Interaction of pharmaceuticals with Schardinger dextrins. II. Interaction with selected compounds.
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Acids↗
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Results for “AMINOSALICYLIC ACID”
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[COMPARATIVE STUDY BETWEEN THE BACTERIOSTATIC ACTIVITY OF BLOOD SERUM TAKEN AFTER INGESTION OF PARANIAZIDE AND THE BACTERIOSTATIC ACTIVITY OF SERUM TAKEN AFTER INGESTION OF INH AND PAS].
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4-Aminobenzoic Acid↗
Activation of peroxidase-catalyzed oxidation of 3,3',5,5'-tetramethylbenzidine with poly(salicylic acid 5-aminodisulfide).
5-Aminosalicylic acid (5-ASA) inhibited by a mixed mechanism the peroxidase catalyzed oxidation of tetramethylbenzidine (TMB) in 0.015 M phosphate-citrate buffer (pH 6.4) supplemented with 5% DMSO and 5% DMF. Poly(salicylic acid 5-aminodisulfide) (poly(SAADS)) in 0.01 M phosphate buffer (pH 6.2-7.4) supplemented with 5% DMSO and 5% DMF effectively activated the peroxidase-catalyzed oxidation of TMB. The activation was quantitatively characterized by coefficients alpha (M-1) determined at different pH values: alpha increased linearly with increase in pH up to the maximal value of 2.44*105 M-1 at pH 7.0. The activating effect of poly(SAADS) on the peroxidase-catalyzed oxidation of TMB is explained by the activator properties of polyelectrolyte, with its anionic form interacting with peroxidase sites responsible for the acid-base catalysis.
Antioxidants↗
Ameliorative effects of sodium ferulate on experimental colitis and their mechanisms in rats.
AIM: To investigate the ameliorative effects of sodium ferulate (SF) on acetic acid-induced colitis and their mechanisms in rats. METHODS: The colitis model of Sprague-Dawley rats was induced by intracolon enema with 8% (V/V) of acetic acid. The experimental animals were randomly divided into model control, 5-aminosalicylic acid therapy group and three dose of SF therapy groups. The 5 groups were treated intracolonically with normal saline, 5-aminosalicylic acid (100 mg x kg(-1)), and SF at the doses of 200, 400 and 800 mg x kg(-1) respectively and daily (8:00 am) for 7 days 24 h following the induction of colitis. A normal control group of rats clystered with normal saline instead of acetic acid was also included in the study. Pathological changes of the colonic mucosa were evaluated by the colon mucosa damage index (CMDI) and the histopathological score (HS). The insulted colonic mucosa was sampled for a variety of determinations at the end of experiment when the animals were sacrificed by decapitation. Colonic activities of myeloperoxidase (MPO) and superoxide dismutase (SOD), and levels of malondialdehyde (MDA) and nitric oxide (NO) were assayed with ultraviolet spectrophotometry. Colonic contents of prostaglandin E2 (PGE2) and thromboxane B2 (TXB2) were determined by radioimmunoassay. The expressions of inducible nitric oxide synthase (iNOS), cyclo-oxygenase-2 (COX-2) and nuclear factor kappa B (NF-kappaB) p65 proteins in the colonic tissue were detected with immunohistochemistry. RESULTS: Enhanced colonic mucosal injury, inflammatory response and oxidative stress were observed in the animals clystered with acetic acid, which manifested as the significant increase of CMDI, HS, MPO activities, MDA and NO levels, PGE2 and TXB2 contents, as well as the expressions of iNOS, COX-2 and NF-kappaB p65 proteins in the colonic mucosa, although the colonic SOD activity was significantly decreased compared with the normal control (CMDI: 2.9+/-0.6 vs 0.0+/-0.0; HS: 4.3+/-0.9 vs 0.7+/-1.1; MPO: 98.1+/-26.9 vs 24.8+/-11.5; MDA: 57.53+/-12.36 vs 9.21+/-3.85; NO: 0.331+/-0.092 vs 0.176+/-0.045; PGE2: 186.2+/-96.2 vs 42.8+/-32.8; TXB2: 34.26+/-13.51 vs 8.83+/-3.75; iNOS: 0.365+/-0.026 vs 0.053+/-0.015; COX-2: 0.296+/-0.028 vs 0.034+/-0.013; NF-kappaB p65: 0.314+/-0.026 vs 0.039+/-0.012; SOD: 28.33+/-1.17 vs 36.14+/-1.91; P<0.01). However, these parameters were found to be significantly ameliorated in rats treated locally with SF at the given dose protocols, especially at 400 mg x kg(-1) and 800 mg x kg(-1) doses (CMDI: 1.8+/-0.8, 1.6+/-0.9; HS: 3.3+/-0.9, 3.1+/-1.0; MPO: 63.8+/-30.5, 36.2+/-14.2; MDA: 41.84+/-10.62, 37.34+/-8.58; NO: 0.247+/-0.042; 0.216+/-0.033; PGE2: 77.2+/-26.9, 58.4+/-23.9; TXB2: 18.07+/-14.83; 15.52+/-8.62; iNOS:0.175+/-0.018, 0.106+/-0.019; COX-2: 0.064+/-0.018, 0.056+/-0.014; NF-kappaBp65: 0.215+/-0.019,0.189+/-0.016; SOD: 32.15+/-4.26, 33.24+/-3.69; P<0.05-0.01). Moreover, a therapeutic dose protocol of 800 mg x kg(-1) SF was observed as effective as 100 mg x kg(-1) of 5-ASA in the amelioration of colonic mucosal injury as evaluated by CMDI and HS. CONCLUSION: Administration of SF intracolonically may have significant therapeutic effects on the rat model of colitis induced by acetic acid enema, which was probably due to the mechanism of antioxidation, inhibition of arachidonic acid metabolism and NF-kappaB expression.
Acetic Acid↗
The pharmacokinetics of olsalazine sodium in healthy volunteers after a single i.v. dose and after oral doses with and without food.
Olsalazine sodium (5,5'-azodisalicylic acid (OLZ] was given to eight healthy volunteers as a 10 mg i.v. bolus dose and as a 1 g oral dose with and without food. To five fasting participants single oral doses of 2 g and 4 g were given. Blood and urine were collected during three weeks after each dose and were assayed for OLZ, a conjugate identified as a sulphate of OLZ (OLZs), 5-aminosalicylic acid (5-ASA), and N-acetyl-5-aminosalicylic acid (ac-5-ASA). The study showed that: 1. OLZ had a very short elimination half-life, mean 56 min. 2. OLZ was absorbed from the intestinal tract to a very small extent, as seen from the low systemic availability and low urinary excretion, 2.3% and 0.31% respectively, for a 1 g dose taken fasting. 3. OLZ was present in the serum partly as a conjugate, which was identified as an O-sulphate. Following the i.v. dose the serum half-life of the O-sulphate was estimated to be 7 days. 4. Food intake did not influence the systemic availability of OLZ and ac-5-ASA. 5. There was no dose-dependent increase of OLZ absorption with single doses up to 2 g, but a 4-g dose showed a more than two-fold increase in the individual peak serum concentration and in the systemic availability of OLZ. However, there was no significant increase in the mean residence time (MRT) for OLZ or in the serum concentration of either 5-ASA or ac-5-ASA at a dose of 4 g.
Administration, Oral↗
MYCOBACTERIA: LABORATORY METHODS FOR TESTING DRUG SENSITIVITY AND RESISTANCE.
In its seventh report, published in 1960, the WHO Expert Committee on Tuberculosis "noted the need for international standards for the definition and determination of drug resistance which will permit comparisons to be made from one area to another, and recommended that the World Health Organization take appropriate steps to establish such standards".(10) Acting on this recommendation, WHO took the first step towards standardization by convening in Geneva, in December 1961, an informal international meeting of specialists in the bacteriology of tuberculosis. At this meeting an attempt was made to formulate prerequisites for reliable sensitivity tests and to specify the technical procedures for them.The first part of the present paper is a joint contribution by the participants in the meeting, summarizing the general conclusions reached and recommendations made with regard to tests of sensitivity to the three main antituberculosis drugs-isoniazid, streptomycin and p-aminosalicylic acid. The other three parts describe, in turn, three different tests for determining drug sensitivity-the absolute-concentration method, the resistance-ratio method and the proportion method-that are generally considered to give reasonably accurate results.
Aminosalicylic Acid↗
A simple and rapid liquid chromatographic method for the determination of major metabolites of sulfasalazine in biological fluids.
A simple and rapid assay for quantitation of sulfasalazine metabolites in rat urine and plasma was developed using high-performance liquid chromatography (HPLC). The method involves dilution of urine or plasma samples (0.1 mL) with methanol for protein precipitation, followed by mixing and centrifugation at 10,000 x g. Chromatography was accomplished with a reversed-phase ODS C-18 column (5 mu; 4.6 x 250 mm). The mobile phase consisted of 20% methanol in 5.0 mM phosphate buffer (pH 6.0), with 0.5 mM tetrabutylammonium chloride as an ion-pairing agent. The flow rate was 1.7 mL/min. An injection volume of 30 microL was used and the metabolites were quantitated by an ultraviolet detector at 254 nm. Benzamide was used as the internal standard. This method is linear in the range of 0.5 to 25 micrograms/mL for 5-aminosalicylic acid (5-ASA), acetylsulfapyridine (Ac-SP), and acetyl-5-aminosalicylic acid (Ac-5-ASA), and from 0.25 to 25 micrograms/mL for sulfapyridine (SP). The percent relative standard deviation ranged from 1 to 7.9% for the metabolite standard curves and precision studies. The limit of detection for 5-ASA, Ac-SP, and Ac-5-ASA is 100 ng/mL, and for SP is 50 ng/mL, in both urine and plasma. This method is rapid, precise, and accurate, and has been used to determine sulfasalazine metabolites in individual rat plasma and urine samples following an oral dose of 60 mg/kg of sulfasalazine.
Administration, Oral↗
Evaluation of two lanthanide complexes for qualitative and quantitative analysis of target proteins via partial least squares analysis.
Two lanthanide complexes, namely 5-aminosalicylic acid ethylenediaminetetraacetate europium(III) (5As-EDTA-Eu3+) and 4-aminosalicylic acid ethylenediaminetetraacetate terbium(III), were evaluated for the analysis of carbonic anhydrase, human serum albumin (HSA), and gamma-globulin. Quantitative analysis is based on their luminescence enhancement upon protein binding and qualitative analysis on their lifetime capability to recognize the binding protein. Analytical figures of merit are presented for the three proteins. The limits of detection with 5As-EDTA-Eu3+ are at the parts per billion level. Partial least square regression analysis is used to determine HSA and gamma-globulin in binary mixtures without previous separation at the concentration ranges typically found in clinical tests of human blood serum.
Carbonic Anhydrases↗
[Research on p-aminobenzoic, p-aminosalicylic, salicylic and gentisic acids].
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4-Aminobenzoic Acid↗
DRUG SENSITIVITY-RESISTANCE DETERMINATION AND SIMPLE ENZYMATIC TESTS FOR THE DIFFERENTIATION OF MYCOBACTERIA.
Tests to determine mycobacterial sensitivity to antituberculosis drugs have become a routine procedure to enable clinicians to apply the most suitable treatment. However, while antimycobacterial drugs have been widely and successfully used in recent years, laboratory techniques for performing drug sensitivity tests have not yet been standardized and thus do not permit international comparison of results.Among the main hindrances to standardization are differences in the sensitivity of culture media, the capacity of some of the ingredients to adsorb certain drugs, the decomposition of some drugs when exposed to high temperatures during coagulation of solid media, and difficulties in the preparation of standard inocula.The techniques described in this paper have been used with success to determine the sensitivity to the three major antituberculosis drugs (isoniazid, streptomycin and p-aminosalicylic acid) of 600 strains of mycobacteria isolated from 200 newly diagnosed cases in a WHO-sponsored field trial. In all these patients, sputum conversion was achieved by treatment with a combination of the three drugs, without the emergence of resistant strains.The cytochemical tests recommended by the authors for routine use in the differentiation of mycobacteria are a combined test for catalase and peroxidase activity and either the niacin test or, preferably, the Virtanen-Griess nitrate test for differentiating Mycobacterium tuberculosis from Myco. bovis.
Aminosalicylic Acid↗
Some aspects of tuberculous meningitis in Surabaya.
Eighty tuberculous meningitis patients who were seen in the neurological clinics in Surabaya between the January 1971 and January 1975 were asked to cooperate in a double blind clinical trial. One group was given isoniazid, streptomycin and p-aminosalicylic acid, the other group was given isioniazid, rifampicin, ethambutol and a protease. The outcome after the treatment with isoniazid, rifampicin and ethambutol was significantly better than that with isoniazed, streptomycin and p-aminosalicylic acid. The clinical and laboratory symptoms and signs are reviewed in detail.
Adolescent↗
Ischemia/reperfusion injury in the rat colon.
This study investigated metabolic and biochemical consequences of colonic ischemia/reperfusion (I/R) in the rat and evaluated whether antioxidants prevent I/R-induced functional damage in the rat colon. The surgical preparation involved a 10 cm segment of the colon and occlusion of the superior mesenteric artery (SMA) to induce I/R. Arterial blood from the aorta and venous blood from the superior mesenteric vein (SMV) was collected to measure blood gases, lactic acid (LA) and arachidonic acid (AA) metabolites. Tissue xanthine oxidase (XO) and thiobarbituric acid (TBA) derivatives were measured before and after reperfusion. In addition, vascular and mucosal permeability, and the effect of MDL 73404 (a water soluble vitamin E analog) and 5-aminosalicylic acid on LA, AA, XO and TBA was measured. After ischemia, the colon displayed a metabolic shift from aerobic to anaerobic course by increasing lactic acid production in the colon (183% increase in SMV lactate level compared 87% in the SMA; p < 0.03). After 10 minutes of reperfusion, circulating 6-keto-prostaglandin F1 alpha increased by 3.85 fold (p < 0.001) and thromboxane B2 increased by 2 to 3 fold. An Ischemia time longer than 60 minutes was required to cause changes in tissue XO levels. Tissue TBA levels showed a good dose response corresponding with I/R time. I/R (60 minutes) caused a three and 16 fold increase (p < 0.01) in vascular and mucosal permeability, respectively. MDL 73404 and 5-aminosalicylic acid significantly inhibited the vascular permeability and decreased LA, AA, XO and TBA. These observations provide the first direct experimental evidence for I/R-induced damage in the colon and some of its effects can be reversed by conventional and novel antioxidants.
6-Ketoprostaglandin F1 alpha↗
Olsalazine or sulphasalazine in first attacks of ulcerative colitis? A double blind study.
Olsalazine (2 g/day) and sulphasalazine (3 g/day) were compared in a double blind three centre trial in 37 patients presenting with first attack of distal colitis. Sigmoidoscopic appearances, rectal biopsies, and symptom and stool diary records were used to assess benefit and adverse effects. Both groups showed a similar decrease in stool frequency (p less than 0.001). The proportion of unformed stools was also decreased, but to a lesser extent (p less than 0.05) in those taking olsalazine (78% v 55%; p less than 0.001) compared with those taking sulphasalazine (72% v 28%; p less than 0.001). There was a diminution in the proportion of stools containing blood in both groups (olsalazine: 61% v 22%; p less than 0.001/sulphasalazine: 67% v 37%; p less than 0.001). Sigmoidoscopic and histological appearances and clinical activity improved significantly and to a similar extent in both groups. Intolerance was encountered in two patients on olsalazine and four on sulphasalazine; intolerance to sulphasalazine being even higher (five of seven patients) in a preliminary study using a dose of sulphasalazine releasing the same amount of 5-aminosalicylic acid as 2 g olsalazine. Olsalazine was at least as effective as sulphasalazine in the treatment of new patients with distal colitis, and in a dose releasing an equivalent amount of 5-aminosalicylic acid was better tolerated.
Adult↗
Tuberculosis therapy: past, present and future.
The major historical landmarks of tuberculosis (TB) therapy include: the discovery of effective medications (streptomycin and para-aminosalicylic acid) in 1944; the revelation of "triple therapy" (streptomycin, para-aminosalicylic acid and isoniazid) in 1952, which assured cure; recognition in the 1970s that isoniazid and rifampin could reduce the duration of treatment from 18 to 9 months; and the observation in the 1980s that adding pyrazinamide to these drugs allowed cures in only 6 months. To combat noncompliance, intermittent regimens, twice or thrice weekly, have been proven to cure even far-advanced TB in as few as 62-78 encounters over 26 weeks. However, these regimens are not sufficiently short or convenient to facilitate effective treatment in resource-poor countries. Therefore, drug-resistant strains have emerged to threaten TB control in various areas of the world, including India, China, Russia and the former Soviet Union. For these reasons, it is vital that new medications are developed to shorten the duration of therapy, increase the dosing interval of intermittent regimens and replace agents lost to resistance. Other special considerations include identifying optimal therapy for persons with acquired immune deficiency syndrome, particularly noting the problems of drug/drug interactions for those receiving antiretroviral treatment. Finally, the Alchemist's Dream of tuberculosis should be pursued: modulating the immune response to shorten treatment and/or overcome drug resistance.
Antitubercular Agents↗
Which component of sulphasalazine is active in rheumatoid arthritis?
Sulphasalazine is known to be effective as a second line agent in the treatment of rheumatoid arthritis. The two chemical constituents of sulphasalazine (sulphapyridine and 5-aminosalicylic acid) were assessed separately in the treatment of rheumatoid arthritis. Over 24 weeks sulphapyridine showed a pronounced second line effect comparable with sulphasalazine and with a similar toxicity profile, whereas 5-aminosalicylic acid showed only a weak first line effect. Thus sulphapyridine appears to be the active moiety responsible for the second line effect of sulphasalazine in rheumatoid arthritis. The efficacy of the antibacterial component of sulphasalazine yet again permits speculation about the role of a bacterial pathogen in the aetiopathogenesis of rheumatoid disease.
Adult↗
Ulcerative colitis: effect of sulphasalazine, its metabolites and indomethacin on the ability of human colonic mucosa to metabolize prostaglandins in vitro.
1 Homogenates of mucosa from human colon metabolize [3H]-prostaglandin E1 in the presence of nicotinamide adenine dinucleotide to 15-oxo prostaglandin E1 or 15-oxo, 13,14 dihydro prostaglandin E1. 2 Metabolic capacity of tissue from patients with active ulcerative colitis under treatment with sulphasalazine (0.021 +/- 0.004 nmol/Mg protein +/- s.e. mean) did not differ from mucosa of normal patients (0.02 +/- 0.004 nmol/mg protein) during 1 h incubation. 3 Sulphasalazine inhibits prostaglandin E1 metabolism by mucosal homogenates in a dose-dependent manner with an ID50 of 125 microM. Its therapeutically active metabolite, 5-aminosalicylic acid (2.6 mM) was without significant inhibitory activity. 4 Indomethacin inhibits prostaglandin E1 metabolism by colonic mucosa with an ID50 of 388 microM. 5 At present we cannot clearly relate the therapeutic benefit of sulphasalazine and its therapeutically active metabolite, 5-aminosalicylic acid, in ulcerative colitis to their effects on prostaglandin E synthesis or metabolism in vitro.
Alprostadil↗
Sulphasalazine-induced reversible male infertility.
A male patient suffering from ulcerative colitis, presented with primary infertility due to sulphasalazine therapy. Sulphasalazine was discontinued and the patient was treated with a 5-aminosalicylic acid preparation (Salofalk) in the form of an enema. After 3 months, the semen quality was dramatically improved and a successful pregnancy ensued. The sulphapyridine moiety of sulphasalazine seems to be responsible for male infertility and depressed semen quality. The metabolite 5-aminosalicylic acid is proposed as a suitable alternative to sulphasalazine in cases of male infertility.
Adult↗
Evidence for the lack of hepatic N-acetyltransferase in suncus (Suncus murinus).
The abilities of liver cytosol fractions from the suncus and Sprague-Dawley (SD) rats to N-acetylate aniline, p-aminobenzoic acid, p-aminosalicylic acid and 2-aminofluorene (AF) were compared. The cytosol from rats N-acetylated these substrates at efficient rates, whereas the cytosol from the suncus did not N-acetylate these substrates at detectable rates. When AF was given to the suncus, 2-acetylaminofluorene (AAF), a metabolite of AF formed by N-acetyltransferase (NAT), was not detectable in serum, whereas the metabolite was seen clearly in rats. Northern blot and Southern blot analyses, using cDNAs coding for human NATs as probes, indicated that not only the transcripts but also the genes of the enzymes were undetectable in suncus. These results suggest that the suncus is among the few species known to lack NATs.
2-Acetylaminofluorene↗