Disease relevance of Trinitrobenzenesulfonic acid

• METHODS: Colitis was induced by trinitrobenzenesulfonic acid [1].
• BACKGROUND & AIMS: We investigated the effects of macrophage migration inhibitory factor (MIF) antibodies in experimental colitis-induced dextran sulfate sodium (DSS) and trinitrobenzenesulfonic acid (TNBS) and examined whether plasma levels of MIF were elevated in patients with inflammatory bowel disease (IBD) [2].
• The ability of 2,4,6 trinitrobenzenesulfonic acid (TNBS)-induced regulatory cells to modulate the generation of contact sensitivity (CS) to picryl chloride has been studied [3].
• The resulting antiserum (anti-PCI-F) bound to PCI-F and TNP-specific factors that suppressed delayed hypersensitivity (TSF) known to be comprised of PCI-F and Lyt-2+ -derived polypeptides released by cells sensitized by injection of trinitrobenzenesulfonic acid (TNBSF) [4].
• L-Alanine dehydrogenase from Bacillus subtilis was inactivated with two different lysine-directed chemical reagents, i.e. 2,4, 6-trinitrobenzenesulfonic acid and N-succinimidyl 3-(2-pyridyldithio)propionate [5].

Psychiatry related information on Trinitrobenzenesulfonic acid

• Rhodanese primary amino groups modification by 2,4,6-trinitrobenzenesulphonic acid is described by a summation of exponential functions of reaction time at pH values of 8.00 or higher, while at lower pH values it is described by a single exponential function of reaction time [6].

High impact information on Trinitrobenzenesulfonic acid

• DiC4PC transport was inhibited by structural analogs (but not by sn-2,3-diC4PC) and by treatment of microsomes with proteases, N-ethylmaleimide, and trinitrobenzenesulfonic acid [7].
• The maturation level of the B-lymphocyte subpopulations involved in trinitrophenyl (TNP)-specific immunological tolerance in adult mice induced by the injection of trinitrobenzenesulfonic acid (TNBS) was investigated using in vitro antigen-specific and nonspecific polyclonal stimulation [8].
• METHODS: Colitis was induced by rectal instillation of trinitrobenzenesulfonic acid (TNBS) in mice with a genetic deficiency of PARS (PARS-/-) and in wild-type littermates [9].
• The aim of this study was to evaluate a possible desensitization of PAF receptors in guinea pig intestinal smooth muscle cells after experimental inflammation induced by trinitrobenzenesulfonic acid (TNB) [10].
• The amount of endogenous phosphatidylethanolamine exposed to the outer leaflet of the plasma membrane was measured by covalent labeling with the impermeant amino reagent, trinitrobenzenesulfonic acid [11].

Chemical compound and disease context of Trinitrobenzenesulfonic acid

• METHODS: Colitis was induced with 2,4,6-trinitrobenzenesulfonic acid/ethanol enemas [12].
• Quercitrin was tested for acute and chronic anti-inflammatory activity in trinitrobenzenesulfonic acid-induced rat colitis [13].
• We compared the effect of rolipram, a selective PDE4 inhibitor, with steroids on the clinical course of experimental colitis induced by 2,4,6-trinitrobenzenesulfonic acid (TNBS) [14].
• Contractions induced by KCl, carbachol, and Bay K 8644 were decreased in circular smooth muscles isolated from 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis rat colon [15].
• To address this issue, we included the nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME) in the drinking water (10 or 100 micrograms/ml) of guinea pigs immediately after induction of ileitis by intraluminal trinitrobenzenesulfonic acid (TNBS 30 mg/kg in 50% ethanol) [16].

Biological context of Trinitrobenzenesulfonic acid

• The receptor responsible for CGRP-induced ion transport and permeability was examined in tissues from animals treated 7 days previously with trinitrobenzenesulfonic acid to induce colitis or in controls [17].
• Bovine type M pyruvate kinase, which normally has hyperbolic kinetics with its substrates, was inactivated by treatment with trinitrobenzenesulfonic acid [18].
• Suppression of antibody responses by cells from mice treated with picryl sulfonic acid: T cells that suppress IgG antibody without inhibiting concomitant IgE responses [19].
• Enrichment of normal whole LDL with TG resulted in a 45% reduction in enzyme activation, a 27% decrease in the number of trinitrobenzenesulfonic acid-reactive lysine groups, and a marked reduction in the immunoaffinity for B1B6 [20].
• The absence or presence of NBD-PS in the outer leaflet was independently verified by employing "back-exchange", trinitrobenzenesulfonic acid derivatization, and decarboxylation with PS decarboxylase experiments [21].

Anatomical context of Trinitrobenzenesulfonic acid

• To answer this question we used spleen cells from mice treated in vivo with the toleragen trinitrobenzenesulfonic acid as regulators of in vitro generation of primary anti-trinitrophenyl self-cytotoxic T lymphocytes [22].
• The transverse distribution of the phospholipids in vesicular H+-translocating membranes prepared from pig gastric mucosa was investigated with the aid of phospholipase C, sphingomyelinase, and trinitrobenzenesulfonic acid [23].
• As CD44 is important in lymphocyte activation and migration, we asked whether Abs against CD44 isoforms influence trinitrobenzenesulfonic acid (TNBS)-induced colitis in mice [24].
• The aminophospholipids of microvesicles released from human erythrocytes on storage or prepared from erythrocyte ghosts by shearing under pressure are susceptible to the action of 2,4,6-trinitrobenzenesulphonic acid [25].
• Suppressor cells, which depress the passive transfer of contact sensitivity appear in the lymph nodes and spleen of mice injected with picryl sulfonic acid (PSA) [26].

Associations of Trinitrobenzenesulfonic acid with other chemical compounds

• The enzyme activation was also positively correlated with the number of trinitrobenzenesulfonic acid-reactive lysine amino groups, which increased with increasing density of LDL [20].
• T cells from mice injected with picryl sulfonic acid (PSA) can inhibit the anti-trinitrophenyl (TNP) antibody responses of mice produced after skin painting with picryl chloride (PCl) [19].
• Female Sprague-Dawley rats received intrarectal trinitrobenzenesulfonic acid (TNBS) or vehicle 3 days following either systemic capsaicin (CP) pretreatment or vehicle [27].
• Based on this consideration, pregnant BALB/c mice were treated with 2,4,6-trinitrobenzenesulfonic acid (TNBS), searching for differences in 2,4,6-trinitrophenyl (TNP) responsiveness in their offspring as compared to litters of untreated mice [28].
• Reaction with the amine labeling reagents isethionylacetimidate and trinitrobenzenesulfonic acid indicated that 40% of the phosphatidylserine and 60% of the phosphatidylethanolamine are present on the external (cytoplasmic) surface of the synaptic vesicle [29].

Gene context of Trinitrobenzenesulfonic acid

• To investigate and clarify the roles of the NOS isoforms in gut inflammation, we induced trinitrobenzenesulfonic acid colitis in eNOS, nNOS, and iNOS knockout (KO) mice, assessing the course of colitis at early and late times [30].
• We investigated hypothalamic neuronal corticotropin-releasing factor (CRF) gene expression changes in response to visceral inflammation induced by 2,4,6-trinitrobenzenesulfonic acid (TNB) and acute stress [31].
• A 2,4,6-trinitrobenzenesulfonic acid sodium salt (TNBS) colitis model was established to examine the effect of selective iNOS inhibition, by S-(2-aminoethyl) isothiouronium bromide (ITU), on colonic mucosal cell damage and inflammation [32].
• The role of nitric oxide (NO) derived from the inducible isoform of NO synthase (iNOS) in epithelial transport dysfunction was studied in a model of colitis induced in mice by intrarectal 2,4, 6-trinitrobenzenesulfonic acid in 30% ethanol [33].
• Painting the skin with a reactive hapten immunizes Ly-1 cells that secrete antigen-binding material, whereas intravenous injection of trinitrobenzenesulfonic acid activates Ly-2 cells to produce a second subunit that does not see antigen [34].

Analytical, diagnostic and therapeutic context of Trinitrobenzenesulfonic acid

• Ileitis was induced in guinea pigs by intraluminal injection of 2,4,6-trinitrobenzenesulfonic acid and experiments were conducted 3, 7, and 14 days after treatment [35].
• The results from mass spectrometry were compared with results obtained from other more traditional methods of immunogen characterization (UV analysis, trinitrobenzenesulfonic acid titrations, and gel electrophoresis) [36].
• Gel filtration experiments showed that factor VIII-related antigen may be dissociated into subunits by galactose oxidase but not by 2,4,6-trinitrobenzenesulfonic acid or sodium periodate [37].
• PEGylated RGD-modified gelatin was synthesized via several steps involving PEG derivations and characterized by high-performance liquid chromatography, mass spectroscopy, gel permeation chromatography, and the trinitrobenzenesulfonic acid method [38].
• Kinetic study of the reaction between trinitrobenzenesulfonic acid and amino acids with a trinitrobenzenesulfonate ion-selective electrode [39].

References