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At least 253 records · Page 14Linked to original sources
PubMed1978

[Pharmacological properties of N-(3',4'-dimethoxycinnamoyl) anthranilic acid (N-5'), a new anti-atopic agent. (3).--Influence on homologous passive cutaneous anaphylaxis mediated by homocytotropic antibody (author's transl)].

N-5' shows a potent inhibitory action on the homologous passive cutaneous anaphylaxis (PCA) in rats mainly through the inhibition of histamine release from mast cells. The present experiment was an attempt to clarify in detail the pharmacological properties of N-5'. Inhibition of PCA was most potent at 30 or 60 min pretreatment with N-5', and negligible at 240 min pretreatment. Given p.o., N-5' produced a dose-dependent, potent inhibitory action at 30-min pretreatment. On the other hand, disodium cromoglycate (DSCG) had little effect on PCA when given orally. On the case of i.v. administration, N-5' (20 mg/kg) and DSCG (5 mg/kg) showed a most potent inhibition of PCA at 5 min pretreatment. The inhibitory action of DSCG was, however, shorter lasting than that of N-5'. Median effective doses (ED50) of DSCG and N-5' on the PCA were estimated to be 0.79 and 8.8 mg/kg i.v., respectively. Inhibitory activity of N-5' in the adrenalectomized rat did not differ from that in sham operated animals. N-5' had a more potent inhibitory action on the PCA in infant rats than in adults. Inhibitory activity of N-5' in the case of 1, 2, 3 and 4 weeks of successive administration was equipotent to that with a single administration.

Administration, Oral↗
PubMed1966

The metabolism of [2-14C] indole in the rat.

1. [2-(14)C]Indole has been synthesized from [(14)C]formate and o-toluidine via N[(14)C]-formyltoluidine. 2. When fed to rats, the (14)C of [(14)C]indole (dose 70-80mg./kg. body wt.) is fairly rapidly excreted, and in 2 days an average of 81% appears in the urine, 11% in the faeces and 2.4% as carbon dioxide in the expired air. 3. Radioactivity is excreted in the urine as indoxyl sulphate (50% of the dose), indoxyl glucuronide (11%), oxindole (1.4%), isatin (5.8%), 5-hydroxyoxindole conjugates (3.1%), N-formylanthranilic acid (0.5%) and unchanged indole (0.07%). The faeces contain indoxyl sulphate (0.4% of the dose) and indole (0.2%), but the major metabolites have not been identified. 4. Fed to rats with biliary cannulae an average of 5.6% of a dose of [(14)C]indole (20-60mg./kg. body wt.) is excreted in the bile in 2 days. Radioactivity is present as indoxyl sulphate (0.8% dose) and 5-hydroxyoxindole conjugates (0.6%). 5. Rats further metabolize indoxyl into N-formylanthranilic acid and anthranilic acid, and oxindole into 5-hydroxyoxindole. 6. With rat-liver microsomes plus supernatant under aerobic conditions, indole gives indoxyl, oxindole, possibly isatin, N-formylanthranilic acid and anthranilic acid, but under anaerobic conditions gives only oxindole. Similarly, under aerobic conditions, oxindole gives 5-hydroxyoxindole, anthranilic acid and o-aminophenylacetic acid. 7. Indole is metabolized by two pathways, one via indoxyl to isatin, N-formylanthranilic acid and anthranilic acid, and the other via oxindole to 5-hydroxyoxindole and possibly to o-aminophenylacetic and anthranilic acid. 8. The following new compounds are described: 4-hydroxy-2-nitrophenylacetic acid, 3-, 4- and 5-benzyloxy-2-nitrophenylacetic acid, 5- and 7-hydroxyoxindole and 5-aminoacridine indoxyl sulphate.

Animals↗
PubMed1965

SOME DIFFERENCES IN THE CONJUGATION OF O-AMINOPHENOL AND P-NITROPHENOL BY THE URIDINE DIPHOSPHATE TRANSGLUCURONYLASE OF MOUSE-LIVER HOMOGENATES.

1. Glucuronide synthesis from uridine diphosphate glucuronate and o-aminophenol or p-nitrophenol in the presence of uridine diphosphate transglucuronylase of mouse-liver homogenates has been studied with respect to inhibition by compounds known to be conjugated under the experimental conditions, and also by thiophenol. 2. Raising the o-aminophenol concentration decreased the inhibition of o-aminophenyl glucuronide synthesis by the alternative glucuronyl acceptors phenol, menthol and benzoic acid, but was without effect on that caused by p-nitrophenol and thiophenol. 3. Raising the p-nitrophenol concentration decreased or abolished the inhibition of p-nitrophenyl glucuronide synthesis due to phenol, menthol, benzoic acid, anthranilic acid, o-aminophenol and thiophenol. 4. The o-aminophenol system was much more readily inhibited by all compounds than the p-nitrophenol system. 5. In tris buffer, pH7.4, over 30% activation of the o-aminophenol system was achieved by 2mm-Mg(2+), but 10mm-Mg(2+) was inhibitory. The p-nitrophenol system showed only inhibition from 2mm-Mg(2+) upwards. 6. The results are discussed as suggesting that there are at least two uridine diphosphate transglucuronylases.

Aminophenols↗
PubMed1998

Structural requirements for the hepatotoxicity of nonsteroidal anti-inflammatory drugs in isolated rat hepatocytes.

Hepatotoxicity is one of the common side effects of nonsteroidal anti-inflammatory drugs (NSAIDs). We investigated the cytotoxicity of 18 acidic NSAIDs (3 salicylic acids, 3 anthranilic acids, 6 arylacetic acids, 6 arylpropionic acids) to freshly isolated rat hepatocytes as assessed by the NSAID-induced leakage of lactate dehydrogenase (LDH) in order to determine structural requirements for the direct hepatotoxicity of the NSAIDs. Diflunisal (salicylic acids), flufenamic acid, mefenamic acid, tolfenamic acid (anthranilic acids), diclofenac, indomethacin, acemetacin (arylacetic acids) and flurbiprofen (arylpropionic acids) caused significant LDH leakage, indicating that substituent position of a carboxyl group does not relate to the hepatotoxicity of the NSAIDs. Because the cytotoxic NSAIDs were of two types as classified by their "skeleton," diphenyl and diphenylamine, we tested the cytotoxicity of the compounds. Diphenyl did not cause LDH leakage, but diflunisal, which has the diphenyl structure, was cytotoxic. On the other hand, diphenylamine induced LDH leakage to the same degree as diclofenac, which has the diphenylamine structure. Therefore, diphenylamine itself was suggested to be responsible for the cytotoxicity of diclofenac and anthranilic acids, whereas a substituted group(s) in addition to diphenyl structure seems to be important for diflunisal cytotoxicity. All of the cytotoxic NSAIDs and diphenylamine extensively decreased hepatocellular ATP content, whereas the noncytotoxic NSAID did not, indicating that the NSAID-induced decrease in ATP, probably by their uncoupling effects on mitochondrial oxidative phosphorylation, is involved in the hepatotoxicity of the NSAIDs.

Adenosine Triphosphate↗
PubMed1990

New pathway for the biodegradation of indole in Aspergillus niger.

Indole and its derivatives form a class of toxic recalcitrant environmental pollutants. The growth of Aspergillus niger was inhibited by very low concentrations (0.005 to 0.02%) of indole, even when 125- to 500-fold excess glucose was present in the medium. When 0.02% indole was added, the fungus showed a lag phase for about 30 h and the uptake of glucose was inhibited. Indole was metabolized by a new pathway via indoxyl (3-hydroxyindole), N-formylanthranilic acid, anthranilic acid, 2,3-dihydroxybenzoic acid, and catechol, which was further degraded by ortho cleavage. The enzymes N-formylanthranilate deformylase, anthranilate hydroxylase, 2,3-dihydroxybenzoate decarboxylase, and catechol dioxygenase were induced by indole as early as after 5 h of growth, and their activities were demonstrated in a cell-free system.

Amidohydrolases↗
PubMed1993

Utilization of aromatic compounds by the Penicillium strain Bi 7/2.

The Penicillium strain Bi 7/2 utilized phenol, catechol, resorcinol, hydroquinone, pyrogallol, hydroxyhydroquinone, phloroglucinol, m- and p-cresol, orcinol, 4-methylcatechol, 4-methoxyphenol, 4-aminophenol, benzyl alcohol, benzoic acid, 2-, 3- and 4-hydroxybenzoic acid, anthranilic acid, protocatechuic acid and gallic acid as sole sources of carbon and energy. The central metabolites catechol, protocatechuic acid and hydroxyquinone could be determined by HPLC with diode-array detection. Pathways for the degradation of aromatic substances were proposed.

Biodegradation, Environmental↗
PubMed1993

Fluorometric determination of cyanate in plasma by conversion to 2,4(1H,3H)-quinazolinedione and separation by high-performance liquid chromatography.

A fluorometric high-performance liquid-chromatographic method is described for the determination of cyanate in human plasma. The method is based on the derivatization of cyanate with 2-aminobenzoic acid (anthranilic acid), leading to a stable cyclic fluorescent product, 2,4(1H,3H)-quinazolinedione. The fluorescent product was extracted with ethyl acetate, passed through a cation-exchange resin to eliminate the excess of derivatization reagent, and then concentrated on a Sep-Pak C-18 cartridge before reversed-phase chromatography and fluorometric detection. The precision of the method was satisfactory (coefficient of variation 2.3%) and the analytical recovery was quantitative (103%). Detection limit was found to be 8 nmol/liter from a 1-ml plasma sample. Cyanate in plasma was stable for 3 months when stored in liquid nitrogen. The mean and SD cyanate level in human plasma from 17 healthy nonsmoking subjects was 45 +/- 21 nmol/liter.

Adult↗
PubMed1999

Characterization of carbohydrates using highly fluorescent 2-aminobenzoic acid tag following gel electrophoresis of glycoproteins.

Application of the most sensitive fluorescent label 2-aminobenzoic acid (anthranilic acid, AA) for characterization of carbohydrates from the glycoproteins ( approximately 15 pmol) separated by polyacrylamide gel electrophoresis is described. AA label is used for the determination of both monosaccharide composition and oligosaccharide map. For the monosaccharide determination, bands containing the glycoprotein of interest are excised from the polyvinylidene fluoride (PVDF) membrane blots, hydrolyzed in 20% trifluoroacetic acid, derivatized, and analyzed by C-18 reversed-phase high-performance liquid chromatography. For the oligosaccharide mapping, bands were digested with peptide N-glycosidase F (PNGase F) in order to release the N-linked oligosaccharides, derivatized, and analyzed by normal-phase anion-exchange chromatography. For convenience, the PNGase F digestion was performed in 1:100 diluted ammonium hydroxide overnight. The oligosaccharide yield from ammonium hydroxide-PNGase F digestion was better or equal to all the other reported procedures, and the presumed "oligosaccharide-amine" product formed in the reaction mixture did not interfere with labeling of the oligosaccharides under the conditions used for derivatization. Sequencing of oligosaccharides can be performed using the same mapping method following treatment with an array of glycosidases. In addition, the mapping method is useful for determining the relative and simultaneous distribution of sialic acid and fucose.

Animals↗
PubMed2003

Increase in conversion of tryptophan to niacin in pregnant rats.

There is the report that the deaths by pellagra in women is approximately twofold excess that in men. In the present experiment, in order to clarify a factor in the etiology of pellagra in female and to get basic information how much niacin should be supplemented in pregnant state, we investigated the effects of pregnant on the metabolism of tryptophan to niacin in rats. The daily urine samples were collected from day -17 and day +6 (the delivery day was designated as day 0) and the intermediates of tryptophan to niacin were measured. The metabolites such as kynurenic acid, xanthurenic acid, anthranilic acid, 3-hydroxyanthranilic acid, quinolinic acid, N1-methylnicotinamide, N1-methyl-2-pyridone-5-carboxamide, N1-methyl-4-pyridone-3-carboxamide were increased with progress in pregnant and returned to normal levels after the delivery. The catabolism of tryptophan is accelerated during pregnancy, indicataing that pregnancy would not be an etiology of pellagra and no niacin supplement needs but tryptohan supplement would need.

Animals↗
PubMed1987

Human macrophages degrade tryptophan upon induction by interferon-gamma.

Human peripheral blood mononuclear cells, monocytes-macrophages and T-cells were stimulated with human recombinant interferon-gamma, interferon-alpha and phytohemagglutinin. The culture supernatants were analyzed for tryptophan, kynurenine, 3-hydroxyanthranilic acid, anthranilic acid and neopterin by high performance liquid chromatography. Tryptophan was decreased and the four other compounds were increased in supernatants of peripheral blood mononuclear cells activated by interferon-gamma (250 U/ml), interferon-alpha (10.000 U/ml) and phytohemagglutinin (1 microgram/ml). After splitting of peripheral blood mononuclear cells by adherence, the monocytes and macrophages but not the T-cells degraded tryptophan upon stimulation by interferon-gamma in a dose dependent manner. Supernatants of phytohemagglutinin stimulated but not of resting T-cells were found to induce tryptophan degradation by macrophages, the active principle being neutralized by an antiserum for interferon-gamma. Thus phytohemagglutinin acts by activating T-cells to release interferon-gamma which in turn induces macrophages to degrade tryptophan. In all experiments the appearance of neopterin in the culture media was correlated to the observed tryptophan degradation.

Cells, Cultured↗