fed oleic anilide as 0.75% of their diet by weight for three weeks. Their lungs were excised and examined for 12-HETE production in vitro. The 12-HETE levels were significantly (p < 0.01) lower in mice fed oleic anilide than in mice fed the oleic acid control diet. This result illustrates eicosanoid production as a target of fatty acid anilide toxicity. The fatty acid composition, including arachidonic acid, of mouse lungs from both dietary groups was not different. This confirms the availability of substrate for 12-lipoxygenase in both groups. Spleen weights were higher in mice fed oleic anilide than in control mice (p < 0.005). These observations are relevant to immunoregulation and the autoimmune syndromes noted in patients of the Toxic Oil Syndrome (TOS).

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1993

Influence of fatty acid anilides present in toxic oils on the metabolism of exogenous arachidonic acid in cultured human endothelial cells.

The effect of fatty acid anilides (FAA) on the exogenous arachidonic acid (AA) metabolism and toxicity of isolated human endothelial cells was studied to clarify their possible role in the etiology of toxic oil syndrome. Confluent cells were incubated with and without linoleic acid anilide (LAA), oleic acid anilide (OAA) and two unrelated samples for 2-24 h prior to the addition of [l-14C]AA alone or with calcium ionophore A-23187. The eicosanoids produced were analyzed by RP-HPLC. A dual stimulatory and inhibitory effect on the conversion of exogenous AA as a function of preincubation time with anilides (100 and 1000 microM) was observed. Treated cells significantly increased (1-3-fold) the production of the main cyclooxygenase-derived prostanoids (6-keto-PGF1 alpha and PGF2 alpha) formed by these cells, with a maximum stimulatory effect after 2-3 h, only when AA was used alone. However, afterwards a time- and dose-dependent decrease in prostanoid formation was observed with LAA (P < 0.05 at 24 h), either in the absence or presence of ionophore A-23187 in the incubation mixture. This inhibitory effect on cyclooxygenase was not observed with OAA, which still stimulate after 24 h of treatment. The changes in prostanoid synthesis were not followed with a parallel release in the lactate dehydrogenase activity in the medium (except with unrelated samples). Moreover, anilide treatment increased the appearance of cytosolic lipid droplets or vacuoles after 2 and 5 h of contact with LAA and OAA, respectively. From these results, it was suggested that anilides impair prostanoid synthesis in endothelial cells; their stimulatory effect could be explained by an unspecific effect on cell membrane, not related to cell toxicity and the inhibitory effect by an inhibition of the cyclooxygenase activity. These observations further contribute to our understanding of the possible role of anilides in the etiology of the toxic oil syndrome.

Anilides↗
PubMed2002

Strain-dependent in vitro and in vivo effects of oleic acid anilides on splenocytes and T cells in a murine model of the toxic oil syndrome.

The toxic oil syndrome is an exogenously-induced autoimmune disease in humans, which is believed to be due to the accidental ingestion of oleic acid anilides. In a previously established murine model anilides-treated A/J mice developed a wasting disease after 1 week. Anilides-treated B10.S mice showed after 6 weeks a hyperimmunglobulinemia with autoantibody production, but no clinical symptoms. We now compared in vitro the effects of anilides on splenocytes and T cells in A/J and B10.S mice. Splenocyte proliferation was similar in both strains. After in vivo treatment of mice with anilides and in vitro restimulation, splenocytes of sick A/J mice showed a significant increase in splenocyte proliferation. Splenocytes from B10.S mice, however, had a suppressed baseline response and did not proliferate on restimulation. Adherent cells were necessary to induce proliferation in A/J mice-derived T cells. Apoptosis in splenocytes was significantly elevated in anilides-treated A/J and in B10.S mice as compared to saline-treated controls. These data show that anilides are able to affect the immune system in a strain-dependent way and may therefore take part in inducing the disease seen in humans and mice.

Anilides↗
PubMed1993

Distribution of oleyl-anilide hydrolysing activity in rat and human tissues.

A method has been developed and tested for the measurement of anilide hydrolysing activity in rat tissues. A concentrated solution of labelled oleyl anilide in isopropanol is added to the tissue homogenates and after incubation, the chloroform/methanol extract of the samples is chromatographed on Silicagel TLC plates and the oleic acid radioactivity is measured. The activity is time-, homogenate- and temperature-dependent, the optimal pH for measurement is 8 and there is no significant spontaneous anilide degradation. In the rat, the activity is widely distributed, with highest protein specific activity in the adipose tissues. The tissue activities of a same animal are fairly well inter-correlated, with rats showing very low activity in all tissues compared with others presenting high overall activity. The levels of activity found can easily explain the fast elimination of anilides administered to rats and their scant toxic effects. Human adipose tissue samples showed a wide range of anilide hydrolase activities per gram of protein, in general lower than in rats and with some values very low. It is postulated that this lack of anilide-hydrolising capability in some humans may be related to the incidence of the toxic oil syndrome.

Adipose Tissue↗
PubMed1997

Palmitic acid anilide-induced respiratory burst in human polymorphonuclear leukocytes is inhibited by a protein kinase C inhibitor, Ro 31-8220.

Human polymorphonuclear leukocytes (PMNL) were exposed to palmitic acid anilide, an impurity in the case oils that caused the Spanish Toxic Oil Syndrome in 1981, and to the corresponding fatty acid, palmitic acid. The effects of these compounds were studied on the production of reactive oxygen metabolites (ROM) and changes in the levels of free intracellular calcium. Palmitic acid anilide induced the production of reactive oxygen metabolites in PMNL. Interestingly, the palmitic acid anilide-induced respiratory burst was completely blocked by a protein kinase C inhibitor, Ro 31-8220. Moreover, palmitic acid anilide additively amplified the production of ROM caused by a chemotactic peptide, formyl-Methionyl-Leucyl-Phenylalanine (FMLP). In contrast, palmitic acid anilide did not have any effect on the production of ROM induced by a tumor promoter, phorbol myristate acetate (PMA). Palmitic acid, in turn, did not markedly induce the production of ROM nor did it amplify the agonist-induced respiratory burst. Neither of the compounds, alone or in combination with FMLP, affected the levels of intracellular calcium in PMNL. These results indicate that the aniline moiety in palmitic acid modifies its effects on the activation of human PMNL, and the subsequent oxidative burst. The present results also suggest that palmitic acid anilide may activate PMNL through a protein kinase C-dependent mechanism.

Adult↗
PubMed2005

Synthesis of structurally defined scaffolds for bivalent ligand display based on glucuronic acid anilides. The degree of tertiary amide isomerism and folding depends on the configuration of a glycosyl azide.

[structures: see text] Syntheses and structural analyses of bivalent carbohydrates based on anilides of glucuronic acid are described. Secondary anilides predominantly adopted the Z-anti structure; there is also evidence for population of the Z-syn isomer. Bivalent tertiary anilides displayed two signal sets in their NMR spectra, consistent with the presence of (i) a major isomer where both amides have E configurations (EE) and (ii) a minor isomer where one amide is E and the other Z (EZ). Qualitative NOE/ROE spectroscopic studies in solution support the proposal that the anti conformation is preferred for E amides. The crystal structure of one bivalent tertiary anilide showed E-anti and E-syn structural isomers; intramolecular carbohydrate-carbohydrate stacking was observed and mediated by carbonyl-pyranose, azide-azide, and pyranose-aromatic interactions. The EE to EZ isomer ratio, or the degree of folding, for tertiary amides, was greatest for a bivalent compound containing two alpha-glycosyl azide groups; this was enhanced in water, suggesting that hydrophobic interactions are partially but not wholly responsible. Computational methods predicted azide-aromatic (N...H-C interaction) and azide-azide interactions for folded isomers. The close contact of the azide and aromatic protons (N...H-C interaction) was observed upon examination of the close packing in the crystal structure of a related monomer. It is proposed that the alpha-azide group is more optimally aligned, compared to the beta-azide, to facilitate interaction and minimize the surface area of the hydrophobic groups exposed to water, and this leads to the increased folding. The alkylation of bivalent secondary anilides induces a switch from Z to E amide that alters the scaffold orientation. The synthesis of a bivalent mannoside, based on a secondary anilide scaffold, for investigation of mannose-binding receptor cross-linking and lattice formation is described.

Amides↗
PubMed1997

Erucic acid and erucic acid anilide-induced oxidative burst in human polymorphonuclear leukocytes.

Human polymorphonuclear leukocytes (PMNL) were exposed to erucic acid or erucic acid anilide to explore their effects on the production of reactive oxygen species (ROS) and the levels of free intracellular calcium. The compounds did not change the levels of intracellular calcium, but both dose-dependently induced respiratory burst in PMNL. Maximal production of ROS by erucic acid exceeded that induced by its anilide 13-fold. A protein kinase C inhibitor, Ro 31-8220, completely inhibited erucic acid and erucic acid anilide-induced production of ROS. Neither erucic acid nor erucic acid anilide modified FMLP-induced production of ROS. However, erucic acid (500 microM) amplified 5 nM PMA-induced ROS production 1.8-fold, but did not have this effect at a lower PMA concentration. On the contrary, erucic acid anilide inhibited PMA-induced oxidative burst, and shifted the peak ROS production induced by PMA to a later time-point. The present results show that aniline moiety modifies the effects of erucic acid on the activation of PMNL, and suggest that both erucic acid and erucic acid anilide may activate PMNL through a protein kinase C-dependent mechanism.

Anilides↗
PubMed1994

Toxic effects of fatty acid anilides on the oxygen defense systems of guinea pig lungs and erythrocytes.

Toxic oil syndrome (TOS) is caused by ingestion of denatured edible oils. Even though the etiology and pathogenesis of this disease are not fully known, it is quite clear that generation of free radicals caused by ingestion of fatty acid anilides is responsible for the pathogenetic mechanism in many TOS patients. Fatty acid anilides may also alter the free radical status of lungs and erythrocytes; this possibility may shed some light on understanding toxic oil syndrome. The present study describes the effects of oral administration of fatty acid anilides on the activities of major enzymes involved in the oxygen defense systems of lungs and erythrocytes. Feeding fatty acid anilides caused an increase in the superoxide dismutase (SOD) activity in erythrocytes, whereas it caused a decrease in the SOD activity in lungs. GSH-Px activity was not significantly changed in erythrocytes but was decreased in lungs. Although the activity of catalase was increased only by a higher dose in the erythrocytes, it was not affected in the lung at any dosage. Even though the ingestion of fatty acid anilides caused an increase in the SOD activity in the erythrocytes and a decrease in the SOD activity in the lungs, there was an increase in the lipid peroxidation in both cases. The increase in lipid peroxidation in erythrocytes is probably caused by the accumulation of H2O2, and that in the lungs is due to the accumulation of superoxide anion.

Anilides↗