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PubMed1984

Improved fixation for immunofluorescence microscopy using light-activated 1,3,5-triazido-2,4,6-trinitrobenzene (TTB).

A new fixation method has been developed for immunofluorescent microscopy using the photosensitive compound 1,3,5-triazido-2,4,6-trinitrobenzene (TTB). Our results show that TTB-fixed cells are well preserved morphologically and that the cellular antigens are better preserved than conventionally fixed cells. By altering one condition at a time in the TTB fixation procedure and analyzing resulting fluorescent antitubulin staining patterns in mammalian tissue culture cells, an optimal procedure was developed. Cells fixed with TTB and stained with antitubulin, antiprekeratin, anti-intermediate filament, anti-alpha-actinin, anti-myosin, antiactin, or anticlathrin were compared with cells fixed by conventional methods and stained with the same antibody. The quality of immunofluorescence images of TTB fixed cells was the same as or better than that of conventionally fixed cells. The most dramatic improvement in image quality was seen when using antiprekeratin or antitubulin. In dividing cells, particularly in metaphase, fluorescent staining with antiactin and anti-alpha-actinin was relatively excluded from the spindle. Antimyosin, on the other hand, stained the spindle and surrounding area more heavily than the subcortical region. We suggest that after TTB fixation, the immunofluorescent patterns of these contractile proteins more closely reflect their relative concentrations in living cells. The exact mechanism for fixation by TTB is not yet known. However, our studies indicated that TTB fixation was not caused by the typical fast photoinduced nitrene diradical mechanism, but rather by some slower, temperature-dependent reaction of a photoactivation product of TTB with the cell.

Actomyosin↗
PubMed1977

Specificity of cytotoxic effector cells directed against trinitrobenzene sulfonate-modified syngeneic cells. Failure to recognize cell surface-bound trinitrophenyl dextran.

Mouse splenic lymphocytes and lymphoid tumor cells were modified with the trinitrophenyl (TNP) group either by treatment with trinitrobenzene sulfonate (TNBS) (which covalently modifies cell surface proteins) or with TNP stearoyl dextran (TSD) (which binds to the cell by noncovalent forces). These cell preparations were compared for their ability to: (a) sensitive syngeneic splenic lymphocytes leading to the generation of cytotoxic effector cells; (b) serve as lysable targets in a 4-h(51)Cr- release assay for effector cells generated in (a); and (c) act as blocking cells in the lysis of TNBS-medified targets lysed by TNP self effector cells generated in (a). In none of these three experimental systems did TSD-medified syngeneic spleen or H-2-matched tumor cells act either as a sensitizing immunogen or as a target antigen, despite the demonstration that quantitatively equivalent mounts of TNP were exposed on the cell surface in the TNBS- and TSD-modified cells. In contrast, TNBS-modified spleen cells sensitized syngeneic lymphocytes to generate effectors against TNBS-modified syageneic targets. Furthermore, TNBS- modified, H-2-matched cells served as specific lysable targets and as inhibiting cells for such effectors. These results indicate that the manner in which TNP is associated with the cell surface is important in the immunogenicity and antigenicity of hapten-modified syngeneic stimulating cells in generating H-2-associated cell-mediated lympholysis (CML) reactions. These findings raise the possibility that a covalent or at least a stable linkage with cell surface proteins (possibly H-2- controlled products) is important for immunological function. Furthermore, these observations do not favor the dual receptor model for H-2-restricted syngeneic CML if it is assumed in such a model that one receptor is specific for the TNP moiety and the second for unmodified self major histocompatibility products.

Animals↗
PubMed1984

Selective modification of myosin SH1 with 1,2,4-trinitrobenzene. VIII. Thiols of myosin.

Myosin has 2 mol of the most reactive thiol, named SH1. 1,2,4-Trinitrobenzene (TNB), a novel dinitrophenyl(DNP)ating reagent [Takahashi et al. (1983) Chem. Lett. 1445-1448], was found to react only with SH1 without any other amino acid residues in myosin under the conditions used. Its reaction with myosin SH1 was about 30 times faster than that with N-acetylcysteine (NAC). The reaction rate of TNB with SH1 was about twice compared with that of NEM, the most reactive selective reagent for SH1 so far found, although its rate with NAC was only one sixtieth that of NEM. As to the lambda max of the absorption spectrum of SH1-DNP-myosin, a large red shift of as much as 20 nm was observed compared with low molecular S-DNP derivatives. This red shift disappeared in 8 M urea. This outstanding feature of SH1 modification with TNB was discussed in terms of affinity labeling by interaction with an aromatic amino acid near SH1.

Adenosine Triphosphatases↗
PubMed2004

Catalposide, a compound isolated from catalpa ovata, attenuates induction of intestinal epithelial proinflammatory gene expression and reduces the severity of trinitrobenzene sulfonic Acid-induced colitis in mice.

Certain irinoid-producing plants have been used as herbal anti-inflammatory remedies. Here we evaluated whether catalposide (CATP), a single compound isolated from irinoid-producing plant Catalpa ovata, has a potential for preventing or ameliorating diseases characterized by mucosal inflammation. Preliminary microarray-based gene expression test revealed that CATP, which alone did not significantly affect expression of any of the >8,000 genes analyzed, attenuated the expression of tumor necrosis factor-alpha (TNF-alpha)-induced proinflammatory genes including interleukin-8 (IL-8) in human intestinal epithelial HT-29 cells. Down-regulation of IL-8 mRNA accumulation was also reflected by the decreased IL-8 secretion in CATP-treated HT-29 cells. The signal transduction study revealed that CATP significantly attenuates TNF-alpha-mediated p38 and extracellular signal-regulated kinase (ERK) phosphorylation. Further, CATP reduced NF-kappaB-mediated transcriptional activation as well as Ikappa-Balpha degradation. To establish the in vivo relevance of these findings, we examined whether CATP could affect intestinal inflammation in vivo using the mouse model of trinitrobenzene sulfonic acid (TNBS)-induced inflammatory colitis. Intrarectal administration of CATP dramatically reduced the weight loss, colonic damage, and mucosal ulceration that characterize TNBS colitis. Moreover, CATP suppressed the expression of TNF-alpha, interleukin-1beta, and intercellular adhesion molecule-1 along with the inhibition of NF-kappa B p65 translocation into nucleus in TNBS colitis. Collectively, current results demonstrate that CATP may be an effective agent for the treatment of diseases characterized by mucosal inflammation.

Animals↗
PubMed2006

Effects of topical treatment of sodium butyrate and 5-aminosalicylic acid on expression of trefoil factor 3, interleukin 1beta, and nuclear factor kappaB in trinitrobenzene sulphonic acid induced colitis in rats.

BACKGROUND AND AIMS: Butyrate enemas have been shown to be effective in treatment of ulcerative colitis, but the mechanism of the effects of butyrate is not totally known. This study evaluates effects of topical treatment of sodium butyrate (NaB) and 5-aminosalicylic acid (5-ASA) on the expression of trefoil factor 3 (TFF3), interleukin 1beta (IL1beta), and nuclear factor kappaB (NFkappaB) in trinitrobenzene sulphonic acid (TNBS) induced colitis in rats. METHODS: Distal colitis was induced in male Wistar rats by colonic administration of TNBS and colonically treated with NaB, 5-ASA, combination of NaB and 5-ASA, and normal saline for 14 consecutive days. Colonic damage score, tissue myeloperoxidase (MPO) activity, TFF3 mRNA expression, serum IL1beta production, and tissue NFkappaB expression were determined, respectively. RESULTS: Treatment of NaB, 5-ASA, and the combination improved diarrhoea, colonic damage score, and MPO activities, increased TFF3 mRNA expression, and decreased serum IL1beta production and tissue NFkappaB expression. The combination therapy of NaB and 5-ASA had better effects than any other single treatment. CONCLUSIONS: The combination of topical treatment of NaB and 5-ASA was effective for relieving and repairing colonic inflammation and the effects were related to stimulation of TFF3 mRNA expression and down-regulation of IL1beta production and NFkappaB expression.

Administration, Topical↗
PubMedDate not supplied

1,3,5-Trinitrobenzene-induced encephalopathy in male Fischer-344 rats.

Administration of 1,3,5-trinitrobenzene (TNB) to male Fischer-344 rats produced ataxia after 6 or 7 oral doses (71 mg/kg). Light microscopic examination after 10 days revealed petechial hemorrhages in the brain stem and cerebellum and bilaterally symmetric degeneration and necrosis (malacia) with reactive gliosis in the cerebellar peduncles. The malacia was dorsal and lateral to the fourth ventricle involving the cerebellar nuclei, medial and lateral vestibular nuclei, and inferior colliculi. Blood vessels associated with the lesion had widened Virchow-Robin spaces, occasionally with extravasated erythrocytes. Rats administered daily oral doses of 35.5 mg/kg of TNB for 10 days and 35.5 and 71 mg/kg of TNB for 1 or 4 days did not have brain lesions.

Administration, Oral↗
PubMedDate not supplied

1,3,5-Trinitrobenzene-induced alpha-2u-globulin nephropathy.

Male and female Fischer-344 (F-344) and male NCI-Black-Reiter (NBR) rats were dosed with 0, 35.5, or 71 mg 1,3,5-trinitrobenzene (TNB)/kg/day for 10 days. Male F-344 rats were dosed with TNB (0 and 35.5 mg/kg) for 20 and 30 days. Hematoxylin and eosin and Mallory-Heidenhain stains and alpha-2u-globulin and proliferating cell nuclear antigen immunohistochemical stains were performed on kidney sections. All treated male F-344 rats exhibited dose-related accumulation of hyaline droplets containing alpha-2u-globulin in proximal tubules. The kidney weights were significantly increased in male and female rats treated with TNB. Significant increases in cell proliferation in proximal tubules were observed in male F-344 rats. Renal changes observed in TNB-treated rats appeared identical to those from other chemicals that induce alpha-2u-globulin nephropathy in male rats. No hyaline droplet accumulation was found in female F-344 and male NBR rats at any doses. We can conclude that TNB induces dose-related exacerbation of hyaline droplets containing alpha-2u-globulin in male rat kidney and subsequent cell proliferation.

Alpha-Globulins↗
PubMedDate not supplied

Reproductive toxicity screen of 1,3,5-trinitrobenzene administered in the diet of Sprague-Dawley rats.

Several Army installations targeted for restoration have measurable quantities of 1,3,5-trinitrobenzene (TNB) in the soil and groundwater. As part of the process of developing environmental and health effects criteria for restoration, a modified Screening Information Data Set (SIDS) reproductive study was performed. Male and female Sprague-Dawley rats received a diet containing approximately 30, 150, or 300 mg TNB/kg diet. Mating occurred following 14 days of treatment. All dams, one-half the males, and representative pups were maintained for a total of 90 days of treatment. No mortality occurred during the study; however, a decrease in mean body weights was noted in both sexes of high-dose rats. A dose-related effect was noted in measurements of sperm function/activity. Sperm depletion and degeneration of the seminiferous tubules were noted histopathologically. Methemoglobinemia and splenic hemosiderosis were common findings in the high- and mid-dose levels of both sexes at necropsy. No adverse effects were noted in mating or fertility indices. No significant treatment-related differences were found in length of gestation, sex ratio, gestation index, or mean number of pups per litter.

Animals↗
PubMed1999

Neurotoxicity of 1,3,5-trinitrobenzene (TNB): immunohistochemical study of cerebrovascular permeability.

1,3,5-Trinitrobenzene (TNB) is a soil and water contaminant at certain military installations. Encephalopathy in rats given 10 daily oral doses of TNB has been reported. The lesion was bilaterally symmetric vacuolation and microcavitation in the cerebellar roof nuclei, vestibular nuclei, olivary nuclei, and inferior colliculi. The contribution of the blood-brain barrier (BBB) in the genesis of these lesions remains uncertain. One of the main goals of the present work was to evaluate the functional state of the BBB. Male Fischer 344 rats (five rats/group) were euthanatized after four, five, six, seven, eight, or 10 daily doses of TNB (71 mg/kg). A different set of rats (five rats/group) was allowed to recover for 10 or 30 days after receiving 10 doses of TNB. Integrity of the BBB was assessed by immunohistochemical staining for extravasated plasma albumin on paraffin-embedded sections. Rats euthanatized after four to eight doses had no lesions, and albumin extravasation in the susceptible regions of the brain was minimal. Rats receiving 10 daily doses of TNB had bilaterally symmetric vacuolation and microcavitation in the cerebellar nuclei, vestibular nuclei, and inferior colliculi in association with multifocal, often confluent foci of extravasated albumin in susceptible nuclei. Albumin was present in vascular walls, extracellular space, and neurons. Immunoreactivity in neurons was of two types: cytoplasmic staining representing pinocytic uptake and homogeneous staining of the entire neuron (nucleus and cytoplasm) due to uncontrolled albumin leakage through the damaged cell membrane. In rats allowed to recover for 10 days, the microcavitated foci were infiltrated by glial and gitter cells. Albumin immunoreactivity was present as extracellular granular debris, and neuronal staining (for albumin) was mild. In rats allowed to recover for 30 days, immunoreactivity to albumin was not seen. This study demonstrates that TNB-mediated tissue damage is accompanied by breakdown of the BBB. The presence of vacuolation and associated extravasated serum proteins in TNB-treated rats is an indication of vasogenic brain edema, which appears to be a critical event in TNB toxicity. Additional studies are needed to determine the reason for selective regional vulnerability and brain microvascular susceptibility to TNB.

Albumins↗
PubMed2006

Toxicities of dinitrotoluenes and trinitrobenzene freshly amended or weathered and aged in a sandy loam soil to Enchytraeus crypticus.

Scientifically based ecological soil-screening levels are needed to identify concentrations of contaminant energetic materials (EMs) in soil that present an acceptable ecological risk at a wide range of military installations. Insufficient information regarding the toxicity of 2,4-dinitrotoluene (2,4-DNT), 2,6-dinitrotoluene (2,6-DNT), and 1,3,5-trinitrobenzene (TNB) to soil invertebrates necessitated toxicity testing. We adapted the standardized Enchytraeid Reproduction Test (International Standardization Organization 16387:2003) and selected Enchytraeus crypticus for these studies. Tests were conducted in Sassafras sandy loam soil, which supports relatively high bioavailability of nitroaromatic EMs. Weathering and aging procedures for EMs amended to test soil were incorporated into the study design to produce toxicity data that better reflect the soil exposure conditions in the field compared with toxicity in freshly amended soils. This included exposing hydrated, EM-amended soils in open glass containers in the greenhouse to alternating wetting and drying cycles. Definitive tests established that the order of EM toxicity to E. crypticus based on the median effect concentration values for juvenile production in either freshly amended or weathered and aged treatments was (from the greatest to least toxicity) TNB > 2,4-DNT > 2,6-DNT. Toxicity to E. crypticus juvenile production was significantly increased in 2,6-DNT weathered and aged soil treatments compared with toxicity in freshly amended soil, based on 95% confidence intervals. This result shows that future investigations should include a weathering and aging component to generate toxicity data that provide more complete information regarding ecotoxicological effects of energetic contaminants in soil.

Animals↗
PubMed1979

Hapten specific unresponsiveness in mice. I. Characteristics of unresponsiveness induced by 2,4,6-trinitrobenzene sulphonic acid.

Injection of mice with the chemically reactive hapten 2,4,6-trinitrobenzene sulphonic acid (TNBSA) induces a specific unresponsiveness as judged by reduction or abolition of the anti-TNP response to TNP-KLH. The normal response to a nonrelated hapten, oxazolone, bound to the same carrier (OX-KLH) is unaffected. Reduction of the anti-TNP response was also observed after TNBSA treatment, in nude mice (nu/nu) and their littermates (nu/+) challenged with TNP-POL, an antigen to which the response is thymus independent. Injection of the chemically non-reactive hapten TNP-glycyl-glycine did not induce unresponsiveness. A similar failure was observed with TNP autologous red cells or serum proteins from mice previously injected with TNBSA. The specific unresponsiveness of spleen cells of TNBSA injected mice was maintained after their transfer into lethally irradiated syngeneic host mice. Finally tolerant cells do not inhibit specifically an adoptive anti-TNP secondary response.

Animals↗
PubMed1979

Cell types required for H-2-restricted cytotoxic responses generated by trinitrobenzene sulfonate-modified syngeneic cells or trinitrophenyl-conjugated proteins.

Murine spleen cells were fractionated over nylon wool or Sephadex G-10 columns, and the cell types involved in the generation of trinitrophenyl (TNP)-specific, H-2 restricted (TNP-self) cytotoxic effector cells were studied from cultures stimulated with trinitrobenzene sulfonate (TNBS)-modified syngeneic cells, TNP-conjugated soluble proteins such as bovine gamma-globulin (TNP-BGG), or bovine serum albumin (TNP-BSA). Unfractionated or nylon nonadherent responding cells generated such effectors, irrespective of whether the cultures were stimulated with TNBS-modified cells or TNP-conjugated proteins. TNP-modified T lymphocytes, B lymphocytes, and phagocyte-enriched spleen cells were all capable of stimulating TNP-self effectors. TNP-self effectors. TNP-self as well as allogeneic cytotoxic responses were dependent on the presence of a radioresistant non-T cell that was removed by Sephadex G-10 fractionation and was replaced by irradiated, Thy 1.2-negative, glass adherent spleen cells, enriched in phagocytic cells. Results obtained by using glass adherent cells that were allogeneic or semi-syngeneic to the responding cells indicated that H-2 homology was not required for efficient glass adherent cell function, and that the H-2 restriction of TNP-self effectors is not determined by these glass adherent cells.

Animals↗
PubMed1997

Testicular effects of 1,3,5-trinitrobenzene (TNB). II. Immunolocalization of germ cells using proliferating cell nuclear antigen (PCNA) as an endogenous marker.

The applicability of PCNA as a tool for the analysis of germ cells in rats treated with 1,3,5-trinitrobenzene (TNB), a potent testicular toxicant, was evaluated. Male Fischer 344 (F344) rats were gavaged with TNB at 71 mg/kg or with corn oil (vehicle). Rats were killed after 10 daily oral doses or were allowed to recover for 10 or 30 d after the 10 doses. Testes from control rats, treated rats, and rats allowed to recover were immunohistochemically stained for PCNA. PCNA labeling in the control rats was confined to the nuclei of spermatogonia, pachytene spermatocytes, and nuclei of elongate spermatocytes. Conventional (hematoxylin and eosin) staining of testes from rats treated with TNB at 71 mg/kg for 10 d revealed loss of germ cells and cessation of spermatogenesis. Immunohistochemical staining of sections from these treated rats revealed only PCNA-positive spermatogonia. Rats allowed a 10-d recovery had both spermatogonial and spermatocytic staining, indicating partial restoration of germ-cell population. In rats allowed to recover for 30 d, the PCNA staining pattern was identical to the control rats. These results indicate that PCNA can be used to assess the proliferative status of spermatogonia (germ cells) in rodent testes exposed to testicular toxicants.

Animals↗
PubMed2000

Tandem mass spectrometric study of 1,3,5-trinitrobenzene molecular ion: an unusual ortho effect involving a hydrogen atom from the aromatic ring

Unimolecular (metastable) and collision-induced dissociation of 1,3, 5-trinitrobenzene molecular ion was studied using linked scans and mass-analyzed ion kinetic energy spectrometry on a hybrid instrument of EBEqQ geometry. An unusual ortho effect leading to the loss of OH radical from the parent molecular ion is observed as a unimolecular dissociation process only in the first-field free region between the ion source and the electric sector, although corresponding dissociation in the ion source is of negligible abundance (<0.1%). This unimolecular process is taken over by other dissociation pathways when the parent ion is collisionally activated, suggesting that this dissociation process occurs only in a very narrow energy window with a rate constant of the order of 2 x 10(5) s(-1). Copyright 2000 John Wiley & Sons, Ltd.

Journal Article↗
PubMed1976

Passive cation movements in the Ehrlich ascites tumor cell: the effects of 2,4,6-trinitrobenzene sulfonic acid.

We have investigated the effects of 2,4,6-trinitrobenzene sulfonic acid (TNBS), an amino reactive reagent, on passive cation movements in Ehrlich ascites tumor cells. Incubation of tumor cells with TNBS (3 mM) results in a two phase association of TNBS with the cells. An initial, rapid phase, presumably at the level of the membrane, is independent of temperature, while the second phase increases linearly in time and is temperature dependent. Kinetic analyses of Na+ movements indicate that TNBS: (1) inhibits Na+ movement from a slowly exchanging cellular compartment, but is without effect on a more rapidly exchanging compartment; (2) does not alter net Na+ accumulation in transport-inhibited cells; and (3) is without effect on non-exchange Na+ efflux at 0 degrees C. The actions of TNBS on K+ movements depend upon temperature and the continued presence of TNBS in the environment. At 22 degrees C two minute exposure of the cells to TNBS leads to 77% inhibition of K+ efflux. With continued exposure to TNBS, the inhibition is only 42%. Reduction of the temperature to 0 degrees C decreases K+ efflux in control cells by 82%. Two minute exposure to TNBS enhances K+ efflux by 50%, while continuous exposure increases it by 144%. These results suggest: (1) TNBS interacts with several classes of membrane sites which are involved with the regulation of passive cation movements; and (2) passive Na+ and K+ movements across the cell membrane proceed by different pathways.

Biological Transport↗
PubMed1995

Effect of leukotriene C4D4 antagonist on colonic damage induced by intracolonic administration of trinitrobenzene sulfonic acid in rats.

We examined the effects of eicosanoid antagonists on colonic damage induced by trinitrobenzene sulfonic acid (TNB) in a rat inflammatory bowel model. TNB (30 mg) dissolved in 0.25 ml of 50% ethanol, was given intrarectally. The appropriate doses of ONO-1078 (a leukotriene C4D4 antagonist), ONO-4057 (a leukotriene B4 antagonist), and OKY-046 (a thromboxane A2 synthetase inhibitor) were given to obtain the same blood level, either 4 h before (pre-treatment model) or 24 h after (the post-treatment model) the administration of TNB (n = 8 in all groups). Drugs were given once daily for 6 days through a gastric feeding tube. Autopsy was performed on the 7th day. Colonic damage was assessed in terms of colonic damage scores, and myeloperoxidase (MPO) activity and eicosanoid concentrations in colonic tissues were measured. Compared with the group given TNB alone, the colonic damage score was reduced to 10% in the pre-treatment model with ONO-1078, but the score was not reduced in other groups, MPO activity was not changed in any group. The concentration of leukotriene C4 was reduced with ONO-1078 treatment, in both pre- and post-treatment models. These results demonstrated that a leukotriene C4D4 antagonist reduced colonic inflammation; however, its anti-inflammatory effect was limited in this colitis model.

Animals↗
PubMed1988

The effect of pyrophosphate on the reaction of myosin with 2,4,6-trinitrobenzene sulphonate.

Myosin was reacted with 2,4,6-trinitrobenzene sulphonate (TNBS) in the presence or absence of Mg-pyrophosphate. The reaction led to trinitrophenylation of lysyl residues which could be divided on the basis of the reaction into three classes: (i) two rapidly reacting lysyl residues (RLR), one residing on each head of myosin, whose rate of reaction depends on the presence of Mg-pyrophosphate; (ii) two lysyl residues which react with intermediate rate (ILR) and reside on the rod segment of myosin; and (iii) the remaining lysyl residues of myosin which react slowly with TNBS. The rate of the trinitrophenylation of RLR was followed spectrophotometrically and enzymatically, measuring an absorbance change at 345 nm, and also changes in K+ (EDTA)-, Mg2+- and Ca2+-activated ATPase activities, respectively. According to analysis of the kinetics of the reaction, Mg-pyrophosphate inhibited the rate of trinitrophenylation in both heads of myosin, not in one head only as was suggested by Miyanishi et al. (J. Biochem Tokyo 85; 1979). Myosin heads (myosin subfragment-1, S-1) were prepared by digesting myosin trinitrophenylated in the absence and presence of Mg-pyrophosphate with chymotrypsin. S-1, with trinitrophenylated RLR, was separated from non-trinitrophenylated S-1 by DEAE cellulose column chromatography. The trinitrophenylated S-1 had a high Mg2+- and a low K+(EDTA)-activated ATPase while the non-trinitrophenylated species had the usual high K+(EDTA)- and low Mg2+-ATPase activity. This results excluded the possibility suggested by Miyanishi et al., that the myosin head, which is resistant to trinitrophenylation in the presence of Mg-pyrophosphate, did not possess K+(EDTA)-activated ATPase activity. The presence of Mg-pyrophosphate during trinitrophenylation substantially affected the enzymic characteristics of the modified myosin. The myosin trinitrophenylated in the presence of Mg-pyrophosphate had a higher K+(EDTA)- and a lower Mg2+-ATPase activity. SH1 (Cys-707) also probably becomes a target of the reaction if myosin is trinitrophenylated in the presence of Mg-pyrophosphate. This is deduced from the following findings: (i) the addition of dithiothreitol after trinitrophenylation partially reversed the loss in the K+(EDTA)-ATPase activity; and (ii) the specific alkylation of the SH1 thiol by 1,5-IAEDANS prior to trinitrophenylation prevented the effect of dithiothreitol on the ATPase activity of myosin. The results indicated that Mg-pyrophosphate induced structural changes in the myosin molecule which influenced the course and possibly the target(s) of trinitrophenylation.

Adenosine Triphosphatases↗
PubMed1993

Experimental ileitis in dogs and colitis in rats with trinitrobenzene sulfonic acid--colonoscopic and histopathologic studies.

Using a novel experimental model of chronic enterocolitis described by Morris et al., we observed sequential changes of mucosal lesions endoscopically and performed histopathological studies. Fisher rats were rectally administered 25 mg of trinitrobenzene sulfonic acid (TNBS) dissolved in 0.5 ml of 50% ethanol (ET). The combination treatment of TNBS and ET produced colitis in rats for over 3 weeks. TNBS itself did not induce any lesions. ET alone induced mucosal lesions, but their severity was much smaller than that induced by TNBS/ET. As an animal model much closer to human inflammatory bowel disease, we have newly developed a canine model of chronic ileitis. Adult mongrel dogs were administered 10 ml of 100% ethanol and 1 g of TNBS dissolved in 10 ml of distilled water (i.e., 100 mg/ml solution) through a 4-lumen double balloon tube which was inserted into the ileum. The TNBS/ET-induced ileitis in dogs persisted for 8 weeks. The mucosal lesions induced by TNBS/ET were characterized as annular or longitudinal ulcers accompanied by extensive lymphocyte infiltration and granulomas, which were similar to macro- and microscopic findings observed in human Crohn's disease. Endoscopic examinations were a valuable tool to obtain sequential information on the development of inflammatory changes in each individual animal. Our canine model would provide various advantages for the study of functional impairment in chronic enterocolitis as well as for the detection of potential therapeutic agents in the human counterpart.

Animals↗