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PubMed2005

Resolvin E1, an endogenous lipid mediator derived from omega-3 eicosapentaenoic acid, protects against 2,4,6-trinitrobenzene sulfonic acid-induced colitis.

Resolvin E1 (RvE1; 5S,12R,18R-trihydroxyeicosapentaenoic acid) is an antiinflammatory lipid mediator derived from omega-3 fatty acid eicosapentaenoic acid (EPA). At the local site of inflammation, aspirin treatment enhances EPA conversion to 18R-oxygenated products, including RvE1, which carry potent antiinflammatory signals. Here, we obtained evidence for reduced leukocyte infiltration in a mouse peritonitis model, where the administration of EPA and aspirin initiated the generation of RvE1 in the exudates. Similar results were obtained with the administration of synthetic RvE1, which blocked leukocyte infiltration. RvE1 also protected against the development of 2,4,6-trinitrobenzene sulfonic acid-induced colitis. The beneficial effect was reflected by increased survival rates, sustained body weight, improvement of histologic scores, reduced serum anti-2,4,6-trinitrobenzene sulfonic acid IgG, decreased leukocyte infiltration, and proinflammatory gene expression, including IL-12 p40, TNF-alpha, and inducible nitric oxide synthase. Thus, the endogenous lipid mediator RvE1 counter-regulates leukocyte-mediated tissue injury and proinflammatory gene expression. These findings show an endogenous mechanism that may underlie the beneficial actions of omega-3 EPA and provide targeted approaches for the treatment of intestinal inflammation.

Animals↗
PubMed1972

Molecular complexes of methoxyindoles with 1,3,5-trinitrobenzene and tetracyanoethylene.

Association constants for 1:1 molecular complexes formed between 1,3,5-trinitrobenzene and various methoxy-substituted indoles have been determined by chemical-shift measurements in their nuclear magnetic resonance spectra. The values of association constants for the molecular complexes are comparable to those obtained by optical spectroscopy. The effect on the association constants and relative chemical shifts of the acceptor protons of the pure complexes of various donors is considered. The association constants and relative chemical shifts of the complexes determined by different protons on the nidoles in the presence of an excess of 1,3,5-trinitrobenzene are different. The possible structure of the complexes is discussed. The molecular complexes between tetracyanoethylene and various methoxyindoles have also been studied.

Journal Article↗
PubMed2002

The role of mast cells in the development of 2, 4, 6-trinitrobenzene sulfonic acid-induced colitis in rats.

BACKGROUND: The role of mast cells in Crohn disease (CD) remains to be established. The aim of this study was to elucidate this in the development of CD-like colitis in rats by the use of mast-cell-deficient Ws/Ws and their control W+/W+ rats. METHODS: CD-like colitis was induced in both groups by an enema of 10 mg of 2,4, 6-trinitrobenzene sulfonic acid (TNBS) in 50% ethanol. Colonic damage, adhesion and colonic weight were measured at 7 and 14 days after the TNBS/ethanol enema. Rat mast cell protease-2 (RMCP-2) in the colonic tissue was also measured at 7 days after the enema. RESULTS: There was no significant difference between W+/W+ and Ws/Ws rats in terms of colonic damage, adhesion or colonic weight. The tissue content of RMCP-2 in Ws/Ws rats treated with either saline or TNBS/ethanol was only maintained at a much lower level than that in W+/W+ rats with the corresponding treatment. CONCLUSIONS: These results demonstrate that mast cells are not essential in the development of 2, 4, 6-trinitrobenzene sulfonic acid-induced colitis in rats.

Animals↗
PubMed2004

The effect of recombinant human growth hormone (rhGH) on trinitrobenzene sulfonic acid-induced colitis in rats: an experimental study.

The limited efficacy of standard medical therapies for inflammatory bowel diseases has resulted in a continuing search for alternative treatments. Growth hormone (GH) has shown to have mutagenic and proliferative effects on intestinal cells. This study was designed to identify the effect of growth hormone on trinitrobenzene slfonic acid-induced colitis (TNBSIC) in rats. This study was carried out on 30 rats, divided in 3 groups: group 1: TNBSIC+ GH, group 2: TNBSIC, group 3: saline enema. Colitis was induced in male Sprague-Dawley rats (200 g-250 g) by intracolonic installation of 2, 4, 6-trinitrobenzene sulphonic acid in 50% ethanol. GH treatment has been started and continued throughout the study after inducing colitis. All rats were killed after 5 weeks and colonic segments were examined histopathologically. Microscopic and macroscopic damage scores were caulculated. Intestinal damage scores were found higher in Goups II when compared with treatment group (P < 0.05). There was no damage in group 3 as expected. Both macroscopic and microscopic scores were highest in group 2 (P < 0.05). The myloperoxidase activity was found lower comparing to group 2 (P < 0.05). In conclusion, growth hormone replacement had protective effects against colonic inflammation while reducing intestinal damage on TNB-induced colitis.

Analysis of Variance↗
PubMed2005

Effects of Changtai granules, a traditional compound Chinese medicine, on chronic trinitrobenzene sulfonic acid-induced colitis in rats.

AIM: To study the effects of Changtai granules (CTG), a traditional compound Chinese medicine, on chronic trinitrobenzene sulfonic acid-induced colitis in rats. METHODS: Healthy adult Sprague-Dawley (SD) rats of both sexes, weighing 250-300 g, were employed in the present study. The rat colitis models were induced by 2,4,6-trinitrobenzene sulfonic acid (TNBS) enemas at a concentration of 100 mg/kg in 50% ethanol. The experimental animals were randomly divided into dexamethasone (DX) treatment, CTG treatment, and model control groups, which were intracolicly treated daily with DX (0.2 mg/kg), CTG at doses of 2.9, 5.7 and 11.4 g crude drug/kg, and the equal amount of saline respectively from 6 h following induction of the colitis in rats inflicted with TNBS to the end of study. A normal control group of rats treated without TNBS but saline enema was also included in the study. After 3 wk of treatment, the animals were assessed for colonal inflammatory and ulcerative responses with respect to mortality, frequency of diarrhea, histology and myeloperoxidase activity (MPO). RESULTS: The therapeutic effect of CTG on ulcerative colitis (UC) was better than DX. CTG effectively inhibited the activity of granulocytes, macrophages and monocytes in a dose-dependent manner. Also it reduced MPO and formation of inflammation in colonic mucosal tissue. Furthermore, administration of CTG significantly prevented body mass loss and death, and decreased frequency of diarrhea in UC rats, when compared with the model control group rats. CONCLUSION: CTG would prove to be an ideal drug for chronic UC, and is warranted to be studied further.

Animals↗
PubMedDate not supplied

Fourteen-day toxicity study of 1,3,5-trinitrobenzene in Fischer 344 rats.

Toxic effects of 1,3,5-trinitrobenzene (TNB) in male and female rats were evaluated by feeding powdered certified laboratory chow diet supplemented with varied concentrations of TNB (0, 50, 200, 400, 800 and 1200 mg kg-1 diet) for 14 days. Food intake by female rats in 400, 800 and 1200 mg TNB diet groups was reduced and resulted in a significant decrease in absolute body weights (BW). Food and water consumption by male rats in high-dose groups (800 and 1200 mg TNB kg-1 diet) was also reduced and resulted in a significant decrease in body weight. The calculated average TNB intake (from 1200 mg TNB kg-1 diet) was 92 mg kg-1 BW day-1 for male rats and 80 mg kg-1 BW day-1 for females. A decrease in testicular weight in males and an increase in spleen weight of both sexes in high-dose groups was noted. In addition, histopathological examinations revealed that the susceptible organs for TNB toxicity were kidney (hyaline droplets), spleen (extramedullary hematopoiesis), brain (hemorrhage, malacia and gliosis) and testes (seminiferous tubular degeneration). Hematology and clinical chemistry studies indicated a decrease in red blood cell count and hematocrit, a decrease in alkaline phosphatase, an increase in Heinz bodies and increased methemoglobin concentration as compared to controls in both sexes. A lowest observed adverse effect level of 4.41 mg TNB kg-1 BW day-1 was established based on the findings of this study.

Anemia↗
PubMedDate not supplied

Percutaneous absorption of trinitrobenzene: animal models for human skin.

The percutaneous absorption of 1,3,5-trinitrobenzene (TNB) was studied in viable skin from hairless guinea pigs (HGP), Fischer 344 rats and humans. Skin was dermatomed and assembled in flow-through diffusion cells followed by TNB application in either an acetone or a water vehicle. Skin absorption was expressed as the percentage of applied dose absorbed into skin and receptor fluid within 24 h. Rapid absorption of TNB by rodent skin was obtained with both vehicles. For HGP skin, TNB absorption was 72.7+/-5.5% in the acetone vehicle and 82.3+/-4.5% in the water vehicle. For rat skin, TNB absorption was 61.0+/-4.1% (acetone) and 66.5+/-4.1% (water). Absorption of TNB from acetone was significantly reduced (38.0+/-11.0%, P = 0.0118) in human skin, but absorption from water remained high (75.5+/-10.8%). Little TNB remained in skin when a thin (200 microm) dermatome section was used (HGP and human skin). A thicker dermatome section was required (350 microm) with haired rat skin, and 13-21% of the absorbed radioactivity remained in the skin at 24 h. Rodent skin did not simulate satisfactorily the barrier properties of human skin when TNB absorption was reduced by application in a volatile solvent.

Animals↗
PubMed1996

Effect of bucillamine on the rat trinitrobenzene sulfonic acid induced model of colitis.

Salicylazosulphapyridine and corticosteroids are the only remedies for inflammatory bowel disease currently in clinical use. They do not, however, necessarily bring about satisfactory therapeutic benefits, so that new agents are needed. In this study, we evaluated the effect of bucillamine, a new antirheumatic agent, in experimental rat colitis induced by trinitrobenzene sulfonic acid enema. Wistar rats were given vehicle alone (n = 16) or treated with 50 (n = 20) or 150 (n = 20) mg/kg of bucillamine daily for three weeks after induction of colitis. Conventional histological sections of the colon stained by haematoxylin and eosin were prepared and observed under a light microscope to determine colonic damage scores. The determinations were significantly lower in the group treated with 50 mg/kg of bucillamine and tended to be lower in the group treated with 150 mg/kg of bucillamine than in the untreated group, which implied that the experimentally induced colonic inflammatory changes and ulcerations were alleviated by bucillamine. Blood tests showed no abnormal values at the end of the treatment. The present observations suggest that bucillamine should be developed further as a possible therapy for inflammatory bowel disease.

Animals↗
PubMed1997

Use of trinitrobenzene as a nitrogen source by Pseudomonas vesicularis isolated from soil.

An aerobic Gram-negative bacterium identified as Pseudomonas vesicularis was isolated from soil contaminated with 2,4, 6-trinitrotoluene (TNT) and 1,3,5-trinitrobenzene (TNB). This bacterium used TNB as the sole source of nitrogen. The TNB was metabolized within 80 h of incubation. The major metabolites produced were dinitroaniline,dinitrobenzene (DNB), nitroaniline, nitrobenzene (NB), and ammonia. The concentrations of DNB and NB produced in the culture medium were nearly stoichiometric. The ammonia concentration in the culture medium increased during the course of incubation. The end product of TNB metabolism was NB,which did not undergo further degradation even after long incubation time. This bacterium could be used in a syntrophic culture system with other NB-degrading bacteria to remove TNB completely from soil and water at contaminated sites.

Biodegradation, Environmental↗
PubMed1994

Quantitation of epsilon-amino group using amino acids as reference standards by trinitrobenzene sulfonic acid. A simple spectrophotometric method for the estimation of hapten to carrier protein ratio.

A simple, sensitive and direct spectrophotometric method is presented for the determination of epsilon-amino groups of L-lysine present in carrier proteins, using the free amino acids L-lysine and L-glutamic acid as reference standards, and 2,4,6-trinitrobenzene 1-sulfonic acid (TNBS) reagent. The amount of epsilon-amino group present in the carrier protein after coupling with hapten is directly quantitated using the standard curve generated by the difference in absorbance observed with L-lysine and L-glutamic acid after their reaction with TNBS reagent. Spectral analysis of L-lysine and L-glutamic acid (27.36 nmol) derivatives of TNBS at 335 nm showed that TNP-L-lysine had twice the absorbance of TNP-L-glutamic acid, since TNBS reagent interacts equally with the alpha-amino and epsilon-amino groups present in L-lysine and the alpha-amino group of L-glutamic acid, respectively. The relationship between absorbance and concentration of epsilon-amino groups (up to 16 micrograms/ml) was found to be linear. The number of epsilon-amino groups of lysine present in carrier proteins such as BSA, HSA, thyroglobulin and the enzyme, horseradish peroxidase, were analyzed by the present method and were found to be similar to the reported values. Various carrier protein-hapten conjugates (protein-mycotoxin/vitamin/steroid hormone conjugates) were made and analyzed by the method developed in order to determine their mole to mole ratio.

Antigens↗
PubMed1979

Cell surface changes during muscle differentiation in vitro: a study with the probe 2,4,6-trinitrobenzene sulphonate.

Cell surface changes during muscle differentiation in vitro, were investigated using the non permeant probe 2,4,6-trinitrobenzene sulphonate (TNBS) in order to label the aminogroups of proteins exposed on the outer surface of the plasma membrane. Surface proteins of chick myotubes and 'mature' unfused myoblasts (myoblasts grown for 7 days in a calcium-depleted medium) were found to bind an equal amount of probe, which is twice the amount bound by surface proteins in 'immature' myoblasts (1--2 days of culture) and fibroblasts. This indicates that a 'remodelling' of the plasma membrane outer surface takes place in the course of muscle cell differentiation even in the absence of cell fusion. Moreover, the total amount of TNBS bound to the surface was 4--5 times greater in myotubes than in unfused myoblasts. This appears to result from the surface expansion which occurs in myotubes during the development of the T tubule system.

Animals↗
PubMed1986

General detection of proteins after electroblotting by trinitrobenzene sulphonic acid derivatization and immunochemical staining with a monoclonal antibody against the trinitrophenyl group.

A sensitive method for the general detection of proteins electroblotted onto nitrocellulose sheets after separation by sodium dodecyl sulfate-polyacrylamide gel electrophoresis is described. The proteins on the blots were reacted with 2,4,6-trinitrobenzene sulphonic acid. The resulting trinitrophenyl groups on the proteins were rendered visible by immunochemical staining with a monoclonal anti-trinitrophenyl antibody, and a peroxidase-conjugated second antibody. Using various proteins, the method was compared to the amidoblack method for staining of protein blots. The method was 10-100-fold more sensitive than the amidoblack method. Amounts as low as 1 ng of human serum albumin could be detected.

Antibodies, Monoclonal↗
PubMed1982

Kupffer cells recognize trinitrobenzene-labeled erythrocytes.

Chemical-modified erythrocytes (trinitrobenzene-modified erythrocytes (TNB-RBC)) are trapped in vivo rapidly by liver macrophages (Kupffer cells). The liver homing of TNB-RBC is dependent on the concentration of TNB-residues coupled to the surface of RBC. High concentrations induce liver homing, low concentrations spleen homing.

Animals↗
PubMed1999

Is administration of n-3 fatty acids by mucosal enema protective against trinitrobenzene-induced colitis in rats?

We investigated the protective role of fish oil (FO-source of n-3 FA) enriched diet (in the first protocol) in 20 rats and FO administration intrarectally (in the second protocol) in 40 rats with trinitrobenzene (TNB) colitis. All colonic specimens were pathologically evaluated, myeloperoxidase enzyme activities were measured, leukotriene B4 (LTB4) and LTC4 levels were determined by radioimmunoassay. In the first protocol 10 rats (group A1) were fed with 8% sunflower and cotton oil enriched diet and (group A2) with 8% FO enriched diet for 6 weeks. At the end of this period, TNB (30 mg in 0.25 ml of 30% ethanol) were intrarectally administered. After 2 weeks, rats were sacrificed. MPO activities (2.47 versus 30.17), LTB4 (34.5 versus 903.3) and LTC4 (77.7 versus 456.0) levels were significantly reduced in group A2 compared with group A1 (P<0.005). There was also a significant difference in pathologic scores (1.55 versus 2.12, P<0.002) between two groups. In the first part of the second protocol, 20 male rats were randomized into two equal groups (B1 and B2) and TNB colitis was induced. After 1 day, 1 ml of saline (group B1) or n-3 FA enemas (group B2) were administered every day for 2 weeks. At the end of this period, rats were sacrificed and evaluated as done for previous groups. Although there was no significant difference between the two groups in comparison with MPO enzyme activities and pathologic scores, the LTB4 (130.1 versus 971.0) and LTC4 (126.0 versus 532.0) levels of FO group were significantly reduced (P<0.005). In the second part of the second protocol, 20 male rats were randomized into two groups. One millilitre of saline (group B3) or FO enemas (group B4) were administered to rats every day for 3 days. At the fourth day, TNB-colitis was induced and after 24 h rats were sacrificed. We could not find any significant difference in MPO activities, pathologic scores, LTB4 and LTC4 levels between groups B3 and B4. In conclusion, FO enriched diet decreased both pathologic damage and tissue LT levels. The second protocol of our study revealed that the long-term FO enemas decreased the LTB4 and LTC4 levels; however, did not have any beneficial effect on the tissue lesions. Short periods of FO enemas did not have a protective role in the occurrence of experimental colitis. The present study showed that FO enemas significantly decreased LT levels. The protective effect of FO (oral and enema) in TNB colitis may open a new insight into the treatment of inflammatory bowel disease.

Animals↗
PubMed1997

Assessment of environmental hazards of 1,3,5-trinitrobenzene.

The remedial investigation/feasibility studies conducted at certain Army installations showed a need to clean up contaminated sites, where high levels of ammunition chemicals such as 2,4,6-trinitrotoluene (TNT), 1,3,5-trinitrobenzene (TNB), 1,3-dinitrobenzene (DNB), and their degradation products/metabolites were detected in surface soil and groundwater. TNB is a photodegradation product of TNT; it is not easily degraded, and persists in the environment. The toxicity data on TNB are scanty. Hence the U.S. Environmental Protection Agency in 1988 (U.S. EPA, 1997) developed a reference dose (RfD) for TNB (0.00005 mg/kg/d for chronic toxicity) based on the toxicity of DNB, which is structurally similar to TNB. Since then we have completed acute, subacute, subchronic, chronic, reproductive, and developmental toxicity studies and toxicokinetics studies. We have reviewed the mammalian toxicity data for TNB and have determined the no observed adverse effect levels (NOAEL) and low observed adverse effect levels (LOAEL) for subchronic, chronic, reproductive, and developmental toxicity. Based on the newly determined NOAEL and LOAEL values, we have now developed a new RfD for TNB (0.03 mg/kg/d), based on the chronic toxic effects on hematology and histopathological changes in testes and kidney.

Administration, Oral↗
PubMedDate not supplied

Chronic toxicity of 1,3,5-trinitrobenzene in Fischer 344 rats.

The chronic toxicity of 1,3,5-trinitrobenzene (TNB) in male and female Fischer 344 (F344) rats was evaluated by feeding a diet containing 0, 5, 60, and 300 ppm of TNB for 2 years. The calculated average TNB intake over 2 years for males and females was 0.22, 2.64, 13.44 and 0.23, 2.68, 13.31 mg/kg body weight (BW)/day respectively. Terminal body weights were decreased and water intake was increased in both sexes (300 ppm), whereas food consumption was decreased in males (60 and 300 ppm groups) only. The relative spleen weights were significantly decreased in both sexes (300 ppm), whereas the relative brain weights were increased in females only (300 ppm). Hematological effects were not observed in animals killed at the 2-year time point, except significant decrease in the mean corpuscular hemoglobin (MCH) in males (300 ppm) and in females (60 and 300 ppm). Methemoglobin levels were increased in both sexes in the high dose group. Histopathological examination showed treatment-related changes in the kidney (hyaline droplets; 60 and 300 ppm) and the spleen (erythroid cell hyperplasia and pigment deposition; 300 ppm) of both sexes. Cytoplasmic hyaline droplets in the kidneys were characterized by immunohistochemistry as alpha-2mu-globulin. We propose a chronic, oral no-observable-adverse-effect level (NOAEL) of 2.68 mg/kg BW/day for TNB in the rat, based on the hematological and renal changes.

Administration, Oral↗
PubMedDate not supplied

Effects of 1,3,5-Trinitrobenzene on cytotoxicity and metabolic activity of type I astrocytes of rats.

1,3,5-Trinitrobenzene (TNB) is a munitions chemical that causes gliovascular lesions in the brain stem of rats similar to those produced by thiamine deficiency and nitroaromatic compounds, including m-dinitrobenzene. To identify neuropathic indices of toxicity, the effects of varying concentrations (0 to 2 mM) of TNB on cytotoxicity and cellular metabolic activity were examined using cultured astrocytes from Fischer-344 rats. The cytotoxicity was assessed by lactate dehydrogenase (LDH) leakage into the culture medium. Astrocyte metabolic activity was assessed by measuring the conversion of a tetrazolium salt to a formazan product. Additionally, the effects of oxidative stress on cellular metabolic activity were determined by varying oxygen tension via alteration of culture media depth. In vitro, the toxic concentration 50% (TC50) of TNB, which induced cell death, was 16 microM following a 24-h exposure. The concentration of TNB that reduced cellular metabolic activity by 50% was 29 microM following a 24-h exposure. Varying the depth of the culture media did not influence the cellular metabolic activity in control or TNB-treated astrocytes. These results support the hypothesis that TNB induced neurotoxicity could partially be mediated via injury to astrocytes, a major component of the blood-brain barrier.

Animals↗
PubMed1995

Hematological effects of 1,3,5-trinitrobenzene (TNB) in rats in vivo and in vitro.

We studied the hematological effects of single and repeated exposure to 1,3,5-trinitrobenzene (TNB) in rats. Male F-344 rats were gavaged with TNB at 35.5 and 71 mg/kg in corn oil. Blood was collected 5 h and 24 h after a single oral dose or 24 h after daily oral doses for 4 or 10 d in four different set of experiments. A dose-dependent methemoglobinemia was present only in blood collected 5 h after a single dose. A highly significant dose-dependent anemia with reduced red cells, hemoglobin, and hemotocrit was present in rats receiving TNB for 4 or 10 d. A dose-dependent decrease in serum triglycerides was present in rats receiving TNB for 10 d. There was no hemolysis when rat erythrocytes were incubated with TNB (in vitro) for 9 h. Spectral changes of hemoglobin recorded during the incubation with TNB confirm methemoglobin formation and progressive denaturation of hemoglobin-forming hemichromes. The significance of methemoglobin and hemichrome formation is discussed, and a probable hypothesis for the hemolytic anemia is suggested.

Anemia, Hemolytic↗