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At least 19 recordsLinked to original sources
PubMed1992

Determination of selenium in urine by isotope dilution gas chromatography-mass spectrometry using 4-nitro-o-phenylenediamine, 3,5-dibromo-o-phenylenediamine, and 4-trifluoromethyl-o-phenylenediamine as derivatizing reagents.

An isotope dilution gas chromatography-mass spectrometry method for selenium determination in urine using 76Se as an internal standard is described. Three different derivatizing reagents, 4-nitro-o-phenylenediamine (NPD), 3,5-dibromo-o-phenylenediamine (DBPD), and 4-trifluoromethyl-o-phenylenediamine (TFMPD) were investigated for their gas chromatographic behavior including memory and precision and accuracy of isotope ratio measurements. By these criteria, the performance of these reagents was TFMPD greater than DBPD greater than NPD. Overall precision values of 1 to 7% were observed in determining Se isotope ratios at the 10-ng level, with no significant difference in using any of the three reagents. Memory effect was observed in the order NPD greater than DBPD greater than TFMPD with TFMPD showing no measurable memory effect. Accuracy of the GC-MS method was verified by quantitation of selenium in the NIST freeze-dried urine reference material SRM 2670.

Gas Chromatography-Mass Spectrometry↗
PubMed1980

Carcinogenicity of 4-chloro-o-phenylenediamine, 4-chloro-m-phenylenediamine, and 2-chloro-p-phenylenediamine in Fischer 344 rats and B6C3F1 mice.

In both male and female Fischer rats, feeding 4-chloro-o-phenylenediamine at 0.5 or 1% in the diet led to a significant increase in hyperplasia, papilloma and carcinoma of the urinary bladder. Neoplastic nodules of the liver and squamous cell papillomas of the stomach were also increased slight. Similar levels of this compound in male and female B6C3F1 mice increased significantly the incidence of hepatocellular adenomas and carcinomas. 4-Chloro-m-phenylenediamine at 0.2 or 0.4% in the diet led to a significant elevation in the incidence of adrenal pheochromocytoma in male rats. At 1 or 2% levels it caused hepatocellular adenoma in female mice. Although the analog, 2-chloro-p-phenylenediamine increased transitional cell hyperplasia of the kidney in both male and female rats, it had no significant neoplastic effect at the 0.15 or 0.3% levels fed.

Animals↗
PubMed1967

Enzymatic oxidation of tetramethyl-p-phenylenediamine and p-phenylenediamine by the electron transport particulate fraction of Azotobacter vinelandii.

The ability of the electron transport particulate fraction of Azotobacter vinelandii strain O to oxidize tetramethyl-p-phenylenediamine (TMPD) and p-phenylenediamine (PPD) was examined in detail. The highest specific activity for TMPD and PPD oxidation concentrated in the A. vinelandii O R(3) fraction. The A. vinelandii O R(3) fraction was used to develop a standard manometric assay which gave optimal oxidation rates for both of these dyes. The conditions of the assay and all essential related enzymatic kinetic parameters are presented. Other para derivatives of phenylenediamines also were oxidized readily, whereas ortho and meta derivatives were not. Hydroquinone, p-hydroxybenzoic acid, p-cresol, tyrosine, pyrogallol, pyrocatechol, and diphenylamine were not able to serve as electron donors for the A. vinelandii O R(3) system. The probable involvement of a particle-bound cytochrome oxidase is indicated by the marked sensitivity of both TMPD and PPD oxidation to cyanide, axide, phenylhydrazine, hydroxylamine, and, to a lesser degree, carbon monoxide.

Aniline Compounds↗
PubMed1981

Teratogenic evaluation of 2-nitro-p-phenylenediamine, 4-nitro-o-phenylenediamine, and 2,5-toluenediamine sulfate in the mouse.

Pregnant outbred albino (CD-1) mice were given 2-nitro-p-phenylenediamine (2NPPD; 32-256 mg/kg/day), 4-nitro-o-phenylenediamine (4NOPD; 16-1024 mg/kg/day) or 2,5-toluenediamine sulfate (2,5TDS; 16-64 mg/kg/day) by subcutaneous injection on Days 6-15 of gestation. The mice were killed on Day 18, the general health and reproductive health of the dams evaluated, and the fetuses examined and processed in order to characterize external, visceral, and skeletal malformations. The 32 and 128 through 256 mg/kg/day dose levels of 2NPPD produced a significant (p less than 0.05) reduction in average weight gain by the dam during pregnancy. There was also a significance reduction in average fetal weight at 128 mg/kg/day and above. Although 2NPPD administration led to a significant increase in the average percentage of malformed fetuses at 160 mg/kg/day and above, these effects occurred only at dosages which produced significant maternal toxicity. Teratogenic effects were observed with 4NOPD, as administration of this dye led to a significance increase in the average percent of malformed fetuses at 256 mg/kg/day and above. A significant reduction in average weight gain by the dam during pregnancy also was observed at these dose levels, as well as significant reduction in average fetal weight. Although 2,5TDS killed 4 of 31 dams at 48 mg/kg/day, and 9 of 11 dams at 64 mg/kg/day, this compound did not cause a significant increase in the average percent of malformed fetuses. There were indications of embryotoxicity, however, as dosages of 32 mg/kg/day and above led to significant reductions in average fetal weight.

Abnormalities, Drug-Induced↗
PubMed1990

The mutagenic modulating effect of p-phenylenediamine on the oxidation of o- or m-phenylenediamine with hydrogen peroxide in the Salmonella test.

The mutagenicity of o- and m-phenylenediamine (PD) was remarkedly enhanced by oxidation; their major mutagenic oxidation products were 2,3- and 2,7-diaminophenazine, respectively. In order to evaluate the modulation effect of p-PD on the oxidation of m- or o-PD, p-PD and mixtures of m- and p-PD (m-PD/p-PD) and o- and p-PD (o-PD/p-PD) were oxidized with hydrogen peroxide and their mutagenicity was tested in Salmonella typhimurium TA98 in the presence or absence of a mammalian metabolic activation system (S9 mix). The H2O2-oxidized m-PD/p-PD and o-PD/p-PD were potent mutagens with S9 mix, whereas H2O2-oxidized p-PD was slightly mutagenic. The major mutagenic oxidation products of m-PD/p-PD and o-PD/p-PD were identified as 2,7- and 2,3-diaminophenazine, respectively, by TLC and HPLC. 2,8-Diaminophenazine was also found as a reaction product in oxidized m-PD/p-PD, and it was weakly mutagenic. The mutagenic potency of oxidized m-PD/p-PD or o-PD/p-PD was lower than that of singly oxidized m-PD or o-PD. The yield of 2,7- and 2,3-diaminophenazine was obviously decreased with increases in p-PD, and it was concluded that the declined mutagenic potency of oxidized m-PD/p-PD or o-PD/p-PD was due to the decrease in diaminophenazines. But the formation of diaminophenazines was not completely inhibited by the addition of a 9-fold molar ratio of p-PD to m-PD or o-PD, 8.6 nmole of 2,7-diaminophenazine and 1882.4 nmole of 2,3-diaminophenazine were formed from 1 mmole of m-PD and o-PD, respectively.

Animals↗
PubMed1979

Bioassay of 4-Nitro-o-phenylenediamine for Possible Carcinogenicity (CAS No. 99-56-9).

4-Nitro-o-phenylenediamine, a component of both semipermanent and permanent hair dye formulations, was selected for bioassay by the National Cancer Institute because of the high incidence of bladder cancer reported among workers in the dye manufacturing industry. A bioassay for the possible carcinogenicity of 4-nitro-o-phenylenediamine was conducted using Fischer 344 rats and B6C3F1 mice. 4-Nitro-o-phenylenediamine was administered in the feed, at either of two concentrations, to groups of 50 male and 50 female animals of each species. Twenty animals of each sex and species were placed on test as controls. The high and low dietary concentrations of 4-nitro-o-phenylenediamine were, respectively, 750 and 375 ppm for rats and 7500 and 3750 ppm for mice. The compound was administered for 103 weeks to rats and for 102 weeks to mice. The period of compound administration was followed by an observation period of 2 weeks for rats and mice. There were no significant positive associations between the concentrations of 4-nitro-o-phenylenediamine administered and mortality in rats or mice of either sex. Adequate numbers of animals in all groups survived sufficiently long to be at risk from late-developing tumors. Distinct dose-related mean body weight depression was observed in mice, indicating that the concentrations of 4-nitro-o-phenylenediamine administered to these animals in this bioassay may have approximated the maximum tolerated concentrations. Since no distinct mean body weightdepression relative to controls, no significantly accelerated mortality, and no other manifestations of chronic toxicity were associated with administration of 4-nitro-o-phenylenediamine to male or female rats, it is possible that these animals may have been able to tolerate a higher dietary concentration. None of the statistical tests for any site in rats or in mice of either sex indicated a significant positive association between compound administration and tumor incidence. Under the conditions of this bioassay, dietary administration of 4-nitro-o-phenylenediamine was not carcinogenic in Fischer 344 rats or B6C3F1 mice. Levels of Evidence of Carcinogenicity: Male Rats: Negative Female Rats: Negative Male Mice: Negative Female Mice: Negative Synonyms: 4-nitro-1,2-benzenediamine; 4-nitro-phenylenediamine; 4-nitro-1,2-diaminobenzene; 1,2-diamino-4-nitrobenzene; 2-amino-4-nitroaniline; 4-NO; 4-NOP; 4-NOPD; 4-N-o-PDA; C.I. 76020

Journal Article↗
PubMed1998

DNA damage induced by m-phenylenediamine and its derivative in the presence of copper ion.

To clarify the mechanism of carcinogenesis by hair dyes, we compared the extent of DNA damage induced by mutagenic m-phenylenediamine and 4-methoxy-m-phenylenediamine, using 32P-5'-end-labeled DNA fragments obtained from the human c-Ha-ras-1 protooncogene and the p53 tumor suppressor gene. Carcinogenic 4-methoxy-m-phenylenediamine caused DNA damage at thymine and cytosine residues in the presence of Cu(II). Catalase and bathocuproine, a Cu(I)-specific chelator, inhibited 4-methoxy-m-phenylenediamine-induced DNA damage, suggesting the involvement of H2O2 and Cu(I). Superoxide dismutase (SOD) enhanced the DNA damage. Formation of 8-hydroxy-2'-deoxyguanosine (8-OH-dG) was induced by 4-methoxy-m-phenylenediamine in the presence of Cu(II). UV-visible spectroscopic studies have shown that Cu(II) mediated autoxidation of 4-methoxy-m-phenylenediamine and SOD accelerated the autoxidation. On the other hand, non-carcinogenic m-phenylenediamine did not cause clear DNA damage and significant autoxidation even in the presence of Cu(II). These results suggest that carcinogenicity of m-phenylenediamines is associated with ability to cause oxidative DNA damage rather than bacterial mutagenicity.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1976

Phenylenediamine restoration of photosynthetic electron flux in DBMIB-inhibited chloroplasts.

Phenylenediamines have been studied and compared as to their effectiveness in stimulating photosynthetic electron flux in DBMIB-inhibited chloroplasts. It has been found that N-substituted as well as C-substituted p-phenylenediamines accelerate the rate of ferricyanide reduction, a photosystem II photoreaction, under conditions where the radical cations of N-substituted p-phenylenediamines are stable. The P/e2 ratios for these partial reactions are between 0.4 and 0.5; this is taken as evidence that N-substituted p-phenylenediamines are reduced by the chloroplasts close to the outer surface. Both N- and C-substituted p-phenylenediamines are capable of bypassing the site of DBMIB inhibition and restoring electron flow from water to methylviologen. N-substituted p-phenylenediamines appear to be more effective even at high concentrations of DBMIB. The P/e2 ratios for these reactions are on the order of 0.75-1.0; this is taken as evidence that the bypass reaction for N-substituted p-phenylenediamines occurs on the inside of the thylakoid membrane.

Chloroplasts↗
PubMed2006

Microbial transformation of aniline derivatives: regioselective biotransformation and detoxification of 2-phenylenediamine by Bacillus cereus strain PDa-1.

A bacterial isolate, strain PDa-1, grew well on basal medium supplemented with 2-phenylenediamine, sucrose, and ammonium nitrate and completely transformed 2-phenylenediamine. The isolate was identified as Bacillus cereus. The product formed from 2-phenylenediamine was identified by EI-MS and NMR as 2-aminoacetanilide; whole cells converted 2-phenylenediamine to the product with a 76% molar yield. Whole cells also showed a broad substrate specificity toward 20 of 26 tested arylamines with substituent groups of various size and positions. Especially 2-aminobenzoic acid, 4-aminosalicylic acid, 5-aminosalicylic acid, and 2-aminofluorene were converted completely to the corresponding product with an aminoacetyl group. Cell extracts of strain PDa-1 had a high arylamine N-acetyltransferase activity. The partially purified enzyme converted 2-phenylenediamine to 2-aminoacetanilide. Strain PDa-1 constitutively expressed the enzyme in the absence of 2-phenylenediamine. Effects of 2-phenylenediamine and 2-aminoacetanilide on growth indicated that this enzyme probably plays a role in the detoxification of toxic arylamines in this strain.

Aniline Compounds↗
PubMed1979

Bioassay of p-phenylenediamine dihydrochloride for possible carcinogenicity.

A bioassay of p-phenylenediamine dihydrochloride for possible carcinogenicity was conducted using Fischer 344 rats and B6C3F1 mice. p-Phenylenediamine dihydrochloride was administered in the feed, at either of two concentrations, to groups of 50 male and 50 female animals of each species. The high and low concentrations of p-phenylenediamine dihydrochloride were, respectively, 1,250 and 625 ppm for both rats and mice. After a 103-week period of compound administration, there were additional observation periods of 2 weeks for rats and 1 week for mice. Twenty animals of each sex and species were placed on test as controls. There were no significant positive associations between the concentrations of p-phenylenediamine dihydrochloride administered and mortality in rats or mice of either sex. Adequate numbers of animals in all groups survived sufficiently long to be at risk from late developing tumors. Slight dose-related mean body weight depression was observed in female rats and the mean body weights among high dose male rats and dosed female mice were slightly depressed in relation to their respective controls, indicating that the concentrations of p-phenylenediamine dihydrochloride administered to these animals in this bioassay may have approximated the maximum tolerated concentrations. Since no distinct mean body weight depression relative to controls, no significant accelerated mortality, and no other signs of toxicity were associated with administration of p-phenylenediamine dihydrochloride to male mice, it is possible that these animals may have been able to tolerate a higher dietary concentration. None of the statistical tests for any site in rats or mice of either sex, including time to leukemia or malignant lymphoma analysis in female mice, indicated a significant positive association between compound administration and tumor incidence. Under the conditions of this bioassay, there was no convincing evidence that dietary administration of p-phenylenediamine dihydrochloride was carcinogenic in Fischer 344 rats or B6C3F1 mice.

Journal Article↗
PubMed1987

Plant activation of m-phenylenediamine by tobacco, cotton, and carrot cell suspension cultures.

Tobacco, cotton, and carrot plant cell suspension cultures activated the promutagen m-phenylenediamine into a mutagen as detected by Salmonella typhimurium strain TA98 with the use of the plant cell/microbe coincubation assay. For each cell line, mid-log phase plant cells at a density of 100-150 mg/ml were coincubated for 1 hr with concentrations of m-phenylenediamine that ranged from 0.1 to 10 mumol per reaction tube in the preincubation test of the plant cell/microbe coincubation assay. Further experiments were conducted to optimize the activation response for each plant cell line. The density of plant cells in the reaction mixture, the time of coincubation of the reaction mixture, and the stage of the growth curve at which the plant cells were harvested for use in the reaction mixture all affected the response. Experiments that used the conditions determined as optimum for each plant cell line were then conducted. With each cell line, the optimized conditions enhanced the activation response that had been observed with the preliminary conditions. A ranking order based on the concentration-response curves indicated a relationship of tobacco cells much greater than carrot cells greater than cotton cells. Tobacco cells were able to activate m-phenylenediamine into a mutagen at concentrations of less than 10 nmol per plate when using TA98 as the genetic indicator organism. Finally, experiments to determine the type of genetic lesion induced by plant-activated m-phenylenediamine were conducted. By using five of the Ames strains, m-phenylenediamine was shown to be active in inducing revertants in strains TA1538 and TA98 following activation by tobacco cells under the optimized conditions. We conclude that m-phenylenediamine is activated by plant cells into a mutagen that primarily induces frameshift mutations.

Biotransformation↗
PubMed2004

Histogranin-like antinociceptive and anti-inflammatory derivatives of o-phenylenediamine and benzimidazole.

Histogranin (HN)-like nonpeptides were designed and synthesized using benzimidazole (compound 1) and o-phenylenediamine (compounds 2-7) as scaffolds for the attachment of phenolic hydroxyl and basic guanidino pharmacophoric elements present in HN. The benzimidazole derivative N-5-guanidinopentanamide-(2R)-yl-2-(p-hydroxybenzyl)-5-carboxybenzimidazole (1) and the o-phenylenediamine derivative N-5-guanidinopentanamide-(2S)-yl-2-N-(p-hydroxyphenylacetyl) phenylenediamine (2) were more potent analgesics than HN in both the mouse writhing (5.5 and 3.5 as potent as HN, respectively) and tail-flick (11.8 and 8.0 as potent as HN, respectively) pain assays. Improvements in the potencies and times of action of compound 2 in the mouse writhing test were obtained by attaching carboxyl (6)or p-Cl-benzoyl (7) groups at position 4 of the (2R) o-phenylenediamine derivative (5). In rats, compounds 2 (80 nmol i.t.), 6 (36 nmol i.t.), and 7 (18 nmol i.t.) were effective in blocking both persistent inflammatory pain in the formalin test and hyperalgesia in the complete Freund adjuvant assay. Compounds 2, 6, and 7, but not compound 1 at 10 nmol (i.c.v.) also mimicked the HN (60 nmol i.c.v.) blockade of N-methyl-D-aspartate (NMDA)-induced convulsions in mice. Finally, in primary cultures of rat alveolar macrophages, HN and compounds 1, 2, 6, and 7 (10(-8) M) significantly blocked lipopolysaccharide-induced cyclooxygenase-2 induction and prostaglandin E(2) secretion. These studies indicate that both derivatives of benzimidazole and o-phenylenediamine mimic the in vivo antinociceptive and in vitro anti-inflammatory effects of HN, but the HN protection of mice against NMDA-induced convulsions is mimicked only by the o-phenylenediamine derivatives.

Analgesics↗
PubMed1984

Apparent correlation between structure and carcinogenicity of phenylenediamines and related compounds.

The carcinogenicity of 23 phenylenediamines and related compounds was reviewed. An extensive analysis of the methods used indicated that the bioassays were conducted well. The data suggest that the carcinogenicity of 4-substituted 1,3-phenylenediamines is reduced substantially or eliminated completely by oxidation of one or both amine groups or by N-substitution. Oxidation of a methyl substituent on nitroaniline to a carboxyl group eliminated all carcinogenic activity. It required dichlorination to make ring-substtuted 1,4-phenylenediamine carcinogenic whereas only one chlorine atom was needed to make 1,2- and 1,3-phenylenediamine carcinogenic. While the available data suggest that as a class, 4-substituted 1,3-phenylenediamines are carcinogenic more often than ring-substituted 1,4-phenylenediamines, the type of added substituent and its position on the benzene ring also are important in exerting carcinogenic activity.

Animals↗