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PubMed1989

[Formulation of effervescent tablets containing acetylsalicylic acid. III. Investigation of the stability of the active principles of tablets].

Parameters influencing the stability of active principles of effervescent tablets containing acetylsalicylic acid were investigated. On the basis of factorial experiment project the effects of contents of citric acid: sodium hydrogen carbonate, polyvinylpyrrolidone and those of storing temperature of tablets and humidity of atmosphere on decomposition of active principle were studied. High performance liquid chromatographic method has been developed for simultaneous determination of acetylsalicylic acid and salicylic acid. It has been established that first of all storing circumstances effect the stability of preparation and composition of tablets also significantly influences the decomposition of acetylsalicylic acid.

Aspirin↗
PubMed1986

Platelet aggregation and thromboxane release induced by arachidonic acid, collagen, ADP and platelet-activating factor following low dose acetylsalicylic acid in man.

The present study was undertaken in order to characterize the dose-dependent nature of acetylsalicylic acid (ASA) on platelet aggregation and plasma thromboxane B2 (TXB2) release in healthy volunteers. Volunteers received either 25, 50, 100 or 500 mg daily for five consecutive days. At the end of the five day period, all dosages of ASA were capable of completely suppressing TXB2 production and arachidonic acid-induced platelet aggregation. At that time, the second phase of ADP-induced aggregation was also blocked. However, while the inhibition following 500 mg ASA was complete after 24 hours, total inhibition with 100, 50 and 25 mg was attained only after two, three and four days, respectively, indicating the cumulative effect of ASA on platelets. Aggregation induced by collagen was also inhibited dose-dependently- yet slower and at no time complete. ASA had no inhibitory effect on aggregation by platelet-activating factor (PAF). It is concluded that a daily dose of 50 mg ASA would suffice in blocking platelet TXA2 production and aggregation induced by most physiological agents.

Adenosine Diphosphate↗
PubMed2005

Acetylsalicylic acid and acetaminophen protect against MPP+-induced mitochondrial damage and superoxide anion generation.

The effects of 1-methyl-4-phenylpyridinium (MPP+) has been extensively researched due to its selective toxicity to dopaminergic neurons. Mitochondrial dysfunction which is common in the etiology of Parkinson's disease (PD), has been widely implicated in MPP+-induced toxicity. MPP+-induced mitochondrial dysfunction is believed to result in the generation of free radicals. This study was therefore performed to assess the effect of MPP+ on mitochondrial function and the ability of MPP+ to generate superoxide free radicals. Furthermore, we assessed the ability of the non-narcotic analgesics, acetaminophen and acetylsalicylic acid to prevent any diliterious effects of the potent neurotoxin, MPP+, on mitochondrial function and superoxide anion generation, in vivo. Acetylsalicylic acid and acetaminophen prevented the MPP+-induced inhibition of the electron transport chain and complex I activity. In addition, acetylsalicylic acid and acetaminophen significantly attenuated the MPP+-induced superoxide anion generation. Furthermore the results provide novel data explaining the ability of these agents to prevent MPP+-induced mitochondrial dysfunction and subsequent reactive oxygen species generation. While these findings suggest the usefulness of non-narcotic analgesics in neuroprotective therapy in neurodegenerative diseases, acetylsalicylic acid appears to be a potential candidate in prophylactic as well as in adjuvant therapy in Parkinson's disease.

1-Methyl-4-phenylpyridinium↗
PubMed1996

In vitro study of the anti-aggregating activity of two nitroderivatives of acetylsalicylic acid.

The antiplatelet activity of two new nitrocompounds, chemically related to acetylsalicylic acid (NCX 4215 and NCX 4016), was studied in vitro to verify the hypothetical dual action of these drugs. Both drugs, in a dose-dependent way, inhibited arachidonic acid-induced platelet aggregation and thromboxane A2 production, measured as thromboxane B2 concentration in whole blood. These effects are likely to be related to cyclo-oxygenase inhibition. NCX 4215 and NCX 4016 in a dose-dependent way inhibited also thrombin-induced aggregation of platelets pretreated with acetylsalicylic acid. These inhibitory effects are related to nitric oxide release and cGMP increase and significantly reversed by oxyhaemoglobin and methylene blue. Either as a cyclo-oxygenase inhibitor or as a nitric oxide donor, NCX 4016 proved to be significantly more potent than NCX 4215.

Arachidonic Acid↗
PubMed1981

[Control of implantation in rats and sows by peroral administration of prostaglandin synthetase inhibitors. 3. Effects of prostaglandin F2 alpha, progesterone/estrone, and acetylsalicylic acid on implantation and biochemical composition of amniotic fluid and fetuses of young sows].

Low pregnancy rate (62.5 per cent), low implantation results (64.7 per cent), high percentage of dead foetuses (5.4 per cent), and low allantois fluid volume/foetus (130.7 ml) are likely to suggest adverse effect of prostaglandin administered in early gravidity since all these values deviate sizeably from control data (81.3, 68.0 and 1.1 per cent, 154.7 ml). On the other hand, those negative phenomena were not reflected in the results obtained from biochemical analysis of amniotic fluid and foetuses. The progesterone/oestron and acetylsalicylic acid doses used obviously had no impact upon pregnancy rates (81.3 and 75.0 per cent) and overall implantates (67.4 and 69.6 per cent), when compared to the controls (81.3 and 68.0 per cent). The lowest foetal loss occurred following application of acetylsalicylic acid (30.4 per cent, but 32.0 per cent for the controls). Increase in allantois fluid volume/foetus by progesterone/oestrone and acetylsalicylic acid was one of the findings of particular interest (progesterone/oestron: 174.4 ml, acetylsalicylic acid: 196.5 ml, control: 154.7 ml). The results obtained from amniotic fluid tests (rises in protein and progesterone concentrations) may, to some extent, suggest the possible existence of a relationship in action between the two substances. No information at all on the type of action of these substances was obtainable by biochemical analysis of foetal composition.

Amniotic Fluid↗
PubMedDate not supplied

Application of liquid chromatography to the simultaneous determination of acetylsalicylic acid, caffeine, codeine, paracetamol, pyridoxine, and thiamine in pharmaceutical preparations.

This paper describes a rapid reversed-phase liquid chromatographic method, with UV detection, for the simultaneous determination of acetylsalicylic acid, caffeine, codeine, paracetamol, pyridoxine, and thiamine in pharmaceutical preparations. A reversed-phase C18 Nucleosil column is used. The mobile phase consists of 2 successive eluants: water (5 min) and acetonitrile-water (75 + 25, v/v; 9 min), both adjusted to pH 2.1 with phosphoric acid. Before determination acetylsalicylic acid is completely converted to salicylic acid by alkaline hydrolysis. Salicylic acid, caffeine, paracetamol, pyridoxine, and thiamine are all detected at 285 nm, whereas codeine is detected at 240 nm. Calibration curves were linear for salicylic acid, caffeine, paracetamol, and pyridoxine in the range of 50-500 mg/L, and for codeine and thiamine in the range of 50-1000 mg/L. The method was applied to the analysis of 13 fortified commercial pharmaceutical preparations. Recoveries ranged from 92.6 to 105.5%, with relative standard deviations of 1.1-5.8%.

Acetaminophen↗
PubMed2002

Inhibitory effect of acetylsalicylic acid on metalloproteinase activity in human lung adenocarcinoma at different stages of differentiation.

The mechanism underlying the anticancer effect of nonsteroidal anti-inflammatory drugs (NSAIDs) is not clear. We addressed the question whether the alterations in collagen content in lung adenocarcinomas reported in previous studies result from dysregulation of gelatinolytic activity and whether the activity is altered by acetylsalicylic acid in vitro. Human lung adenocarcinomas were divided into three groups: well-differentiated (G1), moderately differentiated (G2) and poorly differentiated (G3) tumors. Each group was compared with normal lung tissue with respect to tissue collagen and collagen degradation product content (hydroxyproline assay), gelatinolytic activity (zymography) and the expression of matrix metalloproteinases, MMP-2 and MMP-9 (Western immunoblot). Moreover, in the studied tissues, the effect of acetylsalicylic acid on gelatinolytic activity was measured. The lung adenocarcinoma G1 had a similar collagen content as normal lung tissue but increased amounts of collagen degradation products and free hydroxyproline. These phenomena were accompanied by a marked increase in gelatinolytic activity (MMP-2 and MMP-9) in the G1 tumor. In adenocarcinoma G2, the free hydroxyproline content and gelatinolytic activity were increased, while the collagen and collagen degradation product contents were not markedly altered, compared to control. In contrast, adenocarcinoma G3 had an increased tissue collagen content (by about 60%), decreased percentage of collagen degradation products and similar gelatinolytic activity, compared to normal lung. Acetylsalicylic acid was found to inhibit gelatinolytic activity both in control and adenocarcinoma tissues, preferentially the active forms of gelatinases MMP-2 and MMP-9. The results suggest that human lung adenocarcinoma G1, through an elevated expression of the activated forms of both MMP-2 and MMP-9, may represent a more invasive phenotype than less differentiated tumors G2 or G3. It indicates that lung adenocarcinoma G1 should be considered as a possible target for metalloproteinase inhibitory therapy. Acetylsalicylic acid may be such a therapeutical agent in cancer prevention or early stages of tumor growth.

Adenocarcinoma↗
PubMed1981

The construction and uses of factorial designs in the preparation of solid dosage forms. Part 1: Effervescent acetylsalicylic acid tablets.

The construction and application of a fractional factorial design of the type N = 2(5-2) for the preparation of effervescent acetylsalicylic acid tablets by a new technique was demonstrated. This method involved direct compression of the tablet ingredients, dipping the tablets in a volatile mixed solvent system and subsequent removal of the solvent. With the help of a derived regression equation, the factors considered most likely to have a beneficial effect on tablet hardness were: the compression force, the percent of acetylsalicylic acid content/tablet, the particle size of tablet ingredients and the solvent ratio. The time of dipping was found to have an insignificant effect on tablet hardness. By following the path of the steepest ascent, effervescent acetylsalicylic acid tablets of remarkable hardness, friability and dissolution time were obtained. The optimum conditions for preparing these tablets were determined.

Aspirin↗
PubMed2002

The combination of 1alpha,25(OH2)-vitamin D3, calcium and acetylsalicylic acid affects azoxymethane-induced aberrant crypt foci and colorectal tumours in rats.

Effects of 1alpha,25(OH)(2)-vitamin D(3) and acetylsalicylic acid at various dietary levels of calcium (CaCO(3)) on development of aberrant crypt foci (ACF) and tumours in colon were examined in groups of 16 male F344 rats initiated with azoxymethane and observed for 16 weeks. Calcium was the most potent modulator of ACF development. The total number of ACF increased with low calcium and decreased with high calcium. The number of large ACF decreased with any addition of calcium, acetylsalicylic acid and 1alpha,25(OH)(2)-vitamin D(3). High levels of calcium alone or in combination with 1alpha,25(OH)(2)-vitamin D(3) increased the incidence of tumour-bearing animals. 1alpha,25(OH)(2)-vitamin D(3) and acetylsalicylic acid at 5,000 ppm calcium increased the incidence as well.

Animals↗
PubMed2006

Acetylsalicylic acid and acetaminophen protect against oxidative neurotoxicity.

Due to the implication of oxidative stress in neurodegenerative disorders we decided to investigate the antioxidant properties of acetylsalicylic acid and acetaminophen either alone or in combination. The thiobarbituric acid assay (TBA) and the nitroblue tetrazolium (NBT) assay were used to investigate quinolinic acid (QA)-induced: lipid peroxidation and superoxide anion generation in the rat hippocampus, in vivo. The study also shows, using cresyl violet staining, the preservation of structural integrity of neuronal cells following treatment with acetylsalicylic acid and acetaminophen in QA-lesioned rat hippocampus. Furthermore the study sought to determine whether these agents have any effect on endogenous (QA) formation. This study shows that acetylsalicylic acid and acetaminophen inhibit QA-induced superoxide anion generation, lipid peroxidation and cell damage, in vivo, in the rat hippocampus. In addition these agents inhibit the enzyme, 3-hydroxyanthranilic acid oxygenase (3-HAO), responsible for the synthesis of endogenous QA.

3-Hydroxyanthranilate 3,4-Dioxygenase↗
PubMed2002

Hard to swallow dry: kinetics and mechanism of the anhydrous thermal decomposition of acetylsalicylic acid.

The methods of thermal analysis and mass spectrometry have been used to study the kinetics and mechanism of the anhydrous thermal decomposition of acetylsalicylic acid. Both thermogravimetric analysis (TGA) and differential scanning calorimetry (DSC) show that decomposition occurs in two steps. Mass-spectrometric analysis of the residue left after the first decomposition step (approximately equal to 60% mass loss) suggests that in the condensed phase, acetylsalicylic acid decomposes by first forming linear oligomers that are further converted into cyclic oligomers. Model-free isoconversional kinetic analysis of TGA traces has been used to determine global activation energies as a function of the extent of reaction. This method of analysis has also been used to make kinetic predictions of shelf life at ambient temperatures (20-40 degrees C) under anhydrous conditions for acetylsalicylic acid. Our estimate of a shelf life of 876 days (approximately equal to 2.4 years) for 5% decomposition at 30 degrees C is in good agreement with shelf lives of 2-3 years that are stamped on over-the-counter aspirin bottles. Hence, this approach can be used to systematically study the factors that determine the decomposition kinetics of aspirin and may be used for express screening of pharmaceuticals in order to identify those with desirable thermal stabilities.

Algorithms↗
PubMed1984

Actions and interactions of acetylsalicylic acid, salicylic acid and diflunisal on platelet aggregation.

Acetylsalicylic acid (ASA) is increasingly employed in the secondary prophylaxis of thromboembolic diseases, due to its capacity to inhibit platelet aggregation. The anti-aggregatory effect of ASA on platelets can be inhibited in vitro by a high concentration of salicylic acid (SA). SA is generated in vivo upon ASA administration, and the SA thus formed might impair the antiplatelet effect of ASA. To assess this possibility, the platelet response to ASA was tested in healthy volunteers before and after medication for 1 week with ASA 1 g t.i.d., with SA 1 g t.i.d., and with the SA derivative diflunisal 0.5 g b.i.d. Pre-medication test doses of 1 g ASA always inhibited platelet aggregation in vivo. Neither treatment with SA nor diflunisal, producing plasma steady-state concentrations of about 1.0 and 0.35 mmol/l, respectively, inhibited platelet aggregation. Nor did administration of SA, diflunisal or ASA itself impair the anti-aggregatory effect of a fresh test dose of ASA. ASA inhibited platelet aggregation in vitro at 0.03 mmol/l, whereas SA and diflunisal failed to impair platelet aggregation until concentrations exceeding 2.0 and 0.5 mmol/l, respectively, were reached. These findings make it unlikely that SA formed upon administration of ASA would impair the anti-aggregating capacity of ASA.

Adult↗
PubMed1991

Further investigations on the clastogenicity of paracetamol and acetylsalicylic acid in vitro.

Paracetamol (PCM) and acetylsalicylic acid (ASA), both widely used analgesics, were tested for their clastogenicity in V79 cells in vitro. Rat liver S9 mix and primary rat hepatocytes (PRH) were used as external activation systems. ASA was found to be negative with and without activation system in concentrations up to 10(-2) M. In contrast PCM induced concentration-dependent chromosomal aberrations with and without activation system within the range of 3 x 10(-3) and 10(-2) M. The greatest effects were observed following continuous treatment with PRH activation and without external metabolization. Pulse treatments without external metabolization, with S9 mix and PRH were less effective. The clastogenic potency of PCM seems to be partly independent of metabolic activation. Although clastogenic effects in vitro were observed only in very high concentrations pharmacokinetic data and other published mutagenicity data indicate that there might be a risk for human use. Peak plasma levels of more than 10(-4) M have been reported (Forrest et al., 1982) and 2 groups of investigators (Kocisova et al., 1988; Hongslo et al., 1990) found PCM to be weakly clastogenic in human lymphocytes in vivo in the maximum human therapeutic dose range.

Acetaminophen↗
PubMed1993

Acacia-gelatin microencapsulated liposomes: preparation, stability, and release of acetylsalicylic acid.

Liposomes of dipalmitoylphosphatidylcholine (DPPC) containing acetylsalicylic acid (ASA) have been microencapsulated by acacia-gelatin using the complex coacervation technique as a potential oral drug delivery system. The encapsulation efficiency of ASA was unaltered by the microencapsulation process. The stability of the microencapsulated liposomes in sodium cholate solutions at pH 5.6 was much greater than the corresponding liposomes. The optimum composition and conditions for stability and ASA release were 3.0% acacia-gelatin and a 1- to 2-hr formaldehyde hardening time. Approximately 25% ASA was released in the first 6 hr from microencapsulated liposomes at 23 degrees C and the kinetics followed matrix-controlled release (Q varies; is directly proportional to t1/2). At 37 degrees C, this increased to 75% released in 30 min followed by a slow constant release, likely due to lowering of the phase transition temperature of DPPC by the acacia-gelatin to near 37 degrees C. At both temperatures, the release from control liposomes was even more rapid. Hardening times of 4 hr and an acacia-gelatin concentration of 5% resulted in a lower stability of liposomes and a faster release of ASA. It is concluded that under appropriate conditions the microencapsulation of liposomes by acacia-gelatin may increase their potential as an oral drug delivery system.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1999

Acetylsalicylic acid in the treatment of headache.

Acetylsalicylic acid (ASA) is used to treat a broad range of symptoms and disorders. Since its discovery in 1897, it has been used to treat fever and rheumatic pain, to inhibit the formation of thrombocytes, to prevent myocardial ischemia and strokes, and as preventive medication against neoplasms. ASA is best known, however, as a headache medication. For this function alone, ASA underwent an evolution: from powder to tablet to effervescent and chewable tablets. In addition to these oral formulations, an injectable form was developed in the 1970s for intravenous and intramuscular application. Furthermore, coated (slow-releasing) tablets are now used in the prophylactic treatment of migraine. The various forms of ASA used to treat headache are discussed and the controlled studies conducted to evaluate ASA's efficacy in headache treatment are summarized.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1970

Acetylsalicylic acid--induced hemolysis and its mechanism.

Acetylsalicylic acid (ASA) is known to cause severe hemolytic anemia in some glucose-6-phosphate-dehydrogenase-deficient (G-6-PD-deficient) individuals. To study its mechanism, erythrocytes from an ASA-sensitive patient were transfused into a normal compatible recipient. The administration of 2,5-dihydroxybenzoic (gentisic) acid, a known ASA metabolite with redox properties, to the recipient resulted in a marked decrease in the survival of the patient's erythrocytes. Similar studies with red cells from individuals with A- and Mediterranean variants of G-6-PD revealed no alteration in the erythrocytes' survival. Further studies disclosed that both salicylate and gentisate competitively inhibited the G-6-PD from the ASA-sensitive patient resulting in a marked change in the K(m) for NADP. These drugs also inhibited the A- and Mediterranean variants of G-6-PD. The magnitude of inhibition, however, was comparatively small and not different from that observed with a normal enzyme. The above studies suggested that enzyme inhibition by salicylate and gentisate may play an important role in ASA-induced hemolysis. Such an inhibition would further curtail NADPH regeneration, rendering the cells more vulnerable to oxidants. In this connection, gentisate seems to play a major role in ASA-induced hemolysis for it is both a G-6-PD inhibitor and an "oxidant."

Adolescent↗
PubMed1981

Hypocalcemic effect of acetylsalicylic acid in rats.

Oral administration of acetylsalicylic acid (ASA) at a dose of 200 mg/kg produced a decrease in both total plasma calcium and plasma ionic calcium levels in rats. The percent changes from controls in both total and ionic calcium were similar, being approximately 13% at 3 hr after the administration. A significant (p less than 0.01) decrease in plasma calcium level was also observed at 4 hr after oral administration of salicylic acid at a dose level of 177 mg/kg. However, oral administration of other non-steroidal anti-inflammatory agents such as indomethacin failed to decrease plasma calcium levels in rats. The hypocalcemic effect of ASA was recognized in parathyroidectomized rats, but neither in thyroparathyroidectomized nor in thyroidectomized rats. Therefore, the data suggested that the action of ASA might be mediated by stimulation of calcitonin release, but not by inhibition of prostaglandin biosynthesis.

Animals↗
PubMedDate not supplied

Nasal provocation tests in the diagnosis of urticaria induced by acetylsalicylic acid.

Nasal provocation tests with lysine acetylsalicylic acid (ASA) have been used in the diagnosis of ASA-induced asthma and rhinitis. To establish its possible role in identifying aspirin sensitivity manifested by urticaria or angioedema, 18 patients suffering from chronic or acute recurring urticaria/angioedema (10 ASA-sensitive and 8 ASA-nonsensitive) were submitted to nasal provocation tests with freshly prepared solutions of lysine ASA. Clinical response and variation of nasal expiratory peak-flow were evaluated, classified according to previously defined scores, and compared. The results showed a significant difference between ASA-sensitive and ASA-nonsensitive patients, suggesting that this test can be an important diagnostic tool for ASA-induced urticaria/angioedema.

Adolescent↗