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At least 19 recordsLinked to original sources
PubMed1983

Estimation of N-hydroxy-o-toluidine, a urinary metabolite of o-toluidine and o-nitrosotoluene, by high performance liquid chromatography with electrochemical detection.

High-performance liquid chromatography with electrochemical detection, a highly sensitive and specific method, was used to determine N-hydroxy-o-toluidine and o-toluidine in the urines of male F344 rats after the administration of 0.82 mmol/kg of o-toluidine or o-nitrosotoluene. In a six hour period, 0.11% of the dose was excreted by o-toluidine-treated rats as N-hydroxy-o-toluidine and 3.61% as o-toluidine. In the same period, 0.48% of the dose was excreted by o-nitrosotoluene treated rats as N-hydroxy-o-toluidine and 0.38% as o-toluidine. The urinary excretion of the N-hydroxy-o-toluidine metabolite may play a role in the carcinogenicity of o-nitrosotoluene and o-toluidine toward the rat bladder.

Animals↗
PubMed1988

Induction of xenobiotic biotransformation by the insecticide chlordimeform, a metabolite 4-chloro-o-toluidine and a structurally related chemical o-toluidine.

Chlordimeform, 4-chloro-o-toluidine and o-toluidine have all been found to have carcinogenic properties. Due to an empirical link between such properties and alteration of some biotransformation enzymes, the abilities of these three chemicals to affect cytochrome P-450 mediated biotransformation, epoxide hydrolase and glutathione S-transferase have been examined. Chlordimeform had no effect on the cytochrome P-450 content, aniline p-hydroxylase or glutathione S-transferase activities, but induced ethoxyresorufin-O-deethylase, ethoxycoumarin-O-deethylase and epoxide hydrolase activities and decreased aldrin epoxidase and aminopyrine N-demethylase activities. The metabolite 4-chloro-o-toluidine increased cytochrome P-450, ethoxyresorufin-O-deethylase, ethoxycoumarin-O-deethylase, glutathione S-transferase and epoxide hydrolase activities. o-Toluidine induced cytochrome P-450, ethoxyresorufin-O-deethylase, ethoxycoumarin-O-deethylase, and aldrin epoxidase activities. Ethoxy-resorufin-O-deethylase activity was induced approximately eight times by chlordimeform and 18 times by 4-chloro-o-toluidine and o-toluidine. Induction was seen at 50 mg/kg with chlordimeform and at 10 mg/kg with the other treatments. Chlordimeform increased the 7 alpha and 16 alpha androstenedione hydroxylase pathways. 4-Chloro-o-toluidine increased the 7 alpha, 16 beta and 16 alpha hydroxylase pathways, while o-toluidine increased the 7 alpha, 6 beta, 16 beta and 16 alpha hydroxylase pathways. All three chemicals marginally decreased the testosterone pathways. SDS-PAGE of rat microsomes revealed an increase in a protein band of MW c54,000 for the chlordimeform and 4-chloro-o-toluidine treated groups. Taken together with the increase in ethoxyresorufin-O-deethylase activity these observations are consistent with the induction of hepatic isozyme P-450d. Thus each chemical has been shown to induce various pathways of biotransformation with increases in the P-450c and P-450d specific substrate ethoxyresorufin-O-deethylase being a consistent finding.

Amidines↗
PubMed1983

The toluidine blue-membrane filter method: absorption spectra of toluidine blue stained bacterial cells and the relationship between absorbance and dry mass of bacteria.

Propan-2-ol did not leach dye from toluidine blue stained bacteria on membrane filters but ethanol did. The absorption spectra of toluidine blue stained cells of two Gram-positive and two Gram-negative organisms differed with the latter organisms exhibiting metachromasia. The results suggest that toluidine blue stains the cell envelope. Linear regression equations were derived for each of four organisms, Streptococcus cremoris, Lactobacillus bulgaricus, Pseudomonas fluorescens and Escherichia coli, relating absorbance at the peak of the absorption spectra and the mass of cells on the filters. With these equations it should be possible to determine mass of cells with an error between 3% and 7.5% depending on the organism. Since the regression equations are similar, the amount of toluidine blue retained per milligram of cells may be constant under standard conditions, irrespective of species.

Bacteria↗
PubMed2004

NIR vibrational overtone spectra of toluidines-evidence for steric and electronic effects in o-toluidine.

The near infrared vibrational overtone absorption spectra of liquid phase toluidines are reported. The analysis of the observed CH and NH local mode mechanical frequency values shows that there exists steric and electronic interaction between the amino and methyl groups in o-toluidine. This observation supports the conclusions drawn from structural studies of toluidines by resonance two-photon ionization (R2PI) spectroscopy, ab initio calculations and laser induced fluorescence studies reported earlier.

Spectroscopy, Near-Infrared↗
PubMed1996

NTP Comparative Toxicity and Carcinogenicity Studies of o-Nitrotoluene and o-Toluidine Hydrochloride (CAS Nos. 88-72-2 and 636-21-5) Administered in Feed to Male F344/N Rats.

o-Nitrotoluene and o-toluidine hydrochloride are structurally related chemicals that are suspected and demonstrated animal carcinogens, respectively. The metabolic potential of the gastrointestinal flora is considered an important factor in o-nitrotoluene-induced toxicity and involves the reduction of the nitro group to the corresponding amine (forming o-toluidine). These studies were designed to 1) compare the target organ toxicities of o-nitrotoluene and o-toluidine hydrochloride administered in feed at approximately equimolar doses (5,000 ppm) to male F344/N rats for 13 or 26 weeks, 2) determine the potential progression or reversibility of toxic or proliferative lesions following chemical withdrawal (stop-exposure) for 13 weeks after 13 weeks of exposure, and 3) examine the effect of antibiotic-altered gastrointestinal flora on the toxicity and/or carcinogenicity of o-nitrotoluene. o-Nitrotoluene and o-toluidine hydrochloride caused mesothelial hyperplasia and mesothelioma in male rats after 13 or 26 weeks of dietary exposure. The incidence of mesothelioma was greater and the latency was less in rats administered o-nitrotoluene than in rats administered o-toluidine hydrochloride. Additionally, o-nitrotoluene caused testicular degeneration in rats. Effects of o-nitrotoluene administration in the liver included progressive, irreversible increases in liver weight and irreversible increases in the incidences of cytoplasmic vacuolization and oval-cell hyperplasia. Placental glutathione S-transferase (PGST)-positive foci of cellular alteration occurred in the liver after 13 weeks of o-nitrotoluene exposure, and the number and size (as reflected by the volume fraction) of foci were increased after 26 weeks of continuous exposure. During the recovery period, the number of PGST-positive foci in rats in the stop-exposure group decreased slightly, but the size of the foci continued to increase. After 26 weeks, cholangiocarcinoma occurred in 2 of 20 rats in the stop-exposure group and 1 of 20 rats in the continuous-exposure group administered o-nitrotoluene. In contrast, liver effects in rats administered o-toluidine hydrochloride consisted of minimal hemosiderin accumulation in Kupffer cells; the incidence of this lesion in the stop-exposure group decreased during the recovery period. o-Toluidine hydrochloride caused fewer and much smaller PGST-positive foci than those caused by o-nitrotoluene. o-Nitrotoluene caused an accumulation of hyaline droplets in the renal tubule epithelium; this accumulation did not increase in severity with continued exposure and completely regressed during the recovery period. Exposure to o-toluidine hydrochloride did not cause hyaline droplet accumulation but did cause an accumulation of hemosiderin pigment in renal tubule epithelium. This change progressed in severity during the 26-week continuous-exposure study but decreased in severity in the stop-exposure study during the recovery period. Exposure to o-nitrotoluene or o-toluidine hydrochloride caused increased incidences of hematopoiesis, hemosiderin accumulation, and capsular fibrosis in the spleen. In rats administered o-toluidine, spleen effects were much more prominent and were also reflected by congestion and markedly increased spleen weights. During the recovery period for the stop-exposure groups administered either compound, incidences of hemosiderin accumulation and hematopoiesis were decreased, but the capsular fibrosis did not resolve. Hyperplasia of the transitional epithelium in the urinary bladder was observed only in rats administered o-toluidine hydrochloride; this lesion did not increase in severity after 26 weeks of continuous exposure and completely regressed in the stop-exposure group during the recovery period. Alteration of the gastrointestinal flora by daily gavage administration of antibiotics did not affect the pattern or severity of toxicity at any site or the development of mesothelioma in rats exposed to o-nitrotoluene, although cholangiocarcinomas that occurred in three rats with the normal flora did not occur in groups with the altered intestinal flora. Subsequent studies determined that the antibiotic regimen used was effective only in reducing the gut population of aerobic microorganisms and had little effect on obligate anaerobes, which are thought to play a mayor role in nitro group reduction. In summary, these studies confirmed the target organs and compared the relative toxicity for o-nitrotoluene and o-toluidine hydrochloride administered to male F344/N rats at equimolar concentrations in feed. With the exception of the spleen toxicity observed with each chemical, but more prominently with o-toluidine hydrochloride, morphologic effects of exposure to each of these chemicals in the testis/epididymis, liver, kidney, and urinary bladder were different. The results of these studies demonstrate the somewhat greater relative carcinogenic potential of o-nitrotoluene compared to o-toluidine hydrochloride after 13 or 26 weeks of administration based on the occurrence of mesothelioma and cholangiocarcinoma. The apparently lower potency of o-toluidine hydrochloride relative to o-o-nitrotoluene in the induction of mesothelioma suggests that simple intestinal reduction of the nitro group may not be sufficient for carcinogenic activity in the mesothelium.

Journal Article↗
PubMedDate not supplied

Qualitative and quantitative influences of ortho chlorine substituents on the microsomal metabolism of 4-toluidines.

The influence of ortho chlorine substituents on 4-toluidine rat liver microsomal metabolism was investigated with 4-toluidine, 2-chloro-4-toluidine, and 2,6-dichloro-4-toluidine as substrates. Microsomal metabolic products were identified and quantified by HPLC, chemical assays, and synthesized reference compounds. Metabolites identified include products from aromatic ring hydroxylation, side-chain C-hydroxylation (benzyl alcohols and benzaldehydes), N-hydroxylation (hydroxylamines, nitrosotoluenes, azoxy, azo, and hydrazo derivatives), and two new types of microsomal metabolites: secondary amines [i.e. (halogenated) N-(4'-aminobenzyl)-4-toluidines] and an imine [i.e. N-(4'-amino-3',5'-dichlorobenzylidene)-2,6-dichloro-4-toluidine]. The secondary amine appeared to be a major microsomal metabolite for all three 4-toluidines studied. Quantification of the metabolite patterns demonstrated several influences of the chlorine substituents on metabolism of the 4-toluidine derivatives. The total conversion increased significantly in the order: 4-toluidine < 2-chloro-4-toluidine < 2,6-dichloro-4-toluidine, especially because of a marked increase in microsomal side-chain C-hydroxylation with increasing number of ortho chlorine substituents. The rate of N-hydroxylation varied much less. Aromatic ring hydroxylation was observed to a significant extent only for nonchlorinated 4-toluidine. Additional data from microsomal binding studies and molecular orbital calculations provided insight in possible mechanisms underlying the observed changes in metabolic profiles with increasing number of chlorine substituents at an ortho position with respect to the amine group.

Animals↗