Disease relevance of DINITROPHENYLENE

• METHODS: Balb/C mice were sensitized and challenged with a suboptimal dose of 2.4 dinitrobenzene sulfonic acid to generate a colonic delayed-type hypersensitivity response [1].
• To determine whether deletion of NEP predisposes mice to uncontrolled inflammation, we compared dinitrobenzene sulfonic acid-induced colitis in wild-type and knockout mice [2].
• Adoptive transfer of 2,4-dinitrobenzene sulfonic acid (DNBS)-pulsed DCs directly implicated the defect in DC migration to lymph node with the defect in contact hypersensitivity [3].
• METHODS: Gene transfer was achieved by intraperitoneal injection of non-replicating human type 5 adenovirus bearing the IL-10 gene, either 24 hours before or one hour after intrarectal administration of dinitrobenzene sulphonic acid in rats [4].
• We have previously shown that Corynebacterium parvum treatment reduced tolerance induced by intravenous injection of 2,4-dinitrobenzene sulfonic acid (DNBSO3) or by sensitizing BALB/c mice with a supraoptimal dose of 2,4-dinitrofluorobenzene (DNFB) [5].

High impact information on DINITROPHENYLENE

• Since little information exists, we induced colitis in male Sprague-Dawley rats with dinitrobenzene sulfonic acid and used immunocytochemistry to examine the number and distribution of enteric neurons at times up to 35 days later [6].
• A population of CD8+ T cells from dinitrobenzene sulfonate-primed mice produce soluble effector molecules that down-regulate the magnitude of dinitrophenol-specific contact hypersensitivity reactions [7].
• Antigen-specific T effector cells of delayed-type hypersensitivity (TDH) and Ts cells were induced in vitro by co-culture of spleen lymphocytes with bone marrow-derived antigen-presenting macrophages (BM-MA) pulse-labeled with 2,4-dinitrobenzene sulfonate (DNBSO3) [8].
• E was inactivated with several other reagents that lead to oxidatively inactivated rhodanese including NADH, dithiothreitol, mercaptoethanol, and m-dinitrobenzene [9].
• The fluorescent ADP analog, 1,N6-ethenoadenosine diphosphate (epsilon ADP), has been trapped at the active site of myosin subfragment 1 (SF1) by the chromophoric cross - linkers, 1,5 - difluoro - 2,4' - dinitrobenzene (F2DNB) and 4,4'-difluoro-3,3'-dinitrophenylsulfone (F2DPS) [10].

Chemical compound and disease context of DINITROPHENYLENE

• Both compounds at doses as low as 1 mg/kg administered as a per os (p.o.) twice a day (b.i.d.) regimen abrogated the expression of dinitrobenzene sulfonic acid-induced, Lyt-2+, T suppressor cells and stimulated contact sensitivity to dinitrofluorobenzene in adoptive transfer experiments [11].
• Ts cells from mice tolerized with dinitrobenzene sulfonate produce a DNP-specific, MHC-restricted soluble suppressor factor (SSF) which regulates contact sensitivity to 2,4-dinitro-fluorobenzene [12].
• Contact sensitivity to dinitrochlorobenzene (DNCB) in guinea pigs could be rapidly suppressed by intravenous injection of dinitrobenzene sulfonic acid sodium salt (DNBSO3) [13].
• Melatonin reduces dinitrobenzene sulfonic acid-induced colitis [14].
• Curcumin attenuates DNB-induced murine colitis [15].

Biological context of DINITROPHENYLENE

• Early metabolic changes during m-Dinitrobenzene neurotoxicity and the possible role of oxidative stress [16].
• Protein activity for a subset of GSTs varied widely with seven substrates, and any GST exhibiting greater than marginal activity with chloro-2,4 dinitrobenzene activity also exhibited significant activity with all other substrates, suggesting broad individual enzyme substrate specificity [17].
• Theophylline (THP) and 1,3-dinitrobenzene (DNB) are thought to induce infertility by incapacitating the nurturing Sertoli cells and causing germ cell apoptosis in the testicular seminiferous epithelium, respectively [18].
• 1,3-Dinitrobenzene metabolism and protein binding [19].
• 1,3-Dinitrobenzene (1,3-DNB), which is known to undergo reductive biotransformation in an intact, oxygenated isolated perfused intestinal preparation, was used as a model substrate for reductive enzymes of the small intestine of the rat [20].

Anatomical context of DINITROPHENYLENE

• AmB also interfered with tolerance induction by i.v. dinitrobenzene sulfonic acid, suggesting that its adjuvant effects involve inhibition of suppressor cells or their precursors [21].
• Critical role for mast cells in the pathogenesis of 2,4-dinitrobenzene-induced murine colonic hypersensitivity reaction [22].
• A novel enzyme catalyzing cleavage of the thioether linkage in cysteine conjugates of aromatic compounds, such as 2,4-dinitrobenzene and p-bromobenzene, has been purified about 500-fold from rat liver cytosol [23].
• Specifically, a distinct difference is noted between cells of different types (astrocyte vs neuron-derived cells) with respect to their response to the toxicant m-dinitrobenzene (DNB) [24].
• 1,3-Dinitrobenzene is a testicular toxicant, which produces a lesion in the seminiferous tubules of the rat [19].

Associations of DINITROPHENYLENE with other chemical compounds

• Mice (Balb/c) were skin-sensitized with dinitrofluorobenzene (DNFB; 0.5%, 100 microliters) on two consecutive days and challenged intranasally 5 days later with dinitrobenzene sulphonic acid (0.6%, 50 microliters) [25].
• Previous work demonstrated that the mitochondrial fraction of rat seminiferous tubules is capable of metabolizing 1,3-dinitrobenzene, using NADPH as a cofactor [26].
• The specificity of the ELISA for 1,3-dinitrobenzene was further demonstrated with a variety of other nitroaromatic compounds, of which only 2,4-dinitrotoluene showed significant cross reactivity [27].
• The molecular weight of the dinitrobenzene derivative measured by LC mass spectrometry (MS) led to the detection of two isomeric impurities in tobramycin by LC-MS using an amino column [28].
• Under aerobic conditions, reduction was the major metabolic pathway for m- and p- DNB in hepatocytes with m- and p-nitroaniline accounting for 74.0 +/- 1.2 and 81.0 +/- 0.6% (mean +/- SE, n = 4), respectively, of the radioactivity present after a 30-min incubation [29].

Gene context of DINITROPHENYLENE

• GW274150 also caused a substantial reduction of (i) the degree of colon injury, (ii) the rise in myeloperoxidase (MPO) activity (mucosa), (iii) the increase in staining (immunohistochemistry) for nitrotyrosine, as well as (iv) PARP activation caused by dinitrobenzene sulfonic acid in the colon [30].
• Here, we investigate the effects of the selective iNOS-inhibitor (S)-2-amino-(1-iminoethylamino)-5-thiopentanoic acid (GW274150) on the development of experimental colitis induced by dinitrobenzene sulfonic acid [30].
• The present study investigates the role of regional differences in activation of the mitochondrial permeability transition pore (mtPTP) by DNB in brainstem and cortical astrocytes and examines the expression of Bcl-2 proteins as potential regulators of mtPTP function [31].
• Increased myeloperoxidase activity was also observed in dinitrobenzene sulfonic acid-treated Sprague-Dawley rats and Flinder's Resistant Line rats [32].
• Superoxide dismutase, glutathione peroxidase and glutathione-S-transferase (1-chloro 2, 4 dinitrobenzene) activities were also decreased in the rotavirus infected group [33].

Analytical, diagnostic and therapeutic context of DINITROPHENYLENE

• On the basis of the sequence analysis of the purified chromophoric peptides, Cys16 and Cys55 are cross-linked by both FNPS and DFNB [34].
• Application of ELISA techniques to metabolic disposition studies for 1,3-dinitrobenzene: comparison with HPLC and radiochemical methods [27].
• Determination of 1,3-dinitrobenzene and its metabolites in rat blood by capillary gas chromatography with electron-capture detection [35].
• The present study investigated the occurrence of apoptosis in rat testis 6, 12, 24, or 48 h after administration of 1,3-dinitrobenzene (DNB)(25 mg/kg, i.p.). Apoptotic cells were visualized using TUNEL in situ detection [36].
• Immunotherapy of NMSC has been attempted in the form of dinitrobenzene sensitization followed by topical application on the tumor, intralesional interferon injections, or perilesional interleukin-2 [37].

References