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PubMedDate not supplied

[Depression of rat liver acetyl-CoA-carboxylase activity by salicylate and other compounds].

Two intraperitoneal injections of salicylate at a dose of 250 mg/kg of body weight led to decrease in the acetyl-CoA-carboxylase activity in liver soluble fraction (140000xg) more than by 60%. Salicylate in concentrations 10(-4) and 10(-2) M inhibited the enzyme from rat liver soluble fraction by 25% and 80%, respectively, in vitro: it was found to be as effective inhibitor as kynurenate and clofibrate. Derivatives of salicylate -- acetyl salicylate and salicyl amide also showed this inhibitory effect, but their action was less disinct as compared with salicylate. 2-phenyl-3-methyl-hydroxypentanic and 2,3-diphenyl-3-hydroxypentanic acids (derivatives of deoxymevalonic acid) demonstrated the strong inhibitory effect on acetyl-CoA-carboxylase, comparable to the action of salicylate. The effect of salicylate on the reaction of carboxylation was not related to competition for acetyl-CoA (formation of acetyl salicylate), to interaction with biotin and to allosteric reaction with acetyl-CoA-carboxylase. Possible mechanisms of the salicylate effect on the enzyme activity are discussed.

Acetyl-CoA Carboxylase↗
PubMed1989

Automated zone-electrophoretic sample treatment for the analysis of biological samples by high-performance liquid chromatography.

The automation of zone-electrophoretic sample treatment for liquid chromatography is described. The procedure is completely controlled from a liquid chromatograph. The carry-over of proteins from human serum under different experimental conditions was studied. The influence of the presence of proteins in the sample is illustrated with the anionic compound salicylic acid and the increase in selectivity for cationic compounds is demonstrated with the determination of ephedrine, norephedrine and amphetamine in urine.

Amphetamine↗
PubMed2006

Isolation of a novel ABC-transporter gene from soybean induced by salicylic acid.

This paper reports on the identification and characterization of a new ATP-binding cassette (ABC) transporter which was identified as a salicylic acid-induced gene from soybean (Glycine max cv. Williams 82) in a subtractive suppression hybridization approach. A fragment of an ABC-transporter gene was used to isolate a full-length cDNA clone for this gene with a length of 4750 bp. The encoded protein has a length of 1447 amino acids and is composed of two similar repeat units typical of full-size ABC transporters. The sequence displays a close relationship to plant pleiotropic drug resistance (PDR)-type transporters and, on a homology basis, clusters together with the Arabidopsis thaliana PDR12 gene, suggesting GmPDR12 as a name for the gene isolated from soybean. GmPDR12 is rapidly responsive to salicylic acid and methyl jasmonate. The mRNA starts to accumulate 30 min after the addition of the signalling compounds. Salicylic acid is required for the execution of the hypersensitive reaction in soybean cell suspension cultures inoculated with Pseudomonas syringae pv. glycinea. It has been demonstrated previously that salicylic acid can be substituted by a variety of functional analogues of salicylic acid. All of these compounds lead to a strong and rapid transcriptional activation of GmPDR12, suggesting a shared signalling pathway.

ATP-Binding Cassette Transporters↗
PubMed1999

Phenolic compounds from tournefortia sarmentosa

Three new isoprenylbenzenes, tournefolins A (1), B (2), and C (3), and two new 2-ethoxy-4,5-dihydroxybenzoyl compounds, 4 and 5, together with the known compounds, salicylic acid and allantoin, were isolated from the stems of Tournefortia sarmentosa. The structures of new compounds were elucidated as 2-(4beta-methyltetrahydrofuran-2alpha-yl)-5-(4beta-methyltetrahydrofu ran-2beta-yl)-1,4-dihydroxybenzene (1), methyl 5-(5-hydroxy-2-methoxyphenyl)-3-furoate (2), methyl 5-(2, 5-dihydroxyphenyl)-3-furoate (3), 2-ethoxy-4,5-dihydroxybenzaldehyde (4), and 2-ethoxy-4,5-dihydroxybenzoic acid (5), on the basis of spectral and chemical methods. The relative configuration of 1 was determined by single-crystal X-ray crystallography.

Journal Article↗
PubMed2002

Influence of particles on sonochemical reactions in aqueous solutions.

Numerous publications deal with the possible application of ultrasound for elimination of organic pollutants as a tool for water pollution abatement. Most of the experiments were performed in pure water under laboratory conditions. For developing technologies that hold promise it is necessary to investigate the effect of ultrasound in natural systems or waste water where particulate matter could play an important role. In this paper the influence of quartz particles (2-25 microm) on the chemical effects of ultrasound in aqueous system using a high power ultrasound generator (68-1028 kHz, 100 W, reactor volume 500 ml) is reported. In pure water in dependence on particle size, concentration and frequency the formation rate of hydrogen peroxide under Ar/O2 (4:1) shows a maximum using 206 kHz in presence of 3-5 microm quartz particles (4-8 g/l). Under these conditions the yield of peroxide is higher than without quartz. Additionally under N2/O2 (4:1) besides hydrogen peroxide the formation of nitrite/nitrate was measured. Compared to pure water quartz particle depressed the formation of nitrite/nitrate up to 10-fold but not the formation of H2O2. According to the results of H2O2 formation the elimination of organic compounds by sonolysis (206 kHz) and the influence of quartz particles were investigated. As organic compounds salicylic acid, 2-chlorobenzoic acid and p-toluenesulfonic acid were used. The influence of quartz on the oxidation of organic compounds (206 kHz) is similar to that on the formation of H2O2.

Journal Article↗
PubMed1998

[Research on the separation behavior of acidic drugs in capillary electrophoresis with reversed direction of electroosmotic flow].

The separation behavior of acidic drugs in capillary electrophoresis with reversal of electroosmotic flow was investigated systematically. Acetylsalicylic acid and its related compound salicylic acid were employed as objective drugs. The cationic surfactant cetyltrimethylammonium bromide (CTAB) was used as reversed reagent for electroosmotic flow. The experimental conditions, such as, cationic surfactant concentration, buffer pH and organic additives, which affected migration time, peak shape and column efficiency, were studied in detail. The experimental results indicated that high speed analysis could be achieved in the capillary electrophoresis with reversed electroosmotic flow induced by cationic surfactant when acidic drugs were analysed. The poor peak shape and low column efficiency caused by the interactions of CTAB with acidic anions would be improved by adding proper organic additive, such as, beta-cyclodextrin or acetonitrile.

Aspirin↗
PubMed2002

Aspirin and salicylates inhibit the IL-4- and IL-13-induced activation of STAT6.

Allergic diseases, including asthma, represent a major threat to human health. Over the three last decades, their incidence has risen in western countries. Aspirin treatment has been shown to improve allergic diseases, especially asthma, and the decreased use of aspirin has been hypothesized to contribute to the increase in childhood asthma. Because salicylate compounds suppress a number of enzymatic activities, and signaling through IL-4R participates in the development of allergic responses, we tested the effect of salicylates on IL-4 signal transduction. We found that treatment of cell lines and primary cells with aspirin and salicylates, but not acetaminophen, inhibited the activation of STAT6 by IL-4 and IL-13. This effect correlated with the inhibition of IL-4-induced CD23 expression. Although salicylates inhibited the in vivo activation of Janus kinases, their kinase activity was not affected in vitro by salicylates, suggesting that other kinases were involved in IL-4-induced STAT6 activation. Furthermore, we found that an Src kinase was involved in STAT6 activation because 1) Src kinase activity was induced by IL-4, 2) Src kinase activity, but not Janus kinase, was inhibited by salicylates in vitro, 3) cells expressing viral Src had constitutive STAT6 phosphorylation, and 4) cells lacking Src showed low STAT6 phosphorylation in response to IL-4. Because STAT6 activation by IL-4 and IL-13 participates in the development of allergic diseases, our results provide a mechanism to explain the beneficial effects of aspirin and salicylate treatment of these diseases.

3T3 Cells↗
PubMed2005

Transcriptional profiling of sorghum induced by methyl jasmonate, salicylic acid, and aminocyclopropane carboxylic acid reveals cooperative regulation and novel gene responses.

We have conducted a large-scale study of gene expression in the C4 monocot sorghum (Sorghum bicolor) L. Moench cv BTx623 in response to the signaling compounds salicylic acid (SA), methyl jasmonate (MeJA), and the ethylene precursor aminocyclopropane carboxylic acid. Expression profiles were generated from seedling root and shoot tissue at 3 and 27 h, using a microarray containing 12,982 nonredundant elements. Data from 102 slides and quantitative reverse transcription-PCR data on mRNA abundance from 171 genes were collected and analyzed and are here made publicly available. Numerous gene clusters were identified in which expression was correlated with particular signaling compound and tissue combinations. Many genes previously implicated in defense responded to the treatments, including numerous pathogenesis-related genes and most members of the phenylpropanoid pathway, and several other genes that may represent novel activities or pathways. Genes of the octadecanoic acid pathway of jasmonic acid (JA) synthesis were induced by SA as well as by MeJA. The resulting hypothesis that increased SA could lead to increased endogenous JA production was confirmed by measurement of JA content. Comparison of responses to SA, MeJA, and combined SA+MeJA revealed patterns of one-way and mutual antagonisms, as well as synergistic effects on regulation of some genes. These experiments thus help further define the transcriptional results of cross talk between the SA and JA pathways and suggest that a subset of genes coregulated by SA and JA may comprise a uniquely evolved sector of plant signaling responsive cascades.

Acetates↗
PubMed1969

Renal accumulation of salicylate and phenacetin: possible mechanisms in the nephropathy of analgesic abuse.

Since either aspirin or phenacetin might be causative in the nephropathy of analgesic abuse, studies were designed to examine the renal accumulation and distribution of the major metabolic products of these compounds, salicylate and N-acetyl-p-aminophenol (APAP) respectively, in dogs. Nineteen hydropenic animals were studied, of which seven were given phenacetin, nine received acetyl salicylic acid, two were given both aspirin and phenacetin, and one received APAP directly. Two of three hydrated animals were given phenacetin and one was given aspirin. During peak blood levels of salicylate and (or) APAP, the kidneys were rapidly removed, frozen, sliced from cortex to papillary tip, and analyzed for water, urea, APAP, and salicylate. No renal medullary gradient for salicylate was demonstrable during both hydropenic and hydrated states. In contrast, both free and conjugated APAP concentrations rose sharply in the inner medulla during hydropenia, reaching a mean maximal value at the papillary tip exceeding 10 times the cortical concentration (P < 0.001), a distribution similar to that of urea. Salicylate had no effect on the APAP gradient, but hydration markedly reduced both the APAP and urea gradients in the medulla. The data indicate that APAP probably shares the same renal mechanisms of transport and accumulation as urea and acetamide, and that papillary necrosis from excessive phenacetin may be related to high papillary concentration of APAP.

Analgesics↗
PubMed1999

Feeding is inhibited by sublethal concentrations of toxicants and by heat stress in the nematode Caenorhabditis elegans: relationship to the cellular stress response.

We report that the free-living nematode Caenorhabditis elegans can respond to a variety of stressors (compounds known to induce the production of cellular stress proteins in model biological systems), by ceasing pharyngeal pumping. This phenomenon results in both a reduction in intake of the stressor and a cessation of feeding. The effect of stressors can therefore be conveniently assayed by monitoring the decrease in the density of the bacterial food in liquid cultures of nematodes. A great range of stressors induced this response including alcohols, heavy metals, sulfhydryl-reactive compounds, salicylate, and heat. For several of these stressors, inhibition of pharyngeal pumping occurred at stressor concentrations below the threshold required for the induction of the 16-kDa heat shock proteins. Salicylate, which did not induce 16-kDa heat shock proteins at any concentration, nevertheless inhibited pharyngeal pumping. Heat was also inhibitory, at a temperature where 16-kDa heat shock protein production was near maximal. Some compounds caused only a partial inhibition of feeding while with others the effect was complete. Upon removal of the stressor, the nematodes resumed pharyngeal pumping with a residual inhibitory effect that depended on the concentration and type of stressor that had been applied. A number of C. elegans neurosensory mutant strains also exhibited a cessation of pharyngeal pumping when exposed to stressors suggesting that the mechanism underlying this inhibition was not entirely neurosensory and may be intrinsic to the pharynx. In C. elegans and other invertebrates, stress-induced inhibition of feeding may be an important survival mechanism that limits the intake of toxic solutes.

Alcohols↗
PubMed1988

Co-oxidation of salicylate and cholesterol during the oxidation of metmyoglobin by H2O2.

The reaction between metmyoglobin and H2O2 proceeds with oxidation of the hemo-protein iron to a higher valence state and consumption of the peroxide. This reaction is further associated with (a) O2 evolution; (b) hydroxylation of the aromatic compound salicylate to yield a set of dihydroxybenzoic acid derivatives (analyzed by HPLC with electrochemical detection); (c) autoxidation of cholesterol with formation of 3 beta-hydroxy-5-alpha-cholest-6-ene-5-hydroperoxide; and (d) formation of electronically excited states detected by low-level chemiluminescence. The heterolytic scission of the O-O bond of hydroperoxides by metmyoglobin causes the formation of an oxidizing equivalent capable of promoting peroxidation of linoleate and arachidonate (as indicated by the parallel formation of thiobarbituric acid-reactive material and an enhancement of chemiluminescence intensity). The identity of the oxidizing equivalent(s) is discussed in terms of the formation of a relatively stable higher state of oxidation of heme Fe (FeIV-OH or FeV = O) as well as on possible intermediate species derived during the decomposition of H2O2 by metmyoglobin, such as HO.and 1O2. These species might be involved either simultaneously or sequentially in the peroxidation of fatty acids as well as in the tissue damage associated with the formation of H2O2 in ischemic-reperfusion states.

Cholesterol↗
PubMed1997

Comparative cytotoxicity of 5-aminosalicylic acid (mesalazine) and related compounds in different cell lines.

Nonsteroidal anti-inflammatory drugs can cause serious side-effects such as tubulo-interstitial nephritis. Mesalazine (5-ASA, 5-aminosalicylic acid) is used for the treatment of colitis ulcerosa, Crohn disease, and other diseases; it has been found to induce necrosis of both proximal convoluted tubules and renal papillaries. The comparative cytotoxicity of 3-, 4-, and 5-aminosalicylic acid, acetylsalicylic acid (AcSA), and the parent compound salicylic acid (SA) was investigated for the free acids and for their sodium salts. The interaction with endogenous glutathione (GSH) was also investigated. Four established cell lines were used: MDCK, LLC-PK1, NRK as renal cells, and HepG2 as hepatic cells. The free acid compounds were less toxic than their corresponding salts. Acidic 5-ASA was the most toxic of the three isomers in MDCK and LLC-PK1 cells, while NRK and HepG2 were more susceptible to acidic 3-ASA. Addition of NaOH modified the relative toxicity of 3-ASA and 5-ASA. The LLC-PK1 and HepG2 cells were more sensitive to the test chemicals as their salts than were the NRK and MDCK cells. SA and 5-ASA decreased the GSH content in renal cells and increased it in HepG2. GSH depletion with L-buthionine-(S,R)-sulfoximine enhanced the toxicity only for SA in NRK and for 5-ASA and AcSA in HepG2. No correlation between endogenous GSH and the susceptibility of MDCK and LLC-PK1 to the test compounds was observed. The results suggest that no typical nephrotoxic effect occurred. No explanation could be found for the tubulo-interstitial nephritis caused by 5-ASA therapy.

Aminosalicylic Acid↗
PubMed1982

Effects of sodium salicylate and acetylsalicylic acid on intramural pH and ulceration of rabbit antral mucosa.

This study examines the relationship between the pH within the middle third of antral mucosa (intramural pH [IMpH]) and the development of ulceration caused by salicylates. Luminal soldium salicylate does not significantly alter the IMpH or cause ulceration of mucosa maintained at luminal pH 7. Salicylate at pH 3.5 initially decrease IMpH (7.28 to 6.75), during which time ulceration occurs. IMpH subsequently increase, resulting in profound alkalinization (pH 7.67) associated with increased HCO3 secretion. Salicylate at pH 1 causes a sustained decrease in IMpH (6.57), which is associated with more severe ulceration. Neither sodium salicylate nor acetylsalicylic acid given intravenously affects. IMpH or causes ulceration at luminal pH 7 or 3.5. However, at pH 1 both salicylate compounds cause ulceration and subtle changes in net ion fluxes without altering IMpH. The data suggest that acidification of the midportion of the mucosa in general is not a prerequisite for the occurrence of gross damage, and the damaging effects of intravenous salicylates cannot be explained by thier metabolic actions alone. However, it appears that the metabolic effects of salicylate make the mucosa more susceptible to the deleterious effects of diffusing acid. Since intravenous sodium salicylate and acetylsalicylic acid both cause ulceration but only acetylsalicylic acid alters prostaglandin synthesis, interference with prostaglandin metabolism does not appear to be a prerequisite for the occurrence of ulceration.

Animals↗
PubMed1988

Effects and interaction studies of triflusal and other salicylic derivatives on cyclooxygenase in rats.

Triflusal (TR) is a new salicylic acid derivative used clinically as an antiplatelet drug. Both aspirin (ASA) and TR inhibit platelet cyclooxygenase but the effects of these drugs are different. TR (0.5-2 mM) strongly inhibited platelet aggregation and malondialdehyde formation induced by arachidonic acid. The IC50 was 0.8 mM for TR and less than 0.1 mM for ASA. Deacetylated compounds, salicylic acid (SA) and HTB (the main metabolite of TR) were apparently competitive and reversible inhibitors of cyclooxygenase and HTB was 15 times more potent than SA. They did, however, partially prevent the inhibitory effects of ASA and TR in vitro. A similar effect was observed ex vivo in rats treated with HTB (100 mg/k i.p.) before TR or ASA (20 and 5 mg/kg i.v., respectively). Moreover, TR at 10 and 20 mg/kg i.v., inhibited thromboxane production by more than 50% while its effect on vascular cyclooxygenase was negligible. These findings indicated that TR is a weaker inhibitor of cyclooxygenase than ASA, and that HTB interferes with the effect of TR and ASA, despite the fact that HTB is a more potent reversible inhibitor than SA with probably a higher affinity for this enzyme.

Alprostadil↗
PubMed2003

Phenotypic evidence for inducible multiple antimicrobial resistance in Salmonella choleraesuis.

Multiple antimicrobial resistance (MAR) in Salmonella choleraesuis is becoming a major concern. It has been demonstrated that a MAR phenotype can be induced in Escherichia coli and other members of the Enterobacteriaceae by exposing the isolates to salicylates, various antimicrobials, or organic solvents used to combat and control bacterial infection. Therefore the purpose of the present study was to determine whether this marA-associated MAR-phenotype is inducible in S. choleraesuis. Isolates used in the present study were able to withstand toxic effects of the organic solvent cyclohexane naturally, or following exposure to the inducing compounds salicylate, tetracycline, or chloramphenicol. All isolates possessed fragments of marA with the predicted size of 408 bp when amplified using marA-specific primers by PCR. The resulting PCR products that were sequenced revealed that amplified S. choleraesuis marA was 99% and 85% homologous to the published Salmonella typhimurium and E. coli marA sequences respectively. Minimum inhibitory concentrations of tetracycline (P<0.08), chloramphenicol (P<0.001), rifampin (P<0.08), and nalidixic acid (P<0.001) against cyclohexane-tolerant mutants were significantly increased when compared with wild-type S. choleraesuis. Northern hybridization signals for both marA and acrB were increased in the induced isolates when compared to uninduced controls while soxS expression did not change between induced and uninduced cultures. The results suggest that marA is present in S. choleraesuis and a MAR-phenotype is inducible in S. choleraesuis presumably due to the overexpression of marA and acrB and not to the overexpression of soxS.

Bacterial Proteins↗
PubMed1999

Effects of salicylate and related compounds on fusidic acid MICs in Staphylococcus aureus.

Salicylate, acetyl-salicylate, benzoate and ibuprofen increased fusidic acid MICs for fusidic acid-resistant and -susceptible strains of Staphylococcus aureus representing six genetic lineages. The effects of these substances on fusidic acid resistance levels occurred in a strain-dependent manner. The weak acid acetate, and acetaminophen did not alter fusidic acid resistance levels, while the addition of saligenin, the alcohol of salicylate, reduced gradient plate MICs for all strains studied. These findings indicate that a benzoic acid structure is required for the induction of increased intrinsic fusidic acid resistance levels. When 2 mM salicylate was added to media used in population analyses, the number of cells able to survive on high concentrations of fusidic acid increased. This increase in cell survival was observed in two unrelated fusidic acid-resistant strains, with chromosomal (WBG8287) or plasmid (WBG1576) mediated resistance determinants and two unrelated susceptible strains. The salicylate-induced increase in fusidic acid resistance was phenotypic at low fusidic acid concentrations (relative to resistance phenotype) for WBG8287 and a fusidic acid-susceptible strain. On media containing salicylate and high fusidic acid concentrations, the mutation frequency to higher fusidic acid resistance levels was greater for WBG8287, compared with unsupplemented fusidic acid-containing media. These experiments provide evidence for a novel salicylate inducible fusidic acid resistance mechanism in S. aureus.

Anti-Bacterial Agents↗