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PubMed1993

Induction of (omega-1)-oxidation of monocarboxylic acids by acetylsalicylic acid.

Monocarboxylic acids may be oxidized at the omega- and (omega-1)- positions to form dicarboxylic acids (DCAs) and (omega-1)-hydroxy- or (omega-1)-oxoacids. The significance of this pathway under normal conditions is unknown, but DCAs and (omega-1)-hydroxyacids are prominent features of disease states. The stimulation of this pathway has been linked to induction of fatty acid-binding protein and peroxisomal proliferation. In this study, we examined the effect of acetylsalicylic acid (ASA) on (omega-1)-oxidation. (Omega-1)-oxidation was assessed in subcellular fractions of rat liver. Rats were fed a normal diet or an ASA-supplemented diet. Products were identified by gas chromatography-mass spectrometry (GC-MS) and by comparison with the properties of authentic synthetic standards. Doses of ASA that produced relatively low serum concentrations (12-24 mg/dl) resulted in as much as a 20-fold increase in the capacity for (omega-1)-oxidation of medium (C12-C15) and long chain (C16-C20) monocarboxylic acids. Normal rat liver oxidizes monocarboxylic acids to (omega-1)-oxoacids, while liver from ASA-treated rats converts these substrates to (omega-1)-oxodicarboxylic acids and (omega-1)-oxoacids. The formation of oxoacids and oxodicarboxylic acids may be due to different enzymes. The formation of oxodicarboxylic acids appears to be more labile than the formation of oxoacids. These two processes also are differentially induced by ASA and have different substrate specificities. These results demonstrate that ASA is a potent stimulant of (omega-1)-oxidation and induces the formation of products that can be shortened in peroxisomes to key metabolic intermediates.

Animals↗
PubMedDate not supplied

Effects of highly concentrated omega-3 polyunsaturated fatty acids and acetylsalicylic acid, alone and combined, on bleeding time and serum lipid profile.

Twenty-two patients with stable coronary heart disease were randomly assigned to either of two groups. Group I (n = 11) was given acetylsalicylic acid (ASA) 300 mg daily for 1 week, whereafter a daily supplement of 3,4 g eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) as a highly concentrated ethylester, formulation ("K-85", Norsk Hydro) was added for another 4 weeks. Group II (n = 11) was given 3,4 g daily of EPA and DHA for 4 weeks, after which ASA 300 mg daily was added for another week. Determination of serum fatty acids confirmed satisfying absorption of EPA and DHA. A significant increase of the Ivy bleeding time was registered following administration of both "K-85" (240 to 270 sec, median values) and ASA (270 to 360 sec, median values) alone. A slighter increase was noted by a combination of the two principles. A reduction in serum triglycerides of 17% was noted after "K-85" (median values, both groups). Serum total cholesterol decreased after "K-85" administration in group I, but not so in group II. HDL-cholesterol remained unchanged. Serum lipids remained unaffected by ASA. During administration of "K-85" no adverse effects or bleeding episodes were seen.

Adult↗
PubMed1978

Meseclazone, 5-chlorosalicylic acid and acetylsalicylic acid. Comparison of their effects on in vitro and ex vivo platelet aggregation.

Meseclazone and its major metabolite, 5-chlorosalicylic acid (5-CSA) have been shown to possess anti-inflammatory, analgesic and antipyretic activity. The comparative effects of these compounds on pletelet aggregation were evaluated in vitro and ex vivo with acetylsalicylic acid (ASA). In vitro, meseclazone and ASA exhibited almost identical inhibitory potency of secondary phase ADP aggregation while 5-CSA was less effective. Moreover, collagen aggregation was inhibited by all three agents: ASA greater than meseclazone greater than 5-CSA. Thrombin-induced aggregation was inhibited to approximately the same extent by 5-CSA and ASA while meseclazone was inactive. The in vitro effects on the release-inducing aggregants were confirmed by ex vivo experiments in rats. These demonstrated that ASA and meseclazone inhibited collagen-induced aggregation 1 and 4 hr after oral administration although ASA was three to four times more active. ASA, but not meseclazone, was still effective 24 hr after administration. Bleeding times in rats 1 and 4 hr following oral administration of meseclazone and ASA were not altered. It is concluded that meseclazone and/or 5-CSA inhibit in vitro and ex vivo platelet aggregation initiated by the release reaction similar to ASA and other non-steroidal anti-inflammatory drugs.

Adenosine Diphosphate↗
PubMed1995

Copper(II) interactions with nonsteroidal antiinflammatory agents. I. Salicylic acid and acetylsalicylic acid.

Recently a growing body of evidence has accumulated on the beneficial effects of copper compounds toward various models of inflammation, and copper complexes of nonsteroidal antiinflammatory drugs (NSAIDs) have been shown to be more effective in this respect than the parent agents. However, the origin of this activity remains unclear: The ability of NSAIDs to influence copper metabolism is still questionable, and apart from the claimed SOD-like activity of copper salts in vivo, relatively little is known about how copper-NSAID interactions may help regulate the inflammatory process. Before the potential role of copper-NSAID complexes versus inflammation can be elucidated, speciation studies are necessary (i) to analyze the overall influence of these drugs on copper metabolism and (ii) to discriminate the individual complexes likely to represent the active form of the drug in vivo. In this paper, copper(II) complex equilibria with salicylic and acetylsalicylic acids--and benzoic acid used as a reference--as well as the mixed-ligand complex equilibria generated by these binary systems and L-histidine [main low-molar-mass ligand of copper(II) in blood plasma] have been investigated under physiological conditions (37 degrees C; 0.15-M NaCl). Confirming previous observations by others, resulting simulated plasma copper distributions virtually rule out any quantitative influence of salicylate on copper tissue diffusion at therapeutic levels. Even though, as is presently shown, both salicylate and acetylsalicylate may favor the gastrointestinal absorption of copper, it seems unlikely that salicylate can exert its antinflammatory activity predominantly through copper complexation. The assertion that copper-NSAID complexes represent the active forms of NSAIDs therefore seems to be of limited significance for salicylate.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1992

Gastric potential difference measurement as a quantification of gastrointestinal tolerability comparing a buffered acetylsalicylic acid formulation versus plain acetylsalicylic acid.

Two different acetylsalicylic acid (ASA, CAS 50-78-2) formulations (Aspirin) were compared regarding their gastric mucosal tolerability. After administration of plain ASA, buffered ASA and ASA placebo the decrease of gastric potential difference (GPD) was measured. Evaluation of the GPD parameters showed a better tolerability of buffered ASA than of plain ASA. It was therefore concluded that buffered ASA effects less gastric mucosal irritation than plain ASA.

Adult↗
PubMed1984

Rapid and sensitive determination of acetylsalicylic acid and its metabolites using reversed-phase high-performance liquid chromatography.

A rapid and sensitive high-performance liquid chromatographic technique was developed for the simultaneous determination of gentisic acid, salicyluric acid, acetylsalicylic acid and salicylic acid in plasma and serum. The method involved a single deproteinization step and separation using a reversed-phase column eluted with a buffered methanol (35%) mobile phase. Detection was achieved with a variable-wavelength ultraviolet detector set at 235 nm and a given chromatographic analysis could be completed in less than 10 min. The method was tested in both human and animal (rat) models given a single dose of acetylsalicylic acid.

Animals↗
PubMed2005

Superior efficacy of clopidogrel plus acetylsalicylic acid compared with extended-release dipyridamole plus acetylsalicylic acid in preventing arterial thrombogenesis in healthy volunteers.

INTRODUCTION: Recent ex vivo platelet aggregometry data indicate that clopidogrel 75 mg/day plus acetylsalicylic acid (ASA) 75 mg/day is a more potent antiplatelet regimen than the marketed combination of dipyridamole+ASA. The present study was designed to assess the antithrombotic effect of both dual antiplatelet regimens using a human ex vivo model of arterial thrombosis. MATERIALS AND METHODS: This was a randomized, double-blind, placebo-controlled, crossover study. During two 10-day treatment periods separated by a 14-day washout period, 23 healthy male volunteers received once-daily clopidogrel 75 mg plus acetylsalicylic acid 75 mg, or twice-daily extended-release dipyridamole 200 mg plus acetylsalicylic acid 25 mg. Assessments were made at baseline and on Day 10 of each period. Arterial thrombus formation was induced ex vivo by exposing a collagen-coated surface in a parallel-plate perfusion chamber to native blood for 3 min (arterial wall shear rate 2600 s(-1)). Total platelet and fibrin deposition was determined by immunoenzymatic methods. RESULTS: Compared with baseline values, the mean inhibition of total platelet deposition was 63.9+/-5.9% with clopidogrel plus acetylsalicylic acid, compared with 18.4+/-5.6% for extended-release dipyridamole plus acetylsalicylic acid (67% reduction; 95% CI, 49-79%; p<0.0001). Corresponding figures for fibrin deposition were 64.9+/-4.8% and 18.3+/-9.7%, respectively (58% reduction; 95% CI, 45-67%; p<0.0001). Both treatments were well tolerated. CONCLUSIONS: Clopidogrel plus acetylsalicylic acid showed significantly superior antithrombotic efficacy compared with extended-release dipyridamole plus acetylsalicylic acid in preventing arterial thrombogenesis in humans.

Adolescent↗
PubMed1998

Simultaneous determination of salicylic acid and acetylsalicylic acid in aspirin delayed-release tablet formulations by second-derivative UV spectrophotometry.

A rapid, simple assay procedure was developed for simultaneous analysis of aspirin (ASA) and salicylic acid (SA) in aspirin delayed-release tablet formulation by 'zero crossing' second-derivative UV spectrophotometry. The zero-order absorption spectra and second derivative spectra of ASA and SA were recorded in diluting solution acetonitrile-formic acid (99:1). The accuracy of the method was demonstrated by the determination of ASA and SA in five tablets formulations (each 20 tablets of the same batch) by the described method and by high performance liquid chromatographic method, and the results were in good agreement.

Aspirin↗