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At least 199 records · Page 11Linked to original sources
PubMed1992

Comparison of two classes of non-peptide drugs as antagonists of neutrophil receptors for f-Met-Leu-Phe. Pyrazolons and iodinated radiographic contrast agents.

The radiographic contrast agent sodium diatrizoate (DTR) reportedly inhibits f-Met-Leu-Phe-induced chemotaxis in human neutrophils. DTR is also an ingredient of Ficoll-Paque, a density centrifugation medium widely used to purify human polymorphonuclear leukocytes (PMNs). Exposure of PMNs to DTR during preparation had no detrimental effect on subsequent binding characteristics of tritiated f-Met-Leu-Phe, probably owing to a rapid dissociation of DTR from the PMN receptors. DTR competed directly with f-Met-Leu-Phe for receptor binding, but was 160- and 640-fold less potent than phenylbutazone and 1,2-diphenyl-4-[3-(1-naphthyl)-propyl]-3,5-pyrazolidinedione (DPN; an analog of phenylbutazone), respectively. Iohexol and the methylamide of DTR did not compete with [3H]f-Met-Leu-Phe in receptor binding, supporting the existence of a definite interaction between iodinated aromatic molecules and the f-Met-Leu-Phe receptor. DTR did not inhibit prostaglandin synthesis, as did DPN. Both drugs inhibited chemotactic peptide-induced release of superoxide anion in a concentration-dependent manner, and were relatively selective for f-Met-Leu-Phe, as opposed to C5a. Both drugs at 10 microM interfered non-selectively with chemotactic peptide-induced beta-glucuronidase release from PMNs. Available non-peptide antagonists of f-Met-Leu-Phe exhibited other pharmacodynamic properties that could make them unsuitable for future in vivo studies designed to probe the physiological role of the receptor.

Binding, Competitive↗
PubMed2005

Dielectric relaxation spectroscopy of heteronuclear cobalt(II)-copper(II) complex of 1-phenyl-3-methyl-5-pyrazolone.

A bright green CoCu(PMP)(OH)2(H2O)2 complex was synthesized. Its structure was elucidated and characterized by different spectroscopic techniques. Both cobalt and copper atoms attain tetrahedral geometry. The complex was investigated by the dielectric relaxation spectroscopy. The dielectric parameters are discussed in terms of temperature and frequency changes. The conductivity of the complex decreased as the temperature increased in the temperature range 30-100 degrees C, while above this temperature range stepwise increase in the conductivity was observed.

Antipyrine↗
PubMed2003

Spiro-fused (C2)-azirino-(C4)-pyrazolones, a new heterocyclic system. Synthesis, spectroscopic studies and X-ray structure analysis.

Reaction of 1-substituted 4-acyl-5-hydroxy-3-methyl-1H-pyrazoles (2) with hydroxylamine gives the corresponding "oximes" 3, which are mainly present as (Z)-2,4-dihydro-4-[(hydroxyamino)methylene]-3H-pyrazol-3-ones. Treatment of compounds 3 with trichloroacetyl isocyanate/potassium carbonate in anhydrous diethyl ether affords 7-methyl-1,5,6-triazaspiro[2.4]hepta-1,6-dien-4-ones (4). The structure of compounds 4 was elucidated by means of single-crystal X-ray analysis (4f, 4h) and confirmed by NMR spectroscopic investigations ((1)H, (13)C).

Journal Article↗
PubMed1980

Kinetics and metabolism of pyrazolones (propyphenazone, aminopyrine and dipyrone).

1 Propyphenazone 220 mg was administered orally to volunteers. Maximum plasma concentrations between 1.5 microgram/ml and 3.5 micrograms/ml were found 30 min later. After comparable doses plasma concentrations in dog and rabbit were lower. The distribution volumes were 2 l/kg. 2 The major metabolic route of propyphenazone is demethylation. The main urinary metabolite is the enolglucuronide of N-(2)-demethylpropyphenazone. 3 Aminopyrine is rapidly and almost completely absorbed after oral administration. Maximum plasma concentrations of 10 microgram/ml are reached 1.5 h after a 500 mg dose. The biological half-life is 2-3 h, the relative distribution volume 60% on average, and binding to plasma proteins approximately 15%. 4 Unchanged aminopyrine is only excreted in small quantities. The major routes of metabolism are demethylation (4-methylaminoantipyrine and 4-aminoantipyrine) and acylation (4-acetyl and 4-formylaminoantipyrine). There are other biotransformation products. 5 After oral administration of [14C]-dipyrone 480 mg the maximum serum concentration of 13.4 +/- 0.8 microgram/ml occurred at 1-1.5 hours. 6 Dipyrone was not detectable in serum or urine. Four of seven metabolites were identified, and were identical with the main metabolites of aminopyrine.

Administration, Oral↗
PubMed1980

Inhibition of platelet aggregation by tartrazine and a pyrazolone analogue in normal and allergic individuals.

The effect of tartrazine (T) (yellow dye No. 5) and one of its metabolites an aminopyrazolone analogue (1-sulphophenyl-3-carboxy-5-hydroxypyrazole, SCHP) upon collagen-induced platelet aggregation (C-PA) was investigated in fourteen atopic patients and fourteen normal subjects. Both T and SCHP inhibited C-PA in atopic patients at significantly lower doses than in normal volunteers. The mean inhibitory concentrations of SCHP were similar to aspirin in both atopic and normal individuals. Although the precise mechanism by which these chemicals block C-PA has not been elucidated, this in vitro system may be a useful method of assessing non-immune mechanisms involved in reactions to tartrazine.

Aspirin↗
PubMed1983

Decreasing inhibitory potency of prostaglandin synthetase inhibitors during their cooxidative metabolism. Studies on aminophenols, pyrazolon derivatives and 1,3-diphenylisobenzofuran.

A variety of prostaglandin synthetase inhibitors are cooxygenated during arachidonic acid peroxidation catalyzed by rat renal medulla prostaglandin synthetase or soybean lipoxygenase. Phenylbutazone, aminopyrine, 1,3-diphenylisobenzofuran, paracetamol, p-aminophenol, p-phenetidine and other o- and m-substituted aminophenol derivatives were cooxygenated, whereby prostaglandin synthetase inhibition was significantly weakened due to the formation of less inhibitory metabolites. In contrast, the inhibitory potency of diclofenac, indomethacin and phenacetin and its analogues remained unchanged during prostaglandin synthesis inhibition, because these compounds were no suitable cooxygenation substrates. Evidence is given that quinone imines may not be involved in the cooxidative metabolism of paracetamol and other aminophenols. As to the mechanisms of cooxygenation of suitable substrates dependent on their chemical structures either the arachidonic acid oxygenase or the subsequent hydroperoxidase reaction may trigger the oxygenation. 1,3-Diphenylisobenzofuran is metabolized during the formation of arachidonic acid hydroperoxides in contrast to paracetamol, which requires an additional peroxidase reaction to yield reactive metabolites.

Acetaminophen↗