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At least 19 recordsLinked to original sources
PubMed1985

Frameshift mutagenicity of dinitrobenzene derivatives on Salmonella typhimurium TA98 and Tm elevation of calf thymus DNA by dinitrobenzene derivatives.

1-Chloro-2,4-dinitrobenzene and m-dinitrobenzene were mutagenic on Salmonella typhimurium TA98 without S-9mix. But 1-substituted-2,4-dinitrobenzene derivatives which substituted by electron releasing groups such as OH-, NH2- or CH3- did not show mutagenicity on Salmonella typhimurium TA98 without S-9mix. Tm of calf thymus DNA was elevated by addition of m-dinitrobenzene or 1-chloro-2,4-dinitrobenzene, and falled by addition of 1-substituted-2,4-dinitrobenzenes which substituted by electron releasing substituents such as OH-, NH2- or CH3- groups. The mutagenic dinitrobenzene derivatives such as 1-chloro-2,4-dinitrobenzene showed the special changes in the difference spectra about four bases of the DNA and this compound.

Animals↗
PubMed1980

Induction of tolerance to 1-fluoro-2,4-dinitrobenzene contact sensitivity with hapten-modified lymphoid cells. II. Selective tolerance in F1 mice of T cell subsets recognizing 1-fluoro-2,4-dinitrobenzene associated with parental major histocompatibility complex antigens.

F1 animals were tolerized to 1-fluoro-2,4-dinitrobenzene (DNFB) contact sensitivity with parentally derived, in vitro hapten-modified spleen cells. This tolerant state was found, upon adoptive transfer to naive parental strain recipients, to affect only that T cell subpopulation that recognized the parental haplotype of the cell used as the tolerogen, and did not inhibit the ability of the remaining T cell subset to confer immunity. This demonstrates that this tolerant state involves the inactivation of a cell required for the expression of contact sensitivity by recognizing DNFB in association with self major histocompatibility complex gene products.

Animals↗
PubMed1990

Modulation of m-dinitrobenzene and m-nitrosonitrobenzene toxicity in rat Sertoli--germ cell cocultures.

Previous work has shown that m-dinitrobenzene is a testicular toxicant in rats in vivo, and in vitro produces comparable morphological changes in rat testicular Sertoli-germ cell cocultures. m-Dinitrobenzene is metabolized both in vivo and in the in vitro system to m-nitroaniline m-nitroaniline and m-nitroacetanilide. These metabolites do not provoke testicular toxicity in vivo or in vitro. We have therefore proposed a pathway for the metabolism of m-dinitrobenzene to m-nitroaniline and m-nitroacetanilide, which involved the intermediate m-nitrosonitrobenzene (1-nitroso-3-nitrobenzene, NNB). When tested, m-nitrosonitrobenzene, at equimolar doses to m-dinitrobenzene, produced similar morphological changes in the culture system to those exhibited by m-dinitrobenzene. However, m-nitrosonitrobenzene produced a greater toxicity than did m-dinitrobenzene (as measured by germ cell detachment). When the intracellular thiol levels were reduced in the cocultures pretreated with diethyl maleate, the toxicity of both m-dinitrobenzene and m-nitrosonitrobenzene was enhanced. In contrast, pretreatment of cocultures with agents known to increase cellular thiol (cysteamine) or scavenge reactive intermediates (cysteamine or ascorbate) reduced the toxicity of m-dinitrobenzene and m-nitrosonitrobenzene. We propose that m-dinitrobenzene requires metabolic activation before it can exert its toxicity to Sertoli cells, and it appears that the toxic species is m-nitrosonitrobenzene or a further metabolite of m-nitrosonitrobenzene.

Animals↗
PubMed1989

Relationship between 1-chloro-2,4-dinitrobenzene-induced cytoskeletal perturbations and cellular glutathione.

Exposure of 3T3 cells to micromolar doses of 1-chloro-2,4-dinitrobenzene, a substrate for glutathione-S-transferase, resulted in a rapid depletion of total cellular glutathione accompanied by disassembly of microtubules as visualized by fluorescence microscopy. However, prolonged incubation resulted in cellular recovery from 1-chloro-2,4-dinitrobenzene insult as evidenced by a steady rise in total cellular glutathione accompanied by microtubule reassembly to their normal organization 5 hours after treatment. To evaluate the role of total cellular glutathione in modulating the 1-chloro-2,4-dinitrobenzene-induced cytoskeletal perturbation, we used 1-chloro-2,4-dinitrobenzene and/or buthionine sulfoximine, an effective irreversible inhibitor of glutathione synthesis, to manipulate cellular glutathione levels. Incubation of 3T3 cells with 2.5 microM 1-chloro-2,4-dinitrobenzene and 250 microM buthionine sulfoximine for 5 hours resulted in a complete depletion of total cellular glutathione accompanied by essentially complete loss of microtubules and marked alterations in the density and distribution pattern of microfilaments. Buthionine sulfoximine enhanced markedly the extent and duration of cellular glutathione depletion and the severity of microtubule disruption of 3T3 cells over the level achieved by 1-chloro-2,4-dinitrobenzene treatment alone. Furthermore, buthionine sulfoximine also prevented the restoration of cellular glutathione content and microtubule reassembly that normally were evident 5 hours after 1-chloro-2,4-dinitrobenzene treatment. Exposure of 3T3 cells to 50 microM 2-cyclohexene-1-one, which depletes free glutathione by conjugation, resulted in a complete depletion of total cellular glutathione content without altering the microtubule organization. These results suggest that the total glutathione content may be important for cellular recovery from 1-chloro-2,4-dinitrobenzene-mediated cytoskeletal injuries, and that microtubule disassembly observed in 1-chloro-2,4-dinitrobenzene-treated cells probably results from depletion of cellular glutathione coupled with binding to tubulin and/or other microtubule components.

Animals↗
PubMed1980

Transfer and trapping of excitation energy in photosystem II as studied by chlorophyll alpha 2 fluorescence quenching by dinitrobenzene and carotenoid triplet. The matrix model.

1. The curves representing the reciprocal fluorescence yield of chlorophyll alpha of Photosystem II (PS II) in Chlorella vulgaris as a function of the concentration of m-dinitrobenzene in the states P Q and P Q-, are found to be straight parallel lines; P is the primary donor and Q the primary acceptor of PS II. In the weakly trapping state P Q- the half-quenching of dinitrobenzene is about 0.2 mM, in vitro it is of the order of 10 mM. The fluorescence yield as a function of the concentration of a quencher is described for three models for the energy transfer between the units, and the matrix model. If it is assumed that the rate constant of quenching by dinitrobenzene is high and thus the number of dinitrobenzene molecules per reaction center low, it can be concluded that the pigment system of PS II in C. vulgaris is a matrix of chlorophyll molecules in which the reaction centers are embedded. Theoretical and experimental evidence is consistent with such an assumption. For Cyanidium caldarium the zero fluorescence yield phi 0 and its quenching by dinitrobenzene were found to be much smaller than the corresponding quantities for C. vulgaris. Nevertheless, our measurements on C. caldarium could be interpreted by the assumption that the essential properties (rate constants, dinitrobenzene quenching) of PS II are the same for these two species belonging to such widely different groups. 2. The measured dinitrobenzene concentrations required for half-quenching in vivo and other observations are explained by (non-rate-limiting) energy transfer between the chlorophyll alpha molecules of PS II and by the assumptions that dinitrobenzene is approximately distributed at random in the membrane and does not diffuse during excitation. 3. The fluorescence kinetics of C. vulgaris during a 350 ns laser flash of variable intensity could be simulated on a computer using the matrix model. From the observed fluorescence quenching by the carotenoid triplet (CT) and the measurement of the the number of CT per reaction center via difference absorption spectroscopy, the rate constant for quenching of CT is calculated to be kT = 3.3 . 10(11)s-1 which is almost equal to the rate constant of trapping by an open reaction center (Duysens, L.N.M. (1979) CIBA Foundation Symposium 61 (New Series), pp. 323--340). 4. The fluorescence quenching by CT in non-treated spinach chloroplasts after a 500 ns laser flash (Breton, J., Geacintov, N.E. and Swenberg, C.E. (1979) Biochim, Biophys. Acta 548, 616--635) could be explained within the framework of the matrix model when the value for kT is used as given in point 3. 5. The observations mentioned under point 1 indicate that the fluorescence yield phi 0 for centers in trapping state P Q is probably for a fraction exceeding 0.8 emitted by PS II.

Carotenoids↗
PubMed1987

Mutagenicity of halogenated and other substituted dinitrobenzenes in Salmonella typhimurium TA100 and derivatives deficient in glutathione (TA100/GSH-) and nitroreductase (TA100NR).

In a previous study, it was shown that 1-chloro-2,4-dinitrobenzene (CDNB) was less mutagenic in a glutathione (GSH)-deficient derivative of Salmonella typhimurium TA100 (TA100/GSH-) than in TA100 itself, suggesting that the mutagenicity of the compound is dependent on GSH, possibly mediated by the action of a bacterial nitroreductase(s) on the CDNB-GSH conjugate. In the present study a series of mutagenicity tests were performed to determine how CDNB could be activated after reaction with GSH. In liquid preincubation assays, strains TA100, TA100/GSH- and TA100NR, a nitroreductase-deficient derivative of TA100, were treated with CDNB and its fluoro and bromo analogues (FDNB and BDNB), further with its GSH conjugate (S-GSH-DNB) and possible metabolic products, such as S-cysteine-dinitrobenzene (S-Cys-DNB) and S-methyl-dinitrobenzene (S-methyl-DNB), and with 2 more analogues, O-methyl-dinitrobenzene (O-methyl-DNB) and dinitrobenzene (DNB). CDNB, FDNB and BDNB were found to be mutagenic in TA100 and TA100NR, while TA100/GSH- was much less sensitive to the mutagenic action of these halogenated dinitrobenzenes. DNB, O-methyl-DNB, S-methyl-DNB and S-Cys-DNB induced equal numbers of His+ revertants in TA100 and TA100/GSH-, but were not mutagenic in TA100NR. S-GSH-DNB showed no mutagenic activity in any of the 3 strains under the present experimental conditions. These results suggest that the halogenated aromatics may react with bacterial DNA and produce pre-mutagenic alterations according to 2 mechanisms: direct attack on the DNA through nucleophilic substitution (SN2) of the halogen atoms; activation through GSH conjugation and subsequent nitroreduction of the conjugate or its metabolic products to more reactive intermediates.

Bacterial Proteins↗
PubMedDate not supplied

Application of ELISA techniques to metabolic disposition studies for 1,3-dinitrobenzene: comparison with HPLC and radiochemical methods.

An enzyme-linked immunosorbent assay (ELISA) is reported for the detection and quantitation of 1,3-dinitrobenzene, a widely used chemical intermediate in industrial syntheses and potent testicular toxicant in rats. Radiolabeled [14C]-1,3-dinitrobenzene (25 mg/kg, ip) was administered to rats, and the blood disappearance curve generated with the ELISA assay was compared with HPLC separation and quantitation by using both UV and radiochemical methods. An excellent correlation was found between the two methods. Matrix effects from the blood samples were minimal. Cross reactivity with metabolites of 1,3-dinitrobenzene occurred only at levels that were 3 orders of magnitude greater than for the parent compound. 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. The sensitivity and specificity of the 1,3-dinitrobenzene ELISA demonstrate the usefulness of an approach which, if verified with conventional analytical methods, allows rapid and inexpensive measurement of xenobiotic levels in biological samples.

Animals↗
PubMed1991

Catabolism of 1,3-dinitrobenzene by Rhodococcus sp. QT-1.

The 1,3-dinitrobenzene-degrading Rhodococcus strain QT-1 was isolated under nitrogen limiting conditions from contaminated soil samples. Experimental data indicate tha 1,3-dinitrobenzene is metabolized via 4-nitrocatechol. Both compounds were oxidized by resting cells and nitro groups were completely eliminated as nitrite. Strain QT-1 utilizes both 1,3-dinitrobenzene and 4-nitrocatechol as source of nitrogen in the absence as well as in the presence of high amounts of ammonia. Growth on 4-nitrocatechol does not induce the enzyme(s) for the initial oxidation of 1,3-dinitrobenzene.

Biodegradation, Environmental↗
PubMed1985

Relationship between red blood cell uptake and methemoglobin production by nitrobenzene and dinitrobenzene in vitro.

Nitrobenzene increases methemoglobin formation when incubated with native hemoglobin but not when incubated with red blood cell suspensions. These experiments were designed to determine if transport of nitrobenzene across the red blood cell membrane is a limiting factor for methemoglobin production by red blood cell suspensions. Incubation of [14C]-m-, o- or p-dinitrobenzene, but not mononitrobenzene, with red blood cell suspensions caused a time-dependent increase in methemoglobin. All three dinitrobenzenes and mononitrobenzene crossed the red blood cell membrane and accumulated in the erythrocytes after only 1 min of incubation. Incubation of mononitrobenzene with hemolysates did not result in methemoglobin production. Incubation of red blood cells with the dinitrobenzenes or mononitrobenzene for 1 and 10 min at 4 degrees C did not influence red blood cell uptake of the nitrobenzenes, suggesting that these compounds do not enter the red blood cell by an active process. Dinitrobenzene-induced methemoglobin production was markedly inhibited at 4 degrees C, and may be a result of decreased interaction with hemoglobin and/or decreased metabolism to reactive intermediates which mediate methemoglobin production. These data indicate that red blood cell transport of nitrobenzene is not the limiting factor in methemoglobin production in vitro.

Animals↗
PubMed1988

A comparison of the effects of the three isomers of dinitrobenzene on the testis in the rat.

Sexually mature Alpk/AP (Wistar derived) rats were killed 5 days after a single oral dose of 50 mg/kg of the 1,2-, 1,3-, or 1,4-isomers of dinitrobenzene. Testis weight reductions accompanied by testicular lesions were observed in the animals dosed with 1,3-dinitrobenzene (1,3-DNB) while the 1,2- and 1,4-isomers were without effect on the testis. However, 1,4-dinitrobenzene, but not 1,2-dinitrobenzene, was of a potency similar to that of 1,3-DNB in producing cyanosis and splenic enlargement in these animals, indicating that different mechanisms are probably responsible for these two toxic effects. In a subsequent study the pathogenesis of the testicular damage resulting from a single oral dose of 5, 10, 15, or 25 mg 1,3-DNB/kg was studied in sexually mature rats. Animals were killed 6, 12, 24, 48, and 96 hr after dosing and a detailed histopathological examination of the testes and selected tissues was made. At 12 hr after a single oral dose of 25 mg/kg, 1,3-DNB produced testicular lesions limited to Stages VIII to XI of the spermatogenic cycle. By 24 hr widespread Sertoli cell damage was evident and in some tubules was associated with degeneration of primary spermatocytes. Ultrastructural examination at this time confirmed that there were effects on Sertoli cells in the absence of germ cell damage. Similar effects were seen 48 hr after a single oral dose of 15 mg 1,3-DNB/kg. Doses of 5 or 10 mg 1,3-DNB/kg were without effect on the testis. The Sertoli cell is implicated as the prime target for the toxic action of 1,3-DNB with germ cell damage a secondary event.

Administration, Oral↗
PubMed1978

Urinary catecholamine excretion and blood sugar response during acute poisonings with dinitrobenzenes.

Rats were injected intraperitoneally with 0.015 mmol of p-dinitrobenzene/kg, 0.15 mmol of m-dinitrobenzene/kg and 0.45 mmol of o-dinitrobenzene/kg body wt. The dinitrobenzenes induced methaemoglobin concentrations of 86%, 60% and 49%, respectively, as well as increases of urinary catecholamine excretion and blood sugar concentration. Due to hyperglycaemia the glycolysis may be stimulated as mechanism for energy production in methaemoglobin-induced oxygen deficiency and as mechanism for reduction of methaemoglobin, that means as responses favouring survival after poisoning.

Animals↗
PubMed1981

An enzymatic assay of reduced glutathione using glutathione S-aryltransferase with o-dinitrobenzene as a substrate.

A simple and sensitive enzymatic assay method for the determination of reduced glutathione (GSH) has been developed using glutathione S-aryltransferase with o-dinitrobenzene as a substrate. o-Dinitrobenzene is a good substrate for the enzyme and has low spontaneous reactivity with GSH at neutral pH. GSH can be determined by colorimetrically measuring nitrite released upon the enzymatic conjugation of GSH and o-dinitrobenzene by using a diazo-coupling method with N-(1-naphthyl)ethylenediamine dihydrochloride. This method is capable of quantitating 1 to 40 nmol of GSH, and can be applied to physiological samples containing deproteinizing reagents.

Animals↗
PubMed1992

Functional/metabolic modulation of the brain stem lesions caused by 1,3-dinitrobenzene in the rat.

To determine whether neuronal activity plays a role in the localisation of brain stem lesions in 1,3-dinitrobenzene intoxication we produced asymmetrical changes in auditory input by rupturing the left tympanic membrane in Fischer rats. This raised the auditory threshold on that side from 57-63 dB to 104-122 dB. It also decreased glucose utilisation in the ipsilateral cochlear nucleus and significantly increased utilisation in the contralateral nucleus, resulting in a relative deficit of 72 +/- 6%. Similarly, tympanic membrane rupture led to decreased glucose utilisation in the contralateral and increased utilisation in the ipsilateral inferior colliculus. Additional exposure to "white noise" prevented the decrease in glucose utilisation in the contralateral inferior colliculus. Dosing with dinitrobenzene (10 mg/kg in 4 doses over 48 hr) to otherwise normal rats produces symmetrical vasculonecrotic lesions in these regions, but in animals with left tympanic membrane rupture the severity of morphological changes in the ipsilateral cochlear nucleus and the contralateral inferior colliculus were substantially reduced. Additional exposure to "white noise" increased the degree of damage in the ipsilateral cochlear nucleus and contralateral inferior colliculus. These findings indicate that altered auditory function in rats, with its associated metabolic consequences exercises a significant role in the development of brain stem damage in auditory pathways following dinitrobenzene intoxication.

Acoustic Stimulation↗
PubMed1978

Two-step modification of aspartate aminotransferase with 1,5-difluoro-2,4-dinitrobenzene. Cross-link localization.

At pH 7, the apoenzyme of carboxymethylated and acylated aspartate aminotransferase reacts selectively with 1,5-difluoro-2,4-dinitrobenzene to form a single intramolecular covalent bond with the epsilon-amino group of the functional lysine residue located within the active centre. On shifting the pH to 9, the second fluorine atom of the bifunctional reagent is substituted with the sterically adjacent side groups of cysteine and tyrosine residues. The modified apoenzyme was subjected to partial proteolysis with pronase, and the digest was used to obtain and isolate the labeled products and to localize amino acid residues involved in the reaction. The established structures of several peptides containing Cys-2,4-dinitrobenzene-Lys and Tyr-2,4-dinitrobenzene-Lys allowed the identification of the amino acid residues involved in the reaction with the bifunctional reagent as Lys 258, Cys 390 and probably Tyr-70. The residues of Cys and Tyr are thus located at a distance of approximately 5 A (the length of the dinitrophenylene bridge) from the lysine residue forming an aldimine bond with pyridoxal 5'-phosphate in the active site.

Animals↗
PubMed1985

The inhibition of mitochondrial F1-ATPase by 1,5-difluoro-2,4-dinitrobenzene.

1,5-Difluoro-2,4-dinitrobenzene completely inhibits F1-ATPase when it is used at micromolar concentrations and the inhibitor/enzyme molar ratio is equal to 3. The inhibition can be reversed by dithiothreitol treatment. 7-Chloro-4-nitrobenzofurazan treatment of F1-ATPase does not prevent the reaction of the enzyme with 1,5-difluoro-2,4-dinitrobenzene. The 1,5-difluoro-2,4-dinitrobenzene-induced inhibition is thought to be a result of the modification of a tyrosine residue with pK 9.1.

4-Chloro-7-nitrobenzofurazan↗
PubMed1981

Reactivity of sarcoplasmic reticulum from rabbit cardiac muscle with 1-fluoro- and 1,5-difluoro- 2,4-dinitrobenzene.

Sarcoplasmic reticulum preparations from rabbit cardiac and fast skeletal muscle react differentially with low concentrations of 1-fluoro- and 1,5-difluoro-2,4-dinitrobenzene. Dinitrophenylation of cardiac sarcoplasmic reticulum by 1-fluoro-2,4-dinitrobenzene is not affected by Ca2+ and is limited to the lipoprotein-lipid region. This contrasts sharply with the predominant Ca2+-dependent dinitrophenylation of the ATPase protein of rabbit skeletal sarcoplasmic reticulum by this reagent. Formation of non-serial high mol. wt. oligomers by 1,5-difluoro-2,4-dinitrobenzene is significantly greater in cardiac than in skeletal vesicles. Substrate MgATP2- does not protect rabbit cardiac sarcoplasmic reticulum ATPase activity or Ca2+ uptake from dinitrophenylation when monofunctional and bifunctional reagents are used. Chemical differences in the overall structure of the two kinds of membrane preparations can be ascertained from a comparison of the effects of Ca2+ and MgATP2- on the reactivity of these reagents.

Adenosine Triphosphate↗
PubMed1980

Genotoxic activity in microorganisms of tetryl, 1,3-dinitrobenzene and 1,3,5-trinitrobenzene.

N-Methyl-N,2,4,6-tetranitroaniline (tetryl), 1,3-dinitrobenzene, and 1,3,5-trinitrobenzene were subjected to DNA repair assays using the Escherichia coli W3110/polA+, p3478/polA- system, reverse mutation assays with His-Salmonella typhimurium strains TA1535, TA1537, TA1538, TA98, and TA100, and mitotic recombinogenic tests with the yeast Saccharomyces cerevisiae D5. Tests were carried out in the absence of an exogenous activation system and in tissue homogenate-mediated assays using Aroclor 1254-induced, male rat-liver-derived S9 mix. Mutagenic activity of tetryl was demonstrated with S typhimurium strains TA1537, TA1538, TA98, and TA100. The responses were particularly strong in the absence of S9 mix. Tetryl also induced increases in recombinant numbers and frequencies in the S cerevisiae test without the S9 mix, but not in its presence. 1,3-Dinitrobenzene was demonstrated to be mutagen with S typhimurium strains TA1538, TA98, and TA100. Slight activity was also seen with TA1537. The S9 mix reduced the magnitude of the responses. 1,3,5-Trinitrobenzene was also demonstrated to be mutagenic with S typhimurium strains TA1535, TA1537, TA1538, TA98, and TA100. Again, the S9 mix reduced the magnitude of the responses. In this segment of a programme initiated by military authorities, the genotoxic potential of three nitroaromatic compounds, which have found significant use in explosive preparations, has been demonstrated. Twelve other compounds used in ordnance were not active in any of the test systems. These were octahydro-1-acetyl-3,5,7-trinitro-S-tetramine (SEX), hexahydro-1,3-dinitro-5-acetyl-S-triamine (TAX), ethyl centralite, 2-nitrodiphenylamine, N-nitrosodiphenylamine, diphenylamine, diethyleneglycoldinitrate, nitroguanidine, lead salicylate, lead resorcylate, red phosphorus, and zinc chloride.

Aniline Compounds↗