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At least 19 recordsLinked to original sources
PubMed1989

Gas chromatographic studies on the biodegradation of nitrobenzene and 2,4-dinitrophenol in the nitrobenzene plant wastewater.

The biodegradation of nitrobenzene (NB) and 2,4-dinitrophenol (DNP) in NB plant wastewater has been studied using acclimated activated sludge in a batch bioreactor. The gas chromatographic (GC) monitoring shows simultaneous utilization of these two substrates, and both NB and DNP were ultimately biodegraded. The primary and ultimate biodegradation rates using GC and COD methods, respectively, are compared and reported.

Journal Article↗
PubMed1997

Nucleophilic Substitution Reactions of 1-Halogeno-4-COR-2-nitrobenzenes and 1-Halogeno-6-COR-2-nitrobenzenes with Sodium Benzenethiolate and Piperidine. Can an "Inverted Built-In Solvation" Be Responsible for the Peculiar Activation by an o-Carboxamido Group in S(N)Ar Reactions with an Anionic Nucleophile?

A kinetic study of the title reactions has allowed an interpretation of the higher efficiency of an o-carboxamido group with respect to an o-carbomethoxy group in activating the benzenethiolate-dehalogenation reactions in methanol (k(CONH)()2/k(CO)()2(Me) 2.2-3.0) as due to an interaction between the anionic nucleophile and the hydrogen atoms of the carboxamido group. An inversion of the activating power of the two groups (k(CONH)()2/k(CO)()2(Me) 0.14) in the reactions with the same nucleophile has been observed when they are in a para-position. Moreover, for piperidino-dehalogenation reactions in methanol k(CONH)()2/k(CO)()2(Me) ratios less than unity (0.2-0.6) have been observed independently of the position (ortho or para) of the carboxamido and carbomethoxy groups with respect to the reaction center.

Journal Article↗
PubMed2003

Chromosomal genotoxicity of nitrobenzene and benzonitrile.

In order to investigate the chromosomal genotoxicity of nitrobenzene and benzonitrile, we studied the induction of micronuclei (MN) by these test compounds in V79 cells, as well as effects on the formation and stability of microtubules and on motor protein functions. No cytotoxicity was seen in V79 cell cultures in terms of Neutral red uptake after 18 h treatment with up to 1 mM nitrobenzene or 1 mM benzonitrile. Subsequently, a concentration range up to 100 micro M was used in the experiments on induction of MN. Both test compounds exhibit a weak, but definitely positive test result compared to the solvent (DMSO) control. Minimal effect concentrations of nitrobenzene and benzonitrile appeared as low as 0.01 micro M, and no-effect-concentrations were between 0.001 and 0.005 micro M. Clearly enhanced MN rates were found at 0.1 micro M and higher. Both, nitrobenzene and benzonitrile, induced mostly kinetochor (CREST)-positive micronuclei, thus characterising the chromosomal effects as aneugenic. In cell-free assays, a slight effect on tubulin assembly was observed at 1 mM nitrobenzene without addition of DMSO. Higher concentrations (5 mM) led to secondary effects. In presence of 1% DMSO, nitrobenzene exerted no detectable effect on tubulin assembly up to the solubility limit in water of about 15 mM. For benzonitrile in presence of DMSO, a clear dose-response of inhibition of tubulin assembly at 37 degrees C was seen above the no-effect-concentration of 2 mM, with an IC(50) of 13 mM and protein denaturation starting above a level of about 20 mM. The nature of the effects of nitrobenzene and benzonitrile on the association of tubulin to form microtubules was confirmed by electron microscopy. Treatment by either 5 mM nitrobenzene or 13 mM benzonitrile plus 1% DMSO left the microtubular structure intact whereas 5 mM nitrobenzene, in absence of DMSO, led to irregular cluster formations. The experiments demonstrate that both nitrobenzene and benzonitrile, in millimolar concentration ranges, may lead to interference with tubulin assembly in a cell-free system. The functionality of the tubulin-kinesin motor protein system was assessed using the microtubule gliding assay. Nitrobenzene affected the gliding velocity in a concentration-dependent manner, starting at about 7.5 micro M and reaching complete inhibition of motility at 30 micro M, whereas benzonitrile up to 200 micro M did not affect the kinesin-driven gliding velocity. The micronucleus assay data demonstrate a chromosomal endpoint of genotoxicity of nitrobenzene and benzonitrile. Aneugenic effects of both compounds occur at remarkably low concentrations, with lowest-effect-concentrations being 0.1 micro M. This points to the relevance of interactions with the cellular spindle apparatus.

Animals↗
PubMed1984

Macromolecular covalent binding of [14C]nitrobenzene in the erythrocyte and spleen of rats and mice.

Nitrobenzene exposure is known to produce red blood cell damage as well as engorgement and sinusoidal congestion of the spleen in male Fischer-344 (F-344) rats but not in male B6C3F1 mice. These studies were conducted to investigate the species differences in the covalent binding of [14C]nitrobenzene in the erythrocyte and spleen and to assess the contribution of nitrobenzene-induced erythrocytic damage to the splenic effects. Total and covalently bound 14C concentrations in erythrocytes of rats were 6-13 times greater than those of mice following a single oral dose of 75, 150, 200 or 300 mg/kg [14C]nitrobenzene, suggesting that species differences in nitrobenzene-induced red blood cell toxicity may be related to differences in erythrocytic accumulation of nitrobenzene and its metabolites. Covalently bound 14C in erythrocytes of rats peaked 24 h following administration of 200 mg [14C]nitrobenzene/kg; in contrast, bound radiolabel in erythrocytes from mice plateaued at 10 h. Splenic engorgement increased in a time-related manner in treated rats but not in mice. Species specificity was also observed in the accumulation of bound radiolabel in the spleen. Gel filtration and sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) of lysed, dialyzed erythrocytes from treated rats revealed that hemoglobin was the primary, if not the exclusive, site of macromolecular covalent binding following nitrobenzene treatment. SDS-PAGE of dialyzed rat spleens revealed that 82% of total bound 14C migrated identically to hemoglobin. These data indicate that covalent binding of [14C]nitrobenzene and its metabolites in the spleen is primarily derived from bound 14C from scavenged erythrocytes. Therefore, the species differences in splenic engorgement and accumulation of [14C]nitrobenzene may be related to differences in susceptibility to nitrobenzene-induced red blood cell damage.

Animals↗
PubMed1984

Influence of dietary pectin on intestinal microfloral metabolism and toxicity of nitrobenzene.

Intestinal microfloral metabolism of nitrobenzene is essential for the production of methemoglobin. Since dietary pectin alters intestinal microflora, these studies were designed to examine the effects of dietary pectin on nitrobenzene-induced methemoglobinemia. Male Fischer-344 rats were fed either AIN-76A (purified diet containing 5% cellulose), AIN-76A with 5% pectin replacing the cellulose, or NIH-07 (cereal-based diet containing 8.4% pectin) for 28 days. Following this period, nitrobenzene (200 mg/kg) was administered by gastric intubation, and methemoglobin concentrations were determined after 1, 2, 4, 8, and 24 hr. Nitrobenzene-induced methemoglobinemia was evident as early as 1 hr, peaked at 4 hr, and diminished thereafter in rats fed NIH-07 diet. In contrast, nitrobenzene-induced methemoglobinemia was not detectable in rats fed AIN-76A; however, inclusion of 5% pectin in this diet resulted in methemoglobinemia comparable to that of NIH-07-fed animals at 4, 8, and 24 hr. Administration of 400 or 600 mg/kg nitrobenzene resulted in significant diet-related differences in methemoglobinemia. Administration of 600 mg/kg nitrobenzene to animals fed NIH-07 resulted in the highest methemoglobin concentrations (64 +/- 1%); those fed AIN-76A had the lowest (20 +/- 5%), and those fed AIN-76A containing pectin had intermediate methemoglobin concentrations (44 +/- 6%). No diet-related differences in the microbial population of the stomach or small intestine were observed. However, the number of anaerobes present in the ceca of rats fed AIN-76A containing pectin was 2 to 2.5 times greater than that of rats fed AIN-76A. In vitro reductive metabolism of [14C]nitrobenzene was significantly greater in the cecal contents of rats fed NIH-07 than that in the cecal contents of either of the groups fed the AIN-76A-based diets. These studies indicate that intestinal microfloral metabolism and red blood cell toxicity of nitrobenzene is markedly different in animals fed cereal-based versus purified diets. Furthermore, since inclusion of pectin into the purified diet diminishes the magnitude of these effects, differences in dietary composition of fermentable carbohydrates in cereal-based and purified diets may mediate differences in metabolism and toxicity of nitrobenzene.

Animals↗
PubMed1991

Biotransformation of nitrobenzene by bacteria containing toluene degradative pathways.

Nonpolar nitroaromatic compounds have been considered resistant to attack by oxygenases because of the electron withdrawing properties of the nitro group. We have investigated the ability of seven bacterial strains containing toluene degradative pathways to oxidize nitrobenzene. Cultures were induced with toluene vapor prior to incubation with nitrobenzene, and products were identified by high-performance liquid chromatography and gas chromatography-mass spectrometry. Pseudomonas cepacia G4 and a strain of Pseudomonas harboring the TOL plasmid (pTN2) did not transform nitrobenzene. Cells of Pseudomonas putida F1 and Pseudomonas sp. strain JS150 converted nitrobenzene to 3-nitrocatechol. Transformation of nitrobenzene in the presence of 18O2 indicated that the reaction in JS150 involved the incorporation of both atoms of oxygen in the 3-nitrocatechol, which suggests a dioxygenase mechanism. P. putida 39/D, a mutant strain of P. putida F1, converted nitrobenzene to a compound tentatively identified as cis-1,2-dihydroxy-3-nitrocyclohexa-3,5-diene. This compound was rapidly converted to 3-nitrocatechol by cells of strain JS150. Cultures of Pseudomonas mendocina KR-1 converted nitrobenzene to a mixture of 3- and 4-nitrophenol (10 and 63%, respectively). Pseudomonas pickettii PKO1 converted nitrobenzene to 3- and 4-nitrocatechol via 3- and 4-nitrophenol. The nitrocatechols were slowly degraded to unidentified metabolites. Nitrobenzene did not serve as an inducer for the enzymes that catalyzed its oxidation. These results indicate that the nitrobenzene ring is subject to initial attack by both mono- and dioxygenase enzymes.

Biodegradation, Environmental↗
PubMed2003

Hybrid reactor for priority pollutant nitrobenzene removal.

The performance of a hybrid reactor, comprising of trickling filter and activated sludge process, in treating nitrobenzene wastewater was investigated. Acetate induced cells of mixed consortia was acclimatized with gradual increase of nitrobenzene concentration up to 90 mg/l in 100 days using sodium acetate as co-substrate and considering COD and nitrobenzene concentration as paramount parameters for assessing the growth of biofilm and acclimation. A removal of 60-95.80% COD and 80-90.23% nitrobenzene was observed during acclimation. During hydraulic retention time (HRT) studies, the optimum HRT was found to be 29.55 h at which a maximum of 95.83% COD and 97.93% nitrobenzene removal was observed. Other studies included optimization of C:N ratio, substrate:co-substrate ratio, effect of shock loading and estimation of volatilization losses. The optimum C:N ratio was found to be 100:20 at which maximum 97.93% removal of nitrobenzene was observed. At optimum HRT (29.55 h) and optimum C:N ratio (100:20) optimum substrate:co-substrate ratio was found to be 1:33. From the shock load studies it can be concluded that the system can withstand shock load up to two times of usual nitrobenzene concentration. A loss of 9.44% nitrobenzene was observed due to volatilization and mass balance gave an efficiency of 87.49% biological removal of nitrobenzene.

Bioreactors↗
PubMed1993

Degradation of nitrobenzene by a Pseudomonas pseudoalcaligenes.

A Pseudomonas pseudoalcaligenes able to use nitrobenzene as the sole source of carbon, nitrogen, and energy was isolated from soil and groundwater contaminated with nitrobenzene. The range of aromatic substrates able to support growth was limited to nitrobenzene, hydroxylaminobenzene, and 2-aminophenol. Washed suspensions of nitrobenzene-grown cells removed nitrobenzene from culture fluids with the concomitant release of ammonia. Nitrobenzene, nitrosobenzene, hydroxylaminobenzene, and 2-aminophenol stimulated oxygen uptake in resting cells and in extracts of nitrobenzene-grown cells. Under aerobic and anaerobic conditions, crude extracts converted nitrobenzene to 2-aminophenol with oxidation of 2 mol of NADPH. Ring cleavage, which required ferrous iron, produced a transient yellow product with a maximum A380. In the presence of NAD, the product disappeared and NADH was produced. In the absence of NAD, the ring fission product was spontaneously converted to picolinic acid, which was not further metabolized. These results indicate that the catabolic pathway involves the reduction of nitrobenzene to nitrosobenzene and then to hydroxylaminobenzene; each of these steps requires 1 mol of NADPH. An enzyme-mediated Bamberger-like rearrangement converts hydroxylaminobenzene to 2-aminophenol, which then undergoes meta ring cleavage to 2-aminomuconic semialdehyde. The mechanism for release of ammonia and subsequent metabolism are under investigation.

Aminophenols↗
PubMed1994

Carcinogenicity and toxicity of inhaled nitrobenzene in B6C3F1 mice and F344 and CD rats.

The potential carcinogenicity and toxicity of inhaled nitrobenzene were evaluated following chronic (2-year) exposure in mice and rats. Male and female B6C3F1 mice were exposed to 0, 5, 25, or 50 ppm nitrobenzene, while male and female F344 rats and male CD rats were exposed to 0, 1, 5, or 25 ppm nitrobenzene. All exposures were for 6 hr/day, 5 days/week excluding holidays, for a total of 505 days over 2 years. Survival was not adversely affected by nitrobenzene exposure, and only mild exposure-related decreases in body weights (< 10% of control) were occasionally noted. Nitrobenzene exposure resulted in increased incidence of neoplasia in male B6C3F1 mice (pulmonary alveolar/bronchiolar and thyroid follicular cell neoplasms), female B6C3F1 mice (mammary gland neoplasms), male F344 rats (hepatocellular and renal neoplasms), female F344 rats (endometrial stromal neoplasms), and male CD rats (hepatocellular neoplasms). In addition, there were marginal increases in the incidence of hepatocellular neoplasia in female B6C3F1 mice and thyroid follicular neoplasia in male F344 rats. Groups of nitrobenzene-exposed mice and rats with increased incidence of renal and thyroid neoplasia also had increased incidences of hyperplasia in these tissues. Toxicity resulting from chronic inhalation of nitrobenzene was manifested by methemoglobinemia, anemia, and adaptive or degenerative changes in the nose, liver, and testis. The results indicate that inhaled nitrobenzene is carcinogenic and toxic in mice and rats, and that the spectrum of these responses in animals is dependent on species, sex, and genetic background.

Administration, Inhalation↗
PubMed1997

4-Substituted 1-chloro-2-nitrobenzenes: structure-activity relationships and extension of the substrate model of rat glutathione S-transferase 4-4.

In the present study, eleven 4-substituted 1-chloro-2-nitrobenzenes were tested for their GSH conjugation capacity when catalyzed by base or rat glutathione S-transferase (GST) 4-4. Kinetic parameters (ks and K(m), kcat, and kcat/K(m)) were determined and subsequently used for the description of structure-activity relationships (SAR's). For this purpose, eight physicochemical parameters (electronic, steric, and lipophilic) of the substituents and five computer-calculated parameters of the substrates (charge distributions and several energy values) were used in regression analyses with the kinetic parameters. The obtained SAR's are compared with corresponding SAR's for the GSH conjugation of 2-substituted 1-chloro-4-nitrobenzenes, previously determined [Van der Aar et al. (1996) Chem. Res. Toxicol. 9, 527-534]. The kinetic parameters of the 4-substituted 1-chloro-2-nitrobenzenes correlated well with the Hammett sigma p- constant; the Hammett sigma p constant corrected for "through resonance", while the corresponding kinetic parameters of the 2-substituted 1-chloro-4-nitrobenzenes did not. The base- and GST 4-4-catalyzed GSH conjugation reactions of 2-substituted 1-chloro-4-nitrobenzenes depend to a different extent on the electronic properties of the ortho substituents, suggesting the involvement of different rate-limiting transition states. The base- and GST 4-4-catalyzed conjugation of 4-substituted 1-chloro-2-nitrobenzenes, however, showed a similar dependence on the electronic properties of the para substituents, indicating that these substrates are conjugated to GSH via a similar transition state. Multiple regression analyses revealed that, besides electronic interactions, also steric and lipophilic restrictions appeared to play an important role in the GST 4-4-catalyzed GSH conjugation of 4-substituted 1-chloro-2-nitrobenzenes. Finally, the 4-substituted 1-chloro-2-nitrobenzenes were also used to extend the previously described substrate model for GST 4-4 [De Groot et al. (1995) Chem. Res. Toxicol. 8, 649-658], by which a specific steric restriction of substrates for GST 4-4 became clear.

Animals↗
PubMed1995

Purification and characterization of nitrobenzene nitroreductase from Pseudomonas pseudoalcaligenes JS45.

Pseudomonas pseudoalcaligenes JS45 grows on nitrobenzene as a sole source of carbon, nitrogen, and energy. The catabolic pathway involves reduction to hydroxylaminobenzene followed by rearrangement to o-amino-phenol and ring fission (S. F. Nishino and J. C. Spain, Appl. Environ. Microbiol. 59:2520, 1993). A nitrobenzene-inducible, oxygen-insensitive nitroreductase was purified from extracts of JS45 by ammonium sulfate precipitation followed by anion-exchange and gel filtration chromatography. A single 33-kDa polypeptide was detected by denaturing gel electrophoresis. The size of the native protein was estimated to be 30 kDa by gel filtration. The enzyme is a flavoprotein with a tightly bound flavin mononucleotide cofactor in a ratio of 2 mol of flavin per mol of protein. The Km for nitrobenzene is 5 microM at an initial NADPH concentration of 0.5 mM. The Km for NADPH at an initial nitrobenzene concentration of 0.1 mM is 183 microM. Nitrosobenzene was not detected as an intermediate of nitrobenzene reduction, but nitrosobenzene is a substrate for the enzyme, and the specific activity for nitrosobenzene is higher than that for nitrobenzene. These results suggest that nitrosobenzene is formed but is immediately reduced to hydroxylaminobenzene. Hydroxylaminobenzene was the only product detected after incubation of the purified enzyme with nitrobenzene and NADPH. Hydroxylaminobenzene does not serve as a substrate for further reduction by this enzyme. The products and intermediates are consistent with two two-electron reductions of the parent compound. Furthermore, the low Km and the inducible control of enzyme synthesis suggest that nitrobenzene is the physiological substrate for this enzyme.

Amino Acid Sequence↗
PubMed1990

Toxicity of nitrobenzene compounds towards isolated hepatocytes: dependence on reduction potential.

1. The cytotoxicity of p-substituted nitrobenzenes towards isolated hepatocytes under aerobic or hypoxic conditions has been determined. The nitrobenzene concentration required to cause 50% cytoxicity in 2 h was a function of the one-electron reduction potential of the nitrobenzene, with the more cytotoxic compounds having the strongest electron-withdrawing substituents. 2. The effectiveness of the nitrobenzenes at causing cytotoxicity under aerobic but not hypoxic conditions was markedly increased if hepatocyte catalase was inhibited with azide. 3. Nitrobenzenes at cytotoxic concentrations induced cyanide-resistant respiration in isolated hepatocytes. Their effectiveness correlated with their cytotoxicity. 4. The rate of oxygen activation of these nitrobenzenes by ascorbate was also a function of the one-electron reduction potential. The nitro compounds with the strongest electron-withdrawing substituents were the most rapidly reduced. 5. Most nitrobenzenes were more cytotoxic under aerobic than hypoxic conditions. Ascorbate enhanced hypoxic, but not aerobic, cytotoxicity. 6. It was concluded that the cytotoxicity of different nitrobenzenes is related to their ease of reduction to nitro radical anions and nitrosobenzenes. Aerobic cytotoxicity is probably initiated by redox cycling and oxygen activation by the nitro radical anions whereas hypoxic cytotoxicity is probably initiated by the alkylation of macromolecules by nitrosobenzene metabolites.

Alkylation↗
PubMed2001

Process for degradation of nitrobenzene: combining electron beam irradiation with biotransformation.

Electron beam irradiations of aqueous solutions containing 15-30 mg/L of nitrobenzene at 60 kGy dose removed 78% of the contaminant. Three mononitrophenols were detected as by-products of electron beam treatment of nitrobenzene. A mixed culture enriched on a mixture of 2-, 3-, and 4-nitrophenol degraded both the residual nitrobenzene and the nitrophenol products. Percentage removal of nitrobenzene increased with increasing electron beam dose. This observation led to the conceptual design of a two-stage electron beam microbial process for degradation of nitrobenzene. Three groups of pure isolates were characterized from the mixed culture based on their abilities to grow on cor- responding nitrophenol substrates: Group A, 2NP(-)3NP(-)4NP(+); Group B, 2NP(+)3NP(+)4NP(-); and Group C, 2NP(-)3NP(+)4NP(-). Bacteria that grew on 3-NP transformed nitrobenzene into ammonia in the electron beam-treated nitrobenzene samples.

Biotransformation↗
PubMed2003

Studies on the sorption behaviors of nitrobenzene on marine sediments.

The sorption behaviors of nitrobenzene on marine sediments were systematically investigated in this study. The nitrobenzene sorption on both HCl-treated and untreated sediments accorded well with the linear sorption isotherm. It occurred primarily through partition function of organic carbon of sediments. In comparison, the sorption behavior of nitrobenzene on H2O2-treated sediments was nonlinear and conformed to Langmuir isotherm. Sorption of nitrobenzene on H2O2-treated sediment was mainly through surface function of sediment minerals such as clays. With the increase of ionic strength (salinity), solubility of nitrobenzene in solution would decrease. At the same time, the release of dissolvable part of organic carbon into water solution would also decrease. As a result, partition coefficient and saturate adsorption amount of nitrobenzene on marine sediments increased with increasing salinity of seawater. Contrary to the influence of salinity, partition coefficient and saturate adsorption amount of nitrobenzene decreased with increasing temperature.

Adsorption↗