Disease relevance of symmetric Trinitrobenzene

• Mice treated with anti-mouse CEACAM1-specific monoclonal antibody (mAb) CC1 during the effector phase exhibited a reduced severity of trinitrobenzene sulfonic acid colitis in association with decreased interferon (IFN)-gamma production [1].
• Therapeutic effects of vasoactive intestinal peptide in the trinitrobenzene sulfonic acid mice model of Crohn's disease [2].
• RESULTS: Ghrelin ameliorated significantly the clinical and histopathologic severity of the trinitrobenzene sulfonic acid-induced colitis; abrogating body weight loss, diarrhea, and inflammation; and increasing survival [3].
• Methods: We examined the therapeutic action of DC(VIP) in the colitis induced by intracolonic administration of trinitrobenzene sulfonic acid, evaluating diverse clinical signs of the disease including weight loss, diarrhea, colitis, and histopathology [4].
• After 24 h, mucosal ulceration and hemorrhage were observed in TNB/ethanol-, 50% ethanol-, and to a lesser extent, in TNB/saline-treated rats [5].

Psychiatry related information on symmetric Trinitrobenzene

• An on-line and continuous technique based on electric cell-substrate impedance sensing (ECIS) was developed for measuring the concentration and time response function of fibroblastic V79 cells exposed to mercury chloride and 1,3,5-trinitrobenzene (TNB) [6].

High impact information on symmetric Trinitrobenzene

• Treatment of experimental (Trinitrobenzene sulfonic acid) colitis by intranasal administration of transforming growth factor (TGF)-beta1 plasmid: TGF-beta1-mediated suppression of T helper cell type 1 response occurs by interleukin (IL)-10 induction and IL-12 receptor beta2 chain downregulation [7].
• Suppressor T cells, activated by injection of trinitrobenzene sulphonic acid in DA rats, prevented rejection of LEW kidney allografts in a donor-specific manner when adoptively transferred into syngeneic recipients along with trinitrophenyl (TNP)-haptenated LEW alloantigen [8].
• In initial studies, we showed that i.r. (intrarectal) or i.p. administration of decoy ODNs encapsulated in a viral envelope prevented and treated a model of acute trinitrobenzene sulfonic acid-induced (TNBS-induced) colitis, as assessed by clinical course and effect on Th1 cytokine production [9].
• METHODS: We examined the anti-inflammatory action of ghrelin in the colitis induced by intracolonic administration of trinitrobenzene sulfonic acid [3].
• Inhibition of indoleamine 2,3-dioxygenase augments trinitrobenzene sulfonic acid colitis in mice [10].

Chemical compound and disease context of symmetric Trinitrobenzene

• Colitis was induced in rats by the intrarectal administration of trinitrobenzene sulfonic acid (TNB) dissolved in 50% ethanol, and control rats received saline via the same route [11].
• Curcumin prevents and ameliorates trinitrobenzene sulfonic acid-induced colitis in mice [12].
• Twice daily treatment with indomethacin (0.1-1 mg/kg SC) during the first week after trinitrobenzene sulfonic acid/ethanol administration resulted in dose-dependent increases in the severity of colitis and in the incidence of mortality [13].
• In conclusion, TNB and acetic acid induced colitis can be pharmacologically manipulated by TEMPOL [14].
• The therapeutic effects of NFkappaBD were studied in the trinitrobenzene sulphonic acid, oxazolone and dextran sodium sulphate induced colitis models [15].

Biological context of symmetric Trinitrobenzene

• Effects of LPA on intestinal wound healing in vivo were studied by using the trinitrobenzene model of colitis in rats [16].
• With large molar excesses of the reagent, the reactions obey pseudo-first order kinetics and the rates of inactivations are directly proportional to the concentrations of trinitrobenzene sulfonate; thus, there is no indication of reversible complexation of reagent with enzyme [17].
• Body temperature was monitored by telemetry from conscious, unrestrained male rats treated with trinitrobenzene sulphonic acid or saline [18].
• Formation of the Meisenheimer complex or sigma-complex [1-(S-glutathionyl)-2,4,6-trinitrocyclohexadienate] between glutathione (GSH) and 1,3,5-trinitrobenzene (TNB) can be observed at the active sites of isoenzymes 3-3 and 4-4 of rat liver GSH transferase [19].
• Conversely, CCR6 deficiency alters leukocyte homeostasis and the cytokine environment in the intestinal mucosa; these changes are sufficient to confer susceptibility to trinitrobenzene sulfonic acid-induced intestinal inflammation in the otherwise resistant C57BL/6J mouse strain [20].

Anatomical context of symmetric Trinitrobenzene

• RESULTS: Normal mature IEC expressed low TRAIL levels, whereas, in inflammatory lesions, TRAIL messenger RNA and protein were markedly up-regulated in IEC and lamina propria lymphocytes at levels comparable with trinitrobenzene sulfonic acid-induced colitis [21].
• On the contrary, single intracolonic administration of trinitrobenzene sulfonic acid/ethanol induced a biphasic response consisting of an early pool of radiolabeled feces (T25 = 4.03 +/- 0.55 hours) with a delayed total one (T50 = 11.74 +/- 0.83 hours; T75 = 13.70 +/- 0.49 hours) [22].
• The interval between the release of newly synthesized proteins from ribosomes and their appearance at the cell surface, where they became accessible to trinitrobenzene sulfonic acid, was studied in pulse-chase experiments [23].
• Modification of spleen cells from the strain or origin (129) of this teratoma line with trinitrobenzene sulfonic acid allows the generation of syngeneic killer cells that display a cytotoxic effect against trinitrophenyl-modified splenic targets, but not against trinitrophenyl-modified F9 targets [24].
• Plasma membrane PE was distinguished from intracellular PE by its derivatization with an amino-reactive reagent, trinitrobenzene sulfonic acid, under nonpermeating conditions [25].

Associations of symmetric Trinitrobenzene with other chemical compounds

• Specific thromboxane A2 receptor antagonists, KT1-32 and GR 32191B, did not show any improvement in colonic transit after trinitrobenzene sulfonic acid administration [22].
• Adenosine 5-phosphosulfate (APS) kinase from Penicillium chrysogenum is irreversibly inactivated by trinitrobenzene sulfonate in a pseudo-first order process [26].
• The role of cationic amino acid residues in the binding of porphyrin substrates by purified bovine ferrochelatase (protoheme ferro-lyase, EC 4.99.1.1) have been examined via chemical modification with camphorquinone-10-sulfonic acid, phenylglyoxal, butanedione, and trinitrobenzene sulfonate [27].
• Bovine thyroglobulin was treated with increasing ratios of succinic anhydride, trinitrobenzene sulfonic acid, tetranitromethane, and N-acetylimidazole in an attempt to assess the role of lysine or tyrosine residues in binding to thyroid membrane receptors [28].
• Fibronectin-mediated spreading of trypsinized BHK cells is also inhibited by pre-treatment of cells with several non-penetrating reagents reactive with cell surface amino groups, namely pyridoxal phosphate, trinitrobenzene sulphonate and fluorescein 5-isothiocyanate [29].

Gene context of symmetric Trinitrobenzene

• Recent studies suggest that the induction of HO-1 expression plays a critical protective role in intestinal damage models induced by trinitrobenzene sulphonic acid or dextran sulphate sodium, indicating that activation of HO-1 may act as an endogenous defensive mechanism to reduce inflammation and tissue injury in the intestinal tract [30].
• MATERIALS AND METHODS: Body weight, histological scores, and myeloperoxidase activity were evaluated in trinitrobenzene sulfonic acid colitis [31].
• Gliotoxin reduces the severity of trinitrobenzene sulfonic acid-induced colitis in mice: evidence of the connection between heme oxygenase-1 and the nuclear factor-kappaB pathway in vitro and in vivo [31].
• We studied the effects of HGF in mice with trinitrobenzene sulfonic acid-induced colitis, which shows clinical and molecular resemblance to Crohn's disease [32].
• This pretreatment protected IFN-gamma(-/-) mice from trinitrobenzene sulfonic acid-induced colitis; however, in normal mice this weekly treatment was less protective [33].

Analytical, diagnostic and therapeutic context of symmetric Trinitrobenzene

• Rats with trinitrobenzene sulfonic acid-induced colitis were studied 24 hours after treatment [34].
• Biosynthesized surface components were analyzed by reacting [35S]methionine-labeled macrophages with trinitrobenzene sulfonic acid and purifying trinitrophenyl-substituted surface proteins by immunoprecipitation [35].
• Oral administration of recombinant cholera toxin subunit B inhibits IL-12-mediated murine experimental (trinitrobenzene sulfonic acid) colitis [36].
• In this study, a fluorescence-based fiber-optic biosensor was used to quantify the heterogeneity associated with the binding of a soluble analyte, fluorescently labeled trinitrobenzene, to surface-immobilized monoclonal anti-TNT antibodies [37].
• Furthermore, 1 week after trinitrobenzene sulfonic acid treatment, the production of interleukin-8 by cultured rectal mucosa or cardiac blood mononuclear cells with or without stimulation of lipopolysaccharide for 24 h was also analyzed by enzyme-linked immunosorbent assay [38].

References