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PubMed2004

Kinetics and mechanism of the ferroxime(II)-catalysed biomimetic oxidation of 2-aminophenol by dioxygen. A functional phenoxazinone synthase model.

[Fe(Hdmg)(2)(MeIm)(2)](1), referred to as ferroxime(II), is the precursor of a selective catalyst for the oxidative dehydrogenation of 2-aminophenol (Hap) to 2-amino-3H-phenoxazine-3-one (apx) by dioxygen under ambient conditions. The superoxoferroxime(III) species has been detected by ES-MS, and a 4-substituted 2-aminophenoxyl free radical by the ESR technique. The kinetics of the reaction was followed spectrophotometrically and by monitoring dioxygen uptake at constant pressure. According to the proposed mechanism, solvolysis of 1 is followed by O(2) binding to afford a superoxoferroxime, which abstracts an H-atom from Hap in the rate-determining step via an H-bonded intermediate, generating the free radical. This is supported by the observed primary deuterium kinetic isotope effect of 2.63. The system studied is a functional phenoxazinone synthase model.

Aminophenols↗
PubMed1979

Postnatal development of uridine diphosphate glucuronyltransferase activity towards bilirubin and 2-aminophenol in human liver.

UDP-glucuronyltransferase activities towards 2-aminophenol and bilirubin were studied in a total of 70 human subjects, including premature and full-term newborn babies, infants, children and adults. These two activities have been reported in rat to develop latefoetally and neonatally respectively, but in man they both develop neonatally. There is a linear relationship between the logarithm of each liver transferase activity and the logarithm of the number of days after birth during the first 3 months of life, after which each activity remains constant.

Adult↗
PubMed2005

Contact vitiligo following a strong patch test reaction to triglycidyl-p-aminophenol in an aircraft industry worker: case report and review of the literature.

Epoxy resin systems (ERSs) are a frequent cause of occupational allergic contact dermatitis. A 50-year-old patient developed eczematous skin lesions on the back of his hands, lower arms and eye lids, 2 months after he had started working in aircraft construction. Patch tests showed positive reactions at day 3 to nickel sulfate, epoxy resin based on diglycidyl ether of bisphenol F (DGEBF) and 1,4-butanediol diglycidyl ether (1,4-BDDGE). The chemical triglycidyl-p-aminophenol (TGPAP) applied at 1% and 0.1% induced the strongest (+++ positive) reaction. About 4 months after the patch test with TGPAP, the patient presented with 2 circular depigmented spots in the former TGPAP-patch test areas. Dermatohistopathology confirmed the diagnosis of contact vitiligo.

Aircraft↗
PubMed1990

Filtration failure induced by p-aminophenol in rats is due to raised intratubular pressure and not changes in glomerular function.

1. The p-aminophenol (pAP) model of tubular necrosis displays elevated tubular pressures equivalent to 'stop-flow', with low glomerular filtration rate (GFR) but maintained blood flow and urine output. Renal function, micropuncture, and morphological studies were performed in anaesthetized rats to examine the causes of filtration failure. 2. At the height of pAP-induced renal failure proximal tubular fluid reabsorption (Jv(a] was markedly reduced while proximal and distal free-flow rates measured by tubular fluid collections during venting of the nephron were not significantly different from saline-injected controls. Renal blood flow was maintained over the 4 h observation period despite extensive and selective proximal tubular necrosis. There was no temporal relationship between increased tubular pressure and cast formation. 3. Maintained blood and tubular fluid flow rates indicate that activation of tubuloglomerular feedback plays little or no part in pAP-induced renal failure, which is apparently due to high fluid flow resistance in the region of the connecting tubule, late distal convolution or collecting ducts. Morphological appearances were consistent with compression of these segments.

Absorption↗
PubMed2006

Arylamine N-acetyltransferase responsible for acetylation of 2-aminophenols in Streptomyces griseus.

An arylamine N-acetyltransferase (NAT) responsible for the N acetylation of exogenous 3-amino-4-hydroxybenzoic acid in Streptomyces griseus was identified and characterized. This enzyme was distinct from other eukaryotic and bacterial NATs in that it acetylated various 2-aminophenol derivatives more effectively than it acetylated 5-aminosalicylic acid, and thus it may be involved in the metabolism of xenobiotic compounds.

Acetylation↗
PubMed2000

Airborne occupational allergic contact dermatitis from triglycidyl-p-aminophenol and tetraglycidyl-4,4'-methylene dianiline in preimpregnated epoxy products in the aircraft industry.

BACKGROUND: Very little is known about allergic contact dermatitis (ACD) from preimpregnated epoxy products (prepregs). OBJECTIVE: To describe a patient with occupational ACD from prepregs, and report new quantitative data on the content of prepregs. METHODS AND RESULTS: A laminator developed work-related vesicular hand dermatitis. He worked in an aircraft plant assembling aircraft parts, being exposed to preimpregnated carbon fiber and fiberglass sheets (prepregs), and epoxy adhesive tapes and foams. Triglycidyl-p-aminophenol (TGPAP; 1-0.25%, 2+; 0.05%, 1+) and tetraglycidyl-4,4'-methylene dianiline (TGMDA; 1%, 3+; 0.5-0.05%, 2+) provoked allergic patch test reactions, whereas o-diglycidyl phthalate was negative (1-0.05% pet) and standard epoxy provoked a weak (?+) reaction. Six prepreg products provoking allergic patch test reactions were analyzed for their TGPAP, TGMDA and diglycidyl ether of bisphenol A (DGEBA) content using gas and liquid chromatographic methods, showing up to 10% of TGPAP, 19% of TGMDA and 5% of DGEBA in the prepregs. An epoxy primer contained 61% of TGPAP. CONCLUSION: TGPAP and TGMDA caused occupational ACD. These chemicals need to be used when patch testing patients are exposed to prepregs, because patch testing with DGEBA may be negative.

Adult↗
PubMed1980

Inhibition of p-aminophenol metabolism: a possible mechanism of enhancement of aniline hydroxylation.

The p-hydroxylation of aniline has been traditionally determined by measurement of p-aminophenol (PAP) formation. Comparison of isotopic and colorimetric procedures indicate that the actual amount of aniline metabolized exceeds the among of PAP recovered. Data suggest that enhancement of p-hydroxylation of aniline by acetone, malaoxon and paraoxon may result from inhibition of further metabolism of PAP by the microsomal cytochrome b5-dependent desaturase system. Involvement of the desaturase system is supported by observations that: (a) metabolism of PAP was reduced by starvation and stimulated when starvation was followed by feeding a high carbohydrate diet; (b) enrichment of hepatic microsomes with detergent purified cytochrome b5 decreased the amount of aniline apparently metabolized, as measured by the amount of PAP recovered, and (c) a high correlation occurred between effects of acetone, malaoxon and paraoxon on reoxidation of cytochrome b5 and capacity of these three compounds to enchance aniline metabolism.

Aminophenols↗
PubMed1993

Studies on the mechanism of 4-aminophenol-induced toxicity to renal proximal tubules.

4-Aminophenol (PAP) is known to cause nephrotoxicity in the rat where it produces selective necrosis to renal proximal tubules. The aim of this work was to investigate the toxicity of PAP and its known nephrotoxic metabolite 4-amino-3-S-glutathionylphenol using a well defined suspension of rabbit renal proximal tubules. PAP at a concentration of 0.5 mM and 1 mM caused proximal tubule cell death (measured by lactate dehydrogenase release) in a time-dependent manner over a 4-h exposure. In contrast, 4-amino-3-S-glutathionylphenol at 1 mM produced no proximal tubule cell death over a similar 4-h exposure. At 2 h, 1 mM PAP inhibited proximal tubule respiration by 30% and decreased cellular adenosine triphosphate (ATP) levels by 60%. These events preceded cell death. The addition of PAP to proximal tubules led to a rapid depletion of cellular glutathione, exposure to 0.5 mM causing a 50% depletion within 1 h. The cytochrome P-450 inhibitors SKF525A (1 mM) and metyrapone (1 mM), the iron chelator deferoxamine (1 mM) and the antioxidant N,N'-phenyl-1,4-phenylenediamine (2 microM) had no effect on PAP-induced cell death. However ascorbic acid (0.1 mM), afforded a marked protection against the depletion of cellular glutathione and completely protected against the cell death produced by 1 mM-PAP. These results indicate that oxidation of PAP to generate a metabolite that can react with glutathione is an important step in the toxicity, while mitochondria appear to be a critical target for the reactive intermediate formed.

Adenosine Triphosphate↗
PubMed2000

Thermal behavior of a pharmaceutical solid acetaminophen doped with p-aminophenol.

Thermal behavior of a series of acetaminophen (APAP) doped with p-aminophenol (PANP) was studied by differential scanning calorimetry (DSC) to determine whether it exhibited a eutectic system. Within the temperature range of 120 to 200 degrees C, accurately weighed (1-2 mg) samples sealed in hermetic pans were calorimetrically scanned with a low scanning rate of 1 degrees C/min. The mixture formed a single eutectic with the composition ratio APAP/PANP of 0.6/0.4 at a temperature of 138 degrees C, where it liquefied. Melting began as early as at the eutectic point, which was below the melting temperature of APAP (169 degrees C). The melting point as well as heat of APAP fusion was depressed with the increase in doped PANP. It was postulated that there might be a deficit heat of APAP fusion in APAP doped with PANP, which was coincident with the heat consumed by early liquefaction. The deficit heat was used to correct fraction molten in the van't Hoff law of purity determination. It was found that the purity determination of APAP doped with PANP was comparable to the UV-spectroscopic method up to the maximum doped PANP level of 8 mol percent. It was concluded that DSC was able to approach early heat of liquefaction of APAP doped with PANP. The van't Hoff law may be applicable to the determination of APAP with the presence of PANP as a eutectic impurity.

Acetaminophen↗
PubMed2006

Metabolism of 4-amino-3-hydroxybenzoic acid by Bordetella sp. strain 10d: A different modified meta-cleavage pathway for 2-aminophenols.

Bordetella sp. strain 10d metabolizes 4-amino-3-hydroxybenzoic acid via 2-hydroxymuconic 6-semialdehyde. Cell extracts from 4-amino-3-hydroxybenzoate-grown cells showed high NAD(+)-dependent 2-hydroxymuconic 6-semialdehyde dehydrogenase, 4-oxalocrotonate tautomerase, 4-oxalocrotonate decarboxylase, and 2-oxopent-4-enoate hydratase activities, but no 2-hydroxymuconic 6-semialdehyde hydrolase activity. These enzymes involved in 4-amino-3-hydroxybenzoate metabolism were purified and characterized. When 2-hydroxymuconic 6-semialdehyde was used as substrate in a reaction mixture containing NAD(+) and cell extracts from 4-amino-3-hydroxybenzoate-grown cells, 4-oxalocrotonic acid, 2-oxopent-4-enoic acid, and 4-hydroxy-2-oxovaleric acid were identified as intermediates, and pyruvic acid was identified as the final product. A complete pathway for the metabolism of 4-amino-3-hydroxybenzoic acid in strain 10d is proposed. Strain 10d metabolized 2-hydroxymuconic 6-semialdehyde derived from 4-amino-3-hydroxybenzoic acid via a dehydrogenative route, not via a hydrolytic route. This proposed metabolic pathway differs considerably from the modified meta-cleavage pathway of 2-aminophenol and those previously reported for methyl- and chloro-derivatives.

4-Aminobenzoic Acid↗
PubMed2005

Biomimetic metal-radical reactivity: aerial oxidation of alcohols, amines, aminophenols and catechols catalyzed by transition metal complexes.

The contributions of the authors to the research program 'Radicals in Enzymatic Catalysis' over the last ca. 5 years are summarized. Significant efforts were directed towards the design and testing of phenol-containing ligands for synthesizing radical-containing transition metal complexes as potential candidates for catalysis of organic substrates like alcohols, amines, aminophenols and catechols. Functional models for different copper oxidases, such as galactose oxidase, amine oxidases, phenoxazinone synthase and catechol oxidase, are reported. The copper complexes synthesized can mimic the function of the metalloenzymes galactose oxidase and amine oxidases by catalyzing the aerial oxidation of alcohols and amines. Even methanol could be oxidized, albeit with a low conversion, by a biradical-copper(II) compound. The presence of a primary kinetic isotope effect, similar to that for galactose oxidase, provides compelling evidence that H-atom abstraction from the alpha-C-atom of the substrates is the rate-limiting step. Although catechol oxidase and phenoxazinone synthase contain copper, manganese(IV) complexes containing radicals have been found to be useful to study synthetic systems and to understand the naturally occurring processes. An 'on-off' mechanism of the radicals without redox participation from the metal centers seems to be operative in the catalysis involving such metal-radical complexes.

Alcohols↗
PubMed1987

Urinalysis for detection of chemically induced renal damage (2)--Changes in urinary excretions of enzymes and various components caused by p-aminophenol, puromycin aminonucleoside and hexadimethrine.

In order to establish sensitive methods of detecting minor renal damage, changes of enzymes, protein, tubular cell counts, and creatinine in the urine were investigated in rats to which nephrotoxic chemicals had been administered. Daily administration of p-aminophenol (PAP) dose-dependently increased urinary excretions of lactate dehydrogenase (LDH) and its isoenzymes (LDH5 = LDH4 greater than LDH3 greater than LDH2 = LDH1), aspartate aminotransferase (GOT), alkaline phosphatase (ALP), gamma-glutamyl transpeptidase (gamma-GTP), leucine aminopeptidase (LAP), lysozyme (LZM), N-acetyl-beta-D-glucosaminidase (NAG) and acid protease together with increased counts of tubular cells in the urine. Tubular cell counts, LDH and GOT were more sensitive indicators in the PAP tubulonephritis. Single i.v. injection of puromycin aminonucleoside (PM) dose-dependently increased urinary excretions of LDH and its isoenzymes (LDH1 = LDH5 greater than LDH2 = LDH4 greater than LDH3), GOT, NAG, acid protease and protein but degree of the increases in these enzymes was lower than those in the rats treated with PAP. PM increased excretions of high molecular weight proteins but did not increase ALP, gamma-GTP, LAP, LZM and tubular cells excretions. Single i.v. injection of hexadimethrine increased urinary excretion of LDH and its isoenzymes (LDH1 = LDH5 greater than LDH2 greater than LDH3 = LDH4), GOT, LZM, NAG and acid protease together with increased counts of tubular cells in the urine but did not increase ALP, gamma-GTP and LAP excretions. It is concluded that tubular cell counts, LDH isoenzymes and battery of these enzymes in urine are useful markers for detecting the severity and the site of renal damage in addition that urinary protein is a useful marker for detecting glomerular damage.

Aminophenols↗
PubMed2002

Comparative toxicity study of 3-aminophenol in newborn and young rats.

Repeated dose toxicity of 3-aminophenol was examined on oral administration to newborn and young rats, and susceptibility was analyzed in terms of the no observed adverse effect level (NOAEL) and the unequivocally toxic level. In the 18-day newborn rat study, starting at day 4 after birth, tremors and depression of body weight gain were observed, as well as hypertrophy of thyroid follicular epithelial cells and increases of relative liver and kidney weights at 240 mg/kg. Increase of relative liver weights in males and decrease of blood sugar in females without any histopathological changes at 80 mg/kg were not considered to be adverse effects. No chemical-related changes were observed at 24 mg/kg. Abnormalities of external development and reflex ontogeny in the newborn were not observed. In the 28-day study, starting at 5 weeks of age, depression of body weight gain, tremors, anemia, and liver, kidney and thyroid toxicity were observed at 720 mg/kg. Although slight pigmentation in the renal proximal tubular epithelium was observed in females at 240 mg/kg, this was not considered to be an adverse effect because of the lack of changes in related toxicological parameters. It was concluded that the NOAEL is 80 mg/kg/day in newborn rats and 240 mg/kg/day in young rats, with unequivocally toxic levels of 240 mg/kg/day and 720 mg/kg/day, respectively. Based on these two endpoints, the susceptibility of newborn rats to the chemical was approx. 3 times higher than that of young rats, consistent with our previous results for 4-nitrophenol and 2,4-dinitrophenol.

Aging↗
PubMed1999

The role of glutathione in p-aminophenol-induced nephrotoxicity in the mouse.

p-Aminophenol (PAP) produces nephrotoxicity in rats through a mechanism presumably involving oxidation and conjugation with glutathione (GSH). Recently it was found that PAP also causes nephrotoxicity in mice as evidenced by elevated blood urea nitrogen (BUN) and serum creatinine levels. The objective of this study was to further investigate the mechanism and elucidate the role of GSH in PAP-induced nephrotoxicity in the mouse. Male C57BL/6 mice injected i.p. with various doses of PAP were sacrificed at 12 hr for measurement of BUN and serum creatinine levels and determination of the extent of renal cortical nonprotein sulfhydryl (NPSH) and GSH depletion. PAP depleted renal cortical NPSH content in a dose- and time-dependent manner. Depletion of NPSH in mouse kidney did not occur at PAP doses below 600 mg/kg. Buthionine sulfoximine, an inhibitor of GSH synthesis, decreased nephrotoxicity. Ascorbate, a reducing agent, prevented PAP-induced nephrotoxicity and attenuated renal cortical NPSH depletion. However, acivicin and aminooxyacetic acid, inhibitors of gamma-glutamyltranspeptidase and beta-lyase, respectively, did not prevent toxicity in the mouse. Piperonyl butoxide, an inhibitor of cytochrome P-450 enzymes, enhanced nephrotoxicity and renal cysteine depletion but not GSH depletion. The results suggest that PAP-induced nephrotoxicity in the mouse may involve oxidation and formation of a GSH conjugate.

Aminophenols↗
PubMed1985

3-Hydroxykynurenine, 3-hydroxyanthranilic acid, and o-aminophenol inhibit leucine-stimulated insulin release from rat pancreatic islets.

Individual islets were isolated from rat pancreas to study the effects of tryptophan and its metabolites on leucine-stimulated release of insulin. 3-Hydroxykynurenine, 3-hydroxyanthranilic acid, and o-aminophenol were inhibitors at concentrations below 10 mM whereas tryptophan, kynurenine, kynurenic acid, xanthurenic acid, and anthranilic acid were ineffective inhibitors at concentrations up to 10 mM. A structure-activity analysis of these metabolites demonstrated that vicinal aromatic hydroxy and amino groups with their concomitant electron donating properties are required for inhibition of insulin release. Inhibition of islet insulin release by the three kynurenine metabolites may be involved in the depressed insulin levels found in vitamin B6-deficient rats by other workers.

3-Hydroxyanthranilic Acid↗
PubMed2000

Metabolism of para-aminophenol by rat hepatocytes.

Autoxidation of para-aminophenol (PAP) has been proposed to account for the selective nephrotoxicity of this compound. However, other studies suggest that hepatic metabolites of PAP rather than the parent compound may be responsible for renal damage. These studies were designed to investigate PAP metabolism in isolated hepatocytes. We synthesized several proposed metabolites for analysis by HPLC/mass spectrometry and compared those results with HPLC/mass spectrometric analyses of metabolites found after incubating hepatocytes with PAP. Hepatocytes prepared from male Sprague-Dawley rats were incubated in Krebs-Henseleit buffer at 37 degrees C for 5 h with 2.3 mM PAP under an atmosphere of 5% CO2/95% O2. Aliquots were withdrawn at 0.1 h of incubation and then hourly through 5 h of incubation. Reactions were terminated by the addition of acetonitrile. Hepatocyte viability was unaltered with PAP present in the incubation medium. We found that hepatocytes converted PAP to two major metabolites (PAP-GSH conjugates and PAP-N-acetylcysteine conjugates) and several minor metabolites [PAP-O-glucuronide, acetaminophen (APAP), APAP-O-glucuronide, APAP-GSH conjugates, and 4-hydroxyformanilide]. Preincubating hepatoyctes with 1-aminobenzotriazole, an inhibitor of cytochromes P450, did not alter the pattern of PAP metabolism. In conclusion, we found that PAP was metabolized in hepatocytes predominantly to PAP-GSH conjugates and PAP-N-acetylcysteine conjugates in sufficient quantities to account for the nephrotoxicity of PAP.

Acetylcysteine↗