Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Benzidines”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1975

Metabolic reduction of benzidine azo dyes to benzidine in the rhesus monkey.

Rhesus monkeys were fed azo dyes derived from benzidine (a known human bladder carcinogen). The urinary excretion of free benzidine was assayed and compared to the amount excreted when benzidine itself was fed. A substantial amount of the dye fed was converted to free benzidine. Results indicate that the simple precaution in the use of only azo dyes manufactured from noncarcinogenic aromatic amines, e.g., aniline, for all consumer products appears prudent.

Aminobiphenyl Compounds↗
PubMed1992

Role of N-glucuronidation in benzidine-induced bladder cancer in dog.

The mechanism by which benzidine induces bladder cancer in dog was evaluated by assessing metabolism of [3H]benzidine by dog liver slices and microsomes. Slices incubated with 0.05 mM [3H]benzidine exhibited a 32.5 min incubated with 0.05 mM [3H]benzidine exhibited a 32.5 min peak, which was also produced when microsomal incubations were supplemented with UDP-glucuronic acid. In contrast to microsomes, very little of the 32.5 min peak was produced with the 100,000 g supernatant fraction. Microsomal metabolism was increased 5-fold by pretreatment with Triton X-100. Very little activity was observed with rat microsomes in either the presence or absence of Triton X-100. This metabolite was also generated by incubating benzidine with glucuronic acid at 4 degrees C for 3 days. Thermospray MS identified this metabolite as benzidine N-glucuronide. At 37 degrees C, the t1/2 stability of purified N-glucuronide was 99, 25 and 3 min in dog urine adjusted to pH 7.3, 6.3 and 5.3 respectively. The N-glucuronide was quite stable at pH 9.3, in dog plasma, and in aprotic solvents for 4 h at 37 degrees C. Relative to benzidine, its N-glucuronide is weakly bound to plasma proteins but not more reactive with DNA. Thus, detoxification by liver provides a mechanism for accumulation of benzidine in acidic urine, uptake of benzidine into bladder epithelium, and activation of benzidine in bladder. The liver and N-glucuronidation play a potentially important role in the species specificity of benzidine carcinogenesis.

Animals↗
PubMed1975

Factors modulating benzidine carcinogenicity bioassay.

An integrated series of studies was presented in which several factors were assessed as to their capability to influence the outcome of carcinogenicity of benzidine dihydrochloride in mice. In all studies C57BL/6J X C3HeB/FeJ F1 mice of both sexes were utilized. Animals were either 6 or 1 week of age at the beginning of carcinogenic treatment. Six-week-old mice were exposed to p.o. administration of carcinogen delivered either in food (50 or 100 ppm daily) or by stomach intubation at equivalent dose levels at twice-weekly intervals. In addition, a 150-ppm dose level in food was administered for 39, 54, or 84 weeks. A limited 3-week, daily intubation of benzidine (30 or 100 mug/mouse) was also explored in 1- and 6-week-old mice. Animals were killed in all studies at 90 weeks of age, at which time their tumor incidence was evaluated. Depending upon experimental conditions, benzidine treatment effected development of liver tumors, lung adenomas. Harderian gland cystadenomas, and lymphoreticular neoplasms. Continuous feeding of adult mice for 84 weeks at three dose levels of benzidine resulted in development of liver tumors with a positive dose-response relationship in both sexes. The analysis of data revealed a greater susceptibility of females than of males (94% versus 44% at 150 ppm). Twice-weekly administration of benzidine by stomach intubation was shown to be less hepatocarcinogenic than continuous feeding of equivalent amounts. In the series in which male mice were fed food containing 150 ppm of benzidine for only 34 or 54 weeks, in contrast to the above 84-week schedule, a negative relationship was observed between the incidence of liver tumors and the duration of treatment. Daily administration of 30 mug of benzidine to infants by stomach intubation for a 3-week period significantly enhanced development of liver tumors only in males (66%). Introduction of 150 ppm of benzidine into food offered to mother and offspring from delivery to weaning led to development of liver tumors in 95% of male mice and in 5% of females. No liver tumors developed following similar 3-week treatment of 6-week-old adults.

Administration, Oral↗
PubMedDate not supplied

Mutagenic activation of benzidine requires prior bacterial acetylation and subsequent conversion by prostaglandin H synthase to 4-nitro-4'-(acetylamino)biphenyl.

We have used the Ames test in combination with prostaglandin H synthase (PHS) to study the bioactivation of benzidine as well as other aromatic amines. Previous investigations established that the formation of benzidine mutagens by PHS is dramatically enhanced in Salmonella typhimurium strains with high levels of acetyl CoA-dependent arylamine N-acetyltransferase/arylhydroxylamine O-acetyltransferase activity despite the fact that acetylation of aromatic amines decreases their susceptibility to oxidation by peroxidases. In this study, we used a new strain (YG1012) that has very high acetylation capability to investigate the metabolism and mutagenicity of benzidine and N-acetylbenzidine catalyzed by PHS (from ram seminal vesicle microsomes) and horseradish peroxidase (HRP). YG1012 bacteria rapidly acetylated benzidine to N-acetylbenzidine and N,N'-diacetylbenzidine. Preincubation of the bacteria with benzidine before addition of PHS increased the mutagenicity. Under conditions identical to those used to assess mutagenicity, PHS metabolized benzidine rapidly, but the substrate was not totally consumed, with about 40% of the original concentration remaining intact. These data suggest that conversion to N-acetylbenzidine may be the initial step in the bioactivation of benzidine in the PHS-mediated Ames assay. N-Acetylbenzidine is a cosubstrate for PHS peroxidase activity as measured by 5-phenyl-4-pentenyl hydroperoxide reduction, spectral changes, and formation of protein adducts. N-Acetylbenzidine was converted to mutagens by PHS but not HRP, with enhanced mutagenicity observed in bacteria with high acetylation activity. We used reverse- phase HPLC to characterize the metabolites of N-acetylbenzidine formed by PHS and HRP.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetamides↗
PubMed1992

Mortality and incidence of bladder cancer in benzidine-exposed workers in China.

We examined bladder cancer mortality and incidence to 1981 in 1,972 workers employed in benzidine-exposed jobs in Tianjin, Shanghai, and Jilin, China, between 1972 and 1977, and in 1,974 unexposed workers employed during the same time period. In comparison to general population rates, in the benzidine-exposed group the ratio of observed to expected deaths (SMR) was 17.5 (95% C.I.: 7.5-34.5) and the ratio of observed to expected incident cases (SIR) was 25.0 (95% C.I.: 16.9-35.7). No excess was noted in the unexposed group. The 25-fold increase in bladder cancer incidence in the exposed group was related to level of exposure, with the SIR rising from 4.8 for low exposure to 36.2 for medium exposure, and 158.4 for high exposure. Risks were elevated both for producers of benzidine (SIR = 45.7; 95% C.I.: 20.9-86.8) and for users (SIR = 20.9; 95% C.I.: 12.9-32.0) of benzidine dyes. Benzidine-exposed workers who smoked tobacco had a 31-fold risk (95% C.I.: 20.4-46.4), while non-smoking workers had an 11-fold risk (95% C.I.: 3.6-25.8), suggestive of a multiplicative relationship between these two carcinogens.

Air Pollutants, Occupational↗
PubMed1979

Tetramethylbenzidine--a substitute for benzidine in hemoglobin analysis.

Plasma hemoglobin is routinely measured by some modification of the benzidine-hydrogen peroxide method, particularly at low concentrations. Because benzidine is carcinogenic, and thus impractical for clinical use under current restrictions, the identification of a noncarcinogenic benzidine derivative has become important. 3,3',5,5'-tetramethylbenzidine fulfills this criterion, and consequently a method is described in this paper which uses it for hemoglobin determinations in the range of 1 to 100 mg/dl. Absorption spectra show this method to be far less influenced by plasma proteins and other substances than the benzidine method, and moreover the sensitivity of TMB is at least seven times that of benzidine under comparable conditions.

Benzidines↗
PubMed1978

The benzidine technique for histochemical detection of the SO4 ion.

The benzidine technique for histochemical detection of the SO4 ion was studied analytically on filter paper strips loaded with 0.02 ml of solutions of sulfate containing and sulfate free substances. The influence of the benzidin solution pH on the SO4 and PO4 ion precipitation was analysed and the experimental condition where the SO4 ion was specifically precipitated was established. In basis on this study a benzidine histochemical technique suitable to detect the SO4 ion without interference of the PO4 ion was proposed for tissue sections. This technique has some advantages on the other benzidin techniques previously proposed mainly concerning its specificity.

Anions↗
PubMed1978

Tetramethyl benzidine for horseradish peroxidase neurohistochemistry: a non-carcinogenic blue reaction product with superior sensitivity for visualizing neural afferents and efferents.

Tetramethyl benzidine (TMB) is a presumptively non-carcinogenic chromogen which yields a blue reaction-product at sites of horseradish peroxidase activity. Sixty-six distinct procedures were performed in rats and monkeys in order to determine the optimal incubation parameters for TMB. As a result, a procedure is recommended whose sensitivity greatly surpasses that of a previously described benzidine dihydrochloride method. Indeed, the sensitivity of this new method in demonstrating retrograde transport is markedly superior to that of the previously described benzidine dihydrochloride method. Furthermore, as a consequence of this enhanced sensitivity, many efferent connections of the injection site are also visualized. The injection site demonstrated by this TMB procedure is significantly larger than the one demonstrated when benzidine dihydrochloride or diaminobenzidine is used as a chromogen. Finally, this TMB procedure has been compared to two other TMB procedures and found to provide superior morphology and sensitivity.

Animals↗
PubMed1978

Chlorination of benzidine and other aromatic amines an aqueous environments.

The fate of aniline, N,N-dimethylaniline and benzidine in chlorinated waters was investigated. Conditions were controlled to approximate the process chlorination of raw water supplies and wastewater secondary effluents. As the molar ratio, (Cl2)/(amine), was increased, amine depletions increased and leveled off at about (Cl2)/(amine) = 1. Depletions in distilled water with "free" chlorine were somewhat higher than those in activated sludge/secondary effluent with combined chlorine. For each amine the number and type of products appeared to be independent of the water matrix and the ratio, (Cl2)/(amine). For the monophenyl amines ring chlorination was a significant depletion pathway. Extended chlorination of aniline yielded a precipitated product, while the N-substituted amine, N,N-dimethylaniline did not yield a solid product. In contrast to the monophenyl amines, when benzidine (p,p'-diaminobiphenyl) was exposed to chlorinated waters, a solid product resulted immediately. Infra-red analysis of this product indicated a polymeric structure with no ring chlorination. GLC analysis of the chlorination supernatant showed no ring substituted isomers of benzidine.

Aniline Compounds↗
PubMed1979

[Determination of benzidine in the air using the colorimetry and liquid chromatography methods].

The paper presents selection of analytical methods for determination of airborne benzidine, whose maximum admissible concentration (MAC) comes to zero. Colorimetric method with T chloroamine, allowing to determine 3 microgram of benzidine in m3 of the air, was evaluated. Such advantages of the method as specificity and availability of reagents and measuring apparatus were stressed. Another method presented in the paper is based on liquid chromatography, and its main features are: much better determinability of--0.7 microgram benzidine in m3 of the air and better precision than that of the colorimetric method. Its usefulness is however limited due to the necessity to have a very expensive liquid chromatograph.

Air Pollutants↗
PubMed1977

The Environmental fate of three carcinogens: benzo-(alpha)-pyrene, benzidine, and vinyl chloride evaluated in laboratory model ecosystems.

Radiolabeled benzo-((alpha)-pyrene, benzidine, and vinyl chloride were evaluated in laboratory model ecosystems for environmental fate, degradation pathways, bioconcentration, and food chain accumulation. The comparative effects of microsomal detoxications were evaluated using the inhibitor piperonyl butoxide. The accumulation and bioconcentration of benzo-(alpha)-pyrene and benzidine were closely correlated with their octanol/water partition coefficients and water solubility. Benzo-(alpha)-pyrene as predicted by these parameters was bioaccumulated to substantial levels in several organisms. Vinyl chloride was not accumulated because of its high volatility.

Animals↗
PubMed1992

The in vivo and in vitro genotoxicity of aromatic amines in relationship to the genotoxicity of benzidine.

Benzidine and 12 related aromatic amines have been studied for the effects of substituent groups and pi orbital conjugation on their genotoxicity as measured by their mutagenicity in vitro with Salmonella and by chromosomal aberrations (CA) in vivo in the bone-marrow cells of mice. The in vitro studies indicated increases in mutagenicity with increases in the electron withdrawing ability of para' substituents. Mutagenicity also increases with increased conjugation as shown by the degree of planarity of the biphenyl compounds and by comparing the mutagenicities of biphenyl amines to stilbenes as well as to ethylene bridged diphenyl compounds. The relative in vitro mutagenicity results were not predictive of relative in vivo CA results. The 3 most genotoxic compounds in vivo were the conjugated amines without substituents in the para' position. The CA values for 4-aminostilbene were exceptionally high. These in vivo results indicate increased genotoxicity for benzidine analogs without substitution in the para' position.

Aminobiphenyl Compounds↗
PubMed1975

Testing of some benzidine analogues for microsomal activation to bacterial mutagens.

Analogues of benzidine were assayed for mutagenic activity towards Salmonella typhimurium TA 1538 in the presence and absence of a liver enzyme preparation. Purified 3,3'-dichlorobenzidine and the technical grade material had some direct mutagenic activity, but this was increased over 50-fold by addition of a liver mixed function oxidase preparation. In the presence of the liver preparation, 3,3'-dichlorobenzidine was approximately 10 times more active than benzidine, while 3,3',5,5'-tetrafluorobenzidine was of approximately equipotency. On the other hand, 3,3',5,5'-tetramethylbenzidine had no mutagenic activity alone or in conjunction with a liver preparation. 3,3'-Dianisidine had slight mutagenic activity in the presence of liver but none in its absence.

3,3'-Dichlorobenzidine↗
PubMed1977

Mutagenicity of benzidine and related compounds employed in the detection of hemoglobin.

Seven compounds commonly used as chromagens for the detection of hemoglobin and its derivatives have been assayed for mutagenicity employing the Salmonella/mammalian microsome test. Three of these compounds, benzidine, o-dianisidine, and o-tolidine, were shown to be mutagenic. Since benzidine and o-tolidine are already known to be carcinogens, there is a high probability that o-dianisidine will also prove to be a carcinogen. Four compounds tested with this system, o-anisidine, diphenylamine, guaicol, and o-toluidine, were not mutagenic.

Animals↗
PubMed1977

Risk of bladder tumors among benzidine workers and their serum properdin levels.

Serum properdin levels were determined for 21 benzidine operators at 6-month intervals for 2 years after termination of exposure to this carcinogen. Of this group, 7 developed bladder cancers within a 4-month period prior to the initial assay, and all 7 showed properdin levels below the median for the group as a whole. Two of the 3 workers who had had a brief exposure previously to beta-naphthylamine developed benign bladder tumors but had no malignant neoplasms up to 13 years later. The properdin assays of these 3 men remained consistently at or above the median values. No man developed a bladder tumor who was exposed less than 6 years to benzidine, even though 2 of these men showed low properdin levels. Of the 4 whose properdin levels were initially above the median but dropped below in subsequent assays, 3 developed bladder cancers 0.5, 4, and 9 years later. Only 1 man whose properdin level remained high in 1958-59 developed a bladder cancer 7 years later, and his immunologic picture may have been complicated by recovery from a larynx tumor in 1954. Recurrence of bladder tumors among the original 9 cases has occurred only among the 5 whose properdin levels remained below the median. The 1 whose ranking fell most dramatically (from 13 to 19) has had 13 recurrences in 13 years.

2-Naphthylamine↗
PubMed1975

[Detection of antigens containing benzidine groups in the blood of persons having contact with aniline dyes].

The paper is concerned with the study of a possibility to record 2-naphtylamine and benzidine in serum and formed blood elements of workers being in contact with dyes, which molecule contain radicals of carcinogens. The Ouchterlony method of precipitation in gel in micromodification and the method of a delay in the precipitation reaction have indicated the presence of benzidine as a haptene in blood serum of 25 among 103 workers and in blood clot extracts in 42 among 116 workers from a textile factory under examination. But 2-naphtylamine was not found in the same subjects.

2-Naphthylamine↗