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PubMed1992

Protective influence of oxypurinol on the trinitrobenzene sulfonic acid(TNB) model of inflammatory bowel disease in rats.

Chronic inflammation of the colon and the rectum was induced by intracolonic administration of 25 mg trinitrobenzoic sulfonic acid (TNB) in 0.25 ml 30% ethanol. Three weeks after TNB administration the colon and the rectum showed transmural, granulomatous inflammation which had many similarities to Crohn's disease and furthermore to the morphological and functional changes which occur in early phases of postischemic intestinal damage. In the colon of TNB-treated animals the ATP and GTP levels were markedly decreased. The accumulation of thiobarbituric acid-reactive substances (TBA-RS) demonstrated a free radical-mediated component of the tissue damage. Treatment with oxypurinol radical scavenger and xanthine oxidoreductase inhibitor diminished the morphological changes, the loss of energy-rich nucleotides and the TBA-RS accumulation.

Animals↗
PubMedDate not supplied

Strikingly different effects of dinitrobenzene sulfonic and trinitrobenzene sulfonic acids on various subpopulations of murine lymphoid cells.

Different changes according to T- or B-cell origin occur in dinitrophenyl (DNP)- and trinitrophenyl (TNP)-modified lymphoid cells. The electrophoretic mobility (EPM) or nylon-wool adherent splenic cells (B cell-enriched) modified by TNP and DNP and that of nylon-wool non-adherent splenic cells (T cell-enriched) and thymic cells modified by TNP increase respectively as follows: +24%, +20%, + 6%, and +16%. A relation has been found between these EPM amounts and amino groups which are positively charged on cell surface. The EPM decreases in the case of nylon-wool non-adherent splenic cells (T cell-enriched, -9%) and thymic cells modified by DNP (-4%). The hydrophobic fluorescent probe 1-anilino-8-naphthalene sulphonate used to study conformational changes of cells revealed a slight fluorescence decrease for TNP-modified cells (-11% for thymic cells, -38% for T cells of spleen, and -66% for B cells of spleen), and a fluorescence increase for DNP-modified cells. This fluorescence increase is more important for spleen T cells (+130%) and thymic cells (+233%) than for spleen B cells (+30%).

Animals↗
PubMed1983

Unresponsiveness in hapten-specific cytotoxic T lymphocytes. IV. Functional deletion of T cell subsets required for trinitrophenyl (TNP)-specific cytotoxic T cell generation after acute or chronic treatment with trinitrobenzene sulfonic acid (TNBS).

The generation of cytotoxic T cell responses requires the interaction of a network of immunocompetent cells. Within this network, a dynamic balance of positive and negative immunoregulatory cells and their products modulate the cytotoxic T cell response. We have developed protocols which shift the balance to favor negative immunoregulation and thus result in antigen-specific unresponsiveness. In this report, a variety of approaches have been utilized to examine the effects of acute and chronic tolerance protocols on specific T cell subsets, namely amplifier helper T cells and precursor cytotoxic T cells. The results to be detailed show differential effects on these T cell subsets which are related to the tolerance protocol employed and the strains of mice tested.

Animals↗
PubMed1989

Treatment with 16,16'-dimethyl prostaglandin E2 before and after induction of colitis with trinitrobenzenesulfonic acid in rats decreases inflammation.

Colitis was induced in rats by intrarectal administration of trinitrobenzene sulfonic acid (80 mg/kg, in 30% ethanol). An acute inflammation with ulcers and neutrophil infiltration developed that evolved into a chronic inflammation and luminal narrowing with attendant smooth muscle hypertrophy. We assessed the effects of 16,16-dimethyl prostaglandin E2, administered either before or after trinitrobenzene sulfonic acid, on the development of inflammation. Inflammation was assessed by gross appearance using a grading scale (0-4) and by histology. The number of neutrophils present in inflamed colonic tissue was quantitated by the myeloperoxidase assay. The production of lipoxygenase products was monitored by incubation of colonic specimens with [14C]arachidonic acid and separation of the products by thin-layer chromatography and high-pressure liquid chromatography. Levels of leukotriene B4 were measured in tissue extracts by high-pressure liquid chromatography and ultraviolet absorbance. Eicosanoid production was also assayed by incubating colonic specimens and assaying the media for prostaglandin E2, leukotriene B4, and leukotriene C4 by radioimmunoassay. Trinitrobenzene sulfonic acid treatment resulted in a greatly increased amount of leukotriene B4 in the media. Treatment with 16,16-dimethyl prostaglandin E2 before administration of trinitrobenzene sulfonic acid resulted in a lower inflammation index, lower myeloperoxidase activity, and decreased production of leukotriene B4. Administration of 16,16-dimethyl prostaglandin E2 24 h after administration of trinitrobenzene sulfonic acid was also effective in reducing the inflammatory response. Treatment with 16,16-dimethyl prostaglandin E2 also prevented the development of long-term architectural changes 3 wk after administration of trinitrobenzene sulfonic acid. Rectal administration of dimethyl prostaglandin E2 also diminished the colitis induced by direct injection of trinitrobenzene sulfonic acid into the colonic wall.

16,16-Dimethylprostaglandin E2↗
PubMed1985

Ionization constants of two active-site lysyl epsilon-amino groups of ribulosebisphosphate carboxylase/oxygenase.

Trinitrobenzene sulfonate rapidly inactivates ribulosebisphosphate carboxylase/oxygenase from both spinach and Rhodospirillum rubrum. 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. Saturating levels of the competitive inhibitor 2-carboxyribitol 1,5-bisphosphate reduce the rates of inactivations but do not prevent them, thereby suggesting that the groups subject to arylation remain accessible in the enzyme complexed with competitive inhibitor. Characterization of tryptic digests of the inactivated enzymes reveals that Lys-166 of the R. rubrum enzyme and Lys-334 of the spinach enzyme are the only major sites of arylation. Both of these lysines have been assigned to the catalytic site by prior affinity labeling studies and are found within highly conserved regions of primary structure. As a monoanion over a wide pH range, trinitrobenzene sulfonate, for which the carboxylase lacks high affinity, can thus be used to determine the pKa values of the two active-site lysyl epsilon-amino groups. Based on the pH dependency of inactivation of the R. rubrum enzyme by trinitrobenzene sulfonate, the epsilon-amino group of Lys-166 exhibits a pKa of 7.9 and an intrinsic reactivity (ko) of 670 M-1 min-1. In analogous experiments, Lys-334 of the spinach enzyme exhibits a pKa of 9.0 and a ko of 4500 M-1 min-1. Under deactivation conditions (i.e. in the absence of CO2 and Mg2+), the pKa of Lys-334 becomes 9.8 and the ko is increased to 26,000 M-1 min-1. By comparison, the reaction of trinitrobenzene sulfonate with N-alpha-acetyl-lysine reveals a pKa of 10.8 and a ko of 1250 M-1 min-1. The spinach carboxylase, catalytically inactive as a consequence of selective arylation of Lys-334, still exhibits tight binding of the transition state analogue 2-carboxyarabinitol 1,5-bisphosphate. Therefore, Lys-334 is not required for substrate binding and may serve a role in catalysis. The unusually low pKa of Lys-166 argues that this residue is also important to catalysis rather than substrate binding.

Anions↗
PubMed1980

The humoral antibody response of rats immunized with chemically modified syngeneic brain cells and glioma cells.

Six-month-old Fischer rats (F344) were given the carcinogen methylnitrosourea in their drinking water. Of the induced brain tumors, four were established in culture and propagated as 78FR-G-219 (pleomorphic glioma), 78FR-G-299 (astrocytoma), 78FR-G-284 and 78FR-G-344 (mixed glioma) permanent lines. All cell lines produced S-100 protein and grew as tumors when inoculated s.c. or i.c. in syngeneic hosts. A comparative study of the antigenicity of these lines at different passage levels was carried out using native and chemically modified cells. Syngeneic rats were immunized with cells conjugated with dimethylsulfate and trinitrobenzene sulfonic acid. The immune response was characterized and quantified by an indirect immunofluorescence method and by a complement-dependent microcytotoxicity test. Chemical modification of the tumor cells enhanced antigenicity of the treated cells. The best results were attained with trinitrobenzene sulfonic-acid-treated cells and constituted a two-fold increase in the cytotoxicity index. Cytotoxicity values varied in the different cell lines. Antisera raised with trinitrobenzene sulfonic-acid-modified cells of all lines cross-reacted with cells of all lines. Cytotoxicity values were insignificantly reduced by absorbing the antisera with a variety of syngeneic tissues. Antisera raised against native syngeneic brain cells showed virtually no cytotoxicity for glioma cells. Antisera raised against syngeneic brain cells treated with trinitrobenzene sulfonic acid, however, were slightly cytotoxic for normal brain cells and glioma cells as well. The results of the present studies show that antigenicity of glioma cells can be definitely raised with trinitrobenzene sulfonic acid treatment. Furthermore, it would seem that haptenization of glioma-associated antigens may be a promising approach ot the study of glioma-host interactions.

Animals↗
PubMed1994

Mast cells are not essential to inflammation in murine model of colitis.

A simple rat model of chronic intestinal inflammation was adapted to mice in order to ascertain whether mast cells play an essential role in its induction or perpetuation. Colitis was induced in C57BL mice by intrarectal administration of trinitrobenzene sulfonic acid in 50% ethanol. Higher doses of trinitrobenzene sulfonic acid per gram of body weight were required in mice than rats, with a narrower effective dose range (the upper dose limited by unacceptable mortality and the lower by decreased inflammation). Colons of treated mice were macroscopically inflamed, with transmural damage, adhesions to adjacent structures, and ulcerations. Inflammation was scored subjectively and by tissue weight and myeloperoxidase content; each index was increased dose-dependently by trinitrobenzene sulfonic acid doses of 0.3-10 mg. Six milligrams of trinitrobenzene sulfonic acid induced reproducible inflammation for up to four weeks. Trinitrobenzene sulfonic acid could induce inflammation in both mast-cell-deficient W/Wv mice and their normal +/+ littermates in a similar fashion. Thus it is possible to induce chronic colitis in the mouse. Mast cells are not essential participants in this process.

Animals↗