Formation Of P-aminophenol Research Articles

Preparation and Electrocatalytic Activity of Bimetallic Ni-Cu Micro- and Nanoparticles

Bimetallic Ni/Cu core–shell and Cu-Ni heterostructural micro- and nanoparticles were prepared using two simple successive reduction procedures. Monometallic Ni and Cu particles were synthesized for comparison. The phase constitutions and morphological features of the particles were studied by means of X-ray diffraction, energy-dispersive X-ray spectroscopy, and scanning electron microscopy methods. All the prepared mono- and bimetallic particles were applied as electrocatalysts in the electrohydrogenation of p-nitrophenol (p-NPh). An additional electrochemical reduction of copper cations during the hydrogen saturation of Cu-containing particles was established. The prepared Ni/Cu particles exhibited the highest electrocatalytic activity with an increase in the hydrogenation rate of p-NPh by more than three times compared to its electrochemical reduction on the nonactivated cathode, and p-NPh conversion yielded the maximum values. The main product of p-NPh electrocatalytic hydrogenation over Ni-Cu particles is p-aminophenol, which is an intermediate in the synthesis of many drugs. p-Aminophenol formation is confirmed by UV-Vis spectra.

Sulfur-doped activated carbon supported platinum species as robust catalysts for nitrobenzene hydrogenation to p-Aminophenol

Nitrobenzene catalytic hydrogenation is the main synthesis method for the preparation of p-Aminophenol, but it is a great challenge to manufacture a catalyst with excellent catalytic performance. In this study, the authors explored the impact of S-doping on the catalytic performance of the platinum-based catalyst for the selective hydrogenation of nitrobenzene for p-Aminophenol production. To this end, the activated carbon carrier was modified through high-temperature calcination with an impregnation technique that incorporates organic sulfur. The study further evaluated the effects of the amount of sulfur doping on the particle size of the catalyst as well as its performance. It was theorized that the strong interaction between S and platinum (Pt) resulted in the capture of some of the Pt electrons by the sulfur-doped activated carbon carrier, reducing the reactivity of the catalyst and suppressing the over-hydrogenation side reaction. As a result, the catalyst demonstrated improved selectivity towards the formation of p-Aminophenol.

Photoluminescence as a Valuable Tool in the Optical Characterization of Acetaminophen and the Monitoring of Its Photodegradation Reactions.

In this work, new evidence for the photodegradation reactions of acetaminophen (AC) is reported by photoluminescence (PL), Raman scattering and FTIR spectroscopy. Under excitation wavelength of 320 nm, AC shows a PL band in the spectral range of 340–550 nm, whose intensity decreases by exposure to UV light. The chemical interaction of AC with the NaOH solutions, having the concentration ranging between 0.001 and 0.3 M, induces a gradual enhancement of the photoluminescence excitation (PLE) and PL spectra, when the exposure time of samples at the UV light increases until 140 min, as a result of the formation of p-aminophenol and sodium acetate. This behavior is not influenced by the excipients or other active compounds in pharmaceutical products as demonstrated by PLE and PL studies. Experimental arguments for the obtaining of p-aminophenol and sodium acetate, when AC has interacted with NaOH, are shown by Raman scattering and FTIR spectroscopy.

Mechanistic insights into acetaminophen removal on cashew nut shell biomass-derived activated carbons.

Activated carbons prepared from cashew nut shells by chemical activation with phosphoric acid were tested for the removal of acetaminophen. It was found that an increase in carbonization temperature resulted in increased pore volume and decreased amount of surface functional groups. Potentiometric titration analysis indicated that the majority of surface groups on carbons are acidic. Detailed surface characterization by FT-IR, XPS, and thermal analyses indicated the involvement of surface functional groups in the removal of acetaminophen either via hydrogen bonding or by acid hydrolysis. The carbon obtained at 600°C, which contains high amount of carboxylic groups and high pore volume, exhibited the highest adsorption capacity. For this carbon, the removal of acetaminophen took place mostly via acid hydrolysis with the formation of p-aminophenol and acetic acid adsorbed on the surface. Carbon obtained at 400°C was found to have the highest density of acidic functional groups, which resulted in dimerization reactions and pore blockage. No direct correlation was observed between the adsorption capacities of carbons and their textural or surface characteristics. This suggests the complexity of acetaminophen removal by the cashew nut shell-derived activated carbons, governed by their surface chemistry and supported by high surface area accessible via micro/mesopores.

Theoretical modeling of the mechanism of aniline oxidation by singlet O2

The mechanism of aniline oxidation by singlet oxygen was studied by the DFT-PBE/L2 method. According to the calculations, aniline endoperoxide cannot participate in the reaction because of its energy instability. The addition of 1O2 to aniline proceeds with the simultaneous proton transfer to the oxygen molecule from the NH2 group (for the syn-approach of oxygen) or from the aromatic ring (for the anti-approach). For the syn-approach of the 1O2 molecule, the HNC6H4(H)OOH intermediate is formed, whose decomposition leads to aniline p-hydroperoxide (predominantly) or p-iminoquinone. In the case of the anti-approach, the 1O2 molecule is inserted at the C–H bond to form aniline p-hydroperoxide (H2NC6H4OOH). The decomposition of aniline p-hydroperoxide with the formation of p-aminophenol and H2O2 molecule proceeds via concerted mechanism.

Remediation of a mixture of analgesics in a stirred-tank photobioreactor using microalgal-bacterial consortium coupled with attempt to valorise the harvested biomass

An artificial microalgal-bacterial consortium was used to remediate a mixture of analgesics (ketoprofen, paracetamol and aspirin) in a stirred-tank photobioreactor. A hydraulic retention time (HRT) of 3days supported poor treatment because of the formation of p-aminophenol (paracetamol toxic metabolite). Increasing the HRT to 4days enhanced the bioremediation efficiency. After applying an acclimatization regime, 95% removal of the analgesics mixture, p-aminophenol and COD reduction were achieved. However, shortening the HRT again to 3days neither improved the COD reduction nor ketoprofen removal. Applying continuous illumination achieved the best analgesics removal results. The harvested biomass contained 50% protein, which included almost all essential amino acids. The detected fatty acid profile suggested the harvested biomass to be a good biodiesel-producing candidate. The water-extractable fraction possessed the highest phenolic content and antioxidant capacity. These findings suggest the whole process to be an integrated eco-friendly and cost-efficient strategy for remediating pharmaceutical wastewater.

Evaluation of the degradation of acetaminophen by the filamentous fungus Scedosporium dehoogii using carbon-based modified electrodes.

The nonpathogenic filamentous fungus Scedosporium dehoogii was used for the first time to study the electrochemical biodegradation of acetaminophen (APAP). A carbon fiber microelectrode (CFME) modified by nickel tetrasulfonated phthalocyanine (p-NiTSPc) and a carbon paste electrode (CPE) modified with coffee husks (CH) were prepared to follow the kinetics of APAP biodegradation. The electrochemical response of APAP at both electrodes was studied by cyclic voltammetry and square wave voltammetry. p-NiTSPc-CFME was suitable to measure high concentrations of APAP, whereas CH-CPE gave rise to high current densities but was subject to the passivation phenomenon. p-NiTSPc-CFME was then successfully applied as a sensor to describe the kinetics of APAP biodegradation: this was found to be of first order with a kinetics constant of 0.11day(-1) (at 25°C) and a half-life of 6.30days. APAP biodegradation by the fungus did not lead to the formation of p-aminophenol (PAP) and hydroquinone (HQ) that are carcinogenic, mutagenic, and reprotoxic (CMR). Graphical Abstract The kinetics of APAP biodegradation, followed by a poly-nickel tetrasulfonated phtalocyanine modified carbon fiber microelectrode.

Electrochemical detection of synthetic DNA and native 16S rRNA fragments on a microarray using a biotinylated intercalator as coupling site for an enzyme label

The direct electrochemical detection of synthetic DNA and native 16S rRNA fragments isolated from Escherichia coli is described. Oligonucleotides are detected via selective post-labeling of double stranded DNA and DNA–RNA duplexes with a biotinylated intercalator that enables high-specific binding of a streptavidin/alkaline phosphatase conjugate. The alkaline phosphatase catalyzes formation of p-aminophenol that is subsequently oxidized at the underlying gold electrode and hence enables the detection of complementary hybridization of the DNA capture strands due to the enzymatic signal amplification. The hybridization assay was performed on microarrays consisting of 32 individually addressable gold microelectrodes. Synthetic DNA strands with sequences representing six different pathogens which are important for the diagnosis of urinary tract infections could be detected at concentrations of 60nM. Native 16S rRNA isolated from the different pathogens could be detected at a concentration of 30fM. Optimization of the sensing surface is described and influences on the assay performance are discussed.

Photocatalytic decomposition behavior and reaction pathway of sulfamethazine antibiotic using TiO2

The photocatalytic degradation of sulfanethazine (SMT), one of the sulfonamide antibiotics, in aqueous solution by TiO2 was investigated. The time courses of SMT concentration, the amount of non-purgeable organic carbon, and the concentrations of ions such as SO42−, NH4+, and NO3− formed during the photocatalytic reaction were measured and the structures of seven intermediates formed with the disappearance of SMT were also estimated by LC/MS/MS analyses. In addition to that of SMT, the decomposition behaviors of model compounds sulfanilic acid (SA) and 4-amino-2, 6-dimethylpyrimidine (ADMP) were investigated using the TiO2/UV system. The observed photocatalytic degradation behaviors of SMT, SA, and ADMP gave new insight into the degradation pathway of SMT. Especially, the formation of p-aminophenol during SMT decomposition, which until now has not been reported in previous studies concerning the photocatalytic decomposition of SMT and other sulfonamide antibiotics. These results indicate the existence of a novel photocatalytic degradation pathway for sulfonamides. The direct substitution of the sulfonamide group with a hydroxyl group is suggested.

Facile synthesis of highly catalytic activity Ni–Co–Pd–P composite for reduction of the p-Nitrophenol

A simple hydrothermal method was developed for the one-step synthesis of an urchin-like Ni@Ni3P@CoP2@P composite. p-Nitrophenol can be completely reduced to p-Aminophenol using the as-synthesized composites as catalysts, and the reaction was monitored by UV–vis spectroscopy. Further research implied that the presence of Co greatly improves the catalytic ability of the composites for the reduction of p-Nitrophenol . Palladium (Pd) nanoparticles (NPs) were subsequently loaded into the Ni–Co–P composites to obtain better catalytic effects. Aside from excellent catalytic ability for reducing p-Nitrophenol, the strong magnetism of the as-prepared Ni–Co–Pd–P composites allowed the facile collection of the catalysts from the reaction system. After using the as-synthesized Ni–Co–Pd–P compounds seven times every 15min, recyclability was estimated by monitoring the formation of p-Aminophenol using the catalysts via UV–vis spectroscopy. The as-synthesized Ni–Co–Pd–P composites presented good catalytic ability and excellent recyclability for the reduction of p-Nitrophenol .

Effects and mechanisms of rifampin on hepatotoxicity of acetaminophen in mice

This study examined the effects and possible mechanisms of rifampin against acetaminophen-induced hepatotoxicity in mice. Rifampin significantly enhanced the biotransformation of acetaminophen, evidenced by the increase in p-aminophenol formation in rifampin-treated microsomes and the increase in plasma clearance rate of acetaminophen. Pretreatment with rifampin significantly decreased serum alanine transaminase (ALT) activities, aspartate transaminase (AST) activities and prevented severe liver necrosis following acetaminophen overdose. The contents and activities of microsomal drug-metabolizing enzyme were less affected in rifampin-pretreated mice in comparison to the animals treated with acetaminophen alone. Rifampin was capable of increasing glutathione (GSH) level and GSH reductase activity and reducing GSH depletion and the decrease in GSH reductase activity by acetaminophen in mice. In addition, it was found that the microsomal Ca2+-ATPase activity was not directly related to acetaminophen toxic species generated in the P450 enzyme system in vitro. These findings suggest that rifampin has species-specific effects on the liver against acetaminophen-induced hepatotoxicity in mice, which increase the level of GSH by promoting GSH regeneration.

Hydrogenation of Nitrobenzene to 4-Aminophenol over Supported Platinum Catalysts

The conversion of nitrobenzene (NB) to p-aminophenol (PAP) takes place by way of an initial partial hydrogenation to produce phenylhydroxyl amine (PHA) which then undergoes an in situ acid-catalyzed rearrangement to PAP. This reaction is most commonly run using Pt/C catalysts in the presence of aqueous sulfuric acid and a surfactant to assist in dispersing the NB throughout the reaction medium. The yield of PAP is closely related to those reaction parameters which facilitate first the partial hydrogenation step and second the acid-promoted rearrangement before further hydrogenation to aniline can take place. The effect which a number of reaction parameters such as hydrogen pressure, reaction temperature, stirring rate, and the amounts of NB, the catalyst, and the surfactant present in the reaction mixture had on the rate and selectivity of the hydrogenation was examined. Optimization of these parameters led to the formation of PAP at a selectivity (PAP/AN) of 5.4 with a productivity of over 80,000 g PAP/g...

Hydrogenation of p-nitrophenol to metol using Raney nickel catalyst: Reaction kinetics

Kinetics of the liquid-phase catalytic hydrogenation of p-nitrophenol (PNP) to p-aminophenol (PAP) and its conversion to metol have been investigated over a wide range of operating conditions. The effects of speed of agitation, hydrogen partial pressure, catalyst loading, substrate concentration and temperature on both the reactions have been reported. The effects of various solvents (2-propanol, methanol, dimethylformamide) on both the reactions have been investigated. Both the reactions were found to be first order with respect to the hydrogen partial pressure, first order with respect to PNP concentration for PAP formation and zero order with respect to substrate for metol formation. The experimental data could be fitted to the model involving a surface reaction controlling mechanism with dissociative adsorption of hydrogen for PNP hydrogenation and molecular adsorption of hydrogen for metol formation. The activation energies for the catalytic hydrogenation of PNP and metol formation were found to be 47 and 51 kJ mol −1, respectively.

Degradation of p-nitrophenol in a batch biofilter under sequential anaerobic/aerobic environments

A combined process anaerobic/aerobic in a single reactor was studied, P-nitrophenol (PNP) was used as the model compound. During the anaerobic stage the target compound is modified in such a way that the intermediate product is more readily biodegradable by the aerobic phase. A pilot biofilter was used for the experiment. The biofilter was packed with a volcanic stone (puzolane) to serve as support to the microorganisms and it was inoculated with activated sludge. The microorganisms were acclimated with an initial concentration of 25 mg PNP/l during 75 days (25 cycles). After 230 days of operation, the reaction time of the cycles was reduced to 11.5 h (8 h for the anaerobic phase and 3.5 h for the aerobic one). The PNP was transformed to p-aminophenol (PAP) in the anaerobic phase, with efficiencies near to 100%. A mineralization of 100% of the PAP was found in the oxidative stage. Global efficiencies of PNP mineralization of 98% were obtained. The reaction rates were 16 mg PNP/l-h (PNP uptake), 14 mg PAP/l-h (PAP formation) and 20 mg/l-h (PAP mineralization).

Glucose formation from methylglyoxal in hepatocytes from streptozotocin-induced diabetic mice: the effect of insulin.

Acetol and methylglyoxal are intermediates of the intrahepatic metabolism of acetone leading to pyruvate formation. In hepatocytes prepared from fasted streptozotocin-induced diabetic mice, net glucose production could be measured from methylglyoxal but not from acetone or acetol. Insulin increased glucose formation from methylglyoxal in a concentration-dependent manner, whereas it was ineffective when pyruvate was used as substrate. Drug oxidation, as evidenced by p-aminophenol formation from aniline, was enhanced by methylglyoxal, and insulin proved to be stimulatory in this case as well. It is concluded that insulin might be involved in the regulation of glucose formation from methylglyoxal, but its mode of action is not yet clear.

P-Nitrosophenol Reduction by Liver Cytosol from ADH-Positive and -Negative Deermice (Peromyscus maniculatus)

Liver cytosolic fractions are known to catalyze the reduction of certain C-nitroso compounds to their corresponding hydroxylamines and amines. Alcohol dehydrogenase (ADH), NAD(P)H:quinone oxidoreductase, and xanthine and aldehyde oxidases have been implicated as C-nitroso reductases, To probe the role of these cytosolic enzymes in the reduction of C-nitroso compounds we have studied the effects of classical inhibitors of these enzymes on the ability of liver cytosolic fractions from ADH+ and ADH− deermice to reduce p-nitrosophenol to p-aminophenol. Pyrazole, a potent inhibitor of ADH, inhibited NADH-p-nitrosophenol reduction by ADH+ cytosol by > 85%. Thus, ADH contributes substantially to NADH-C-nitroso reduction by cytosol from ADH+ deermice. The NAD(P)H: quinone oxidoreductase inhibitor, dicumarol, inhibited NADH-dependent p-aminophenol formation by about 25%; however, dicumarol potently inhibited the NADPH-dependent formation (90-95%). As expected, cytosol from ADH− deermice did not catalyze pyrazole-sensitive (ADH-dependent) C-nitroso reduction with NADH as the cofactor. Both NADPH- and NADH-p-nitrosophenol reduction by ADH− cytosol were inhibited >90% by dicumarol. The xanthine oxidase/aldehyde oxidase inhibitor, allopurinol, was without effect on NAD(P)H cytosolic p-nitrosophenol reduction from ADH− and ADH+ deermice under either aerobic or anaerobic conditions. Our findings suggest that in the ADH+ animal, ADH contributes significantly to NADH-dependent C-nitroso reduction by cytosol relative to NAD(P)H:quinone oxidoreductase. NADPH-dependent p-nitrosophenol reduction by liver cytosol of ADH+ animals is mostly dicumarol-sensitive, which implicates NAD(P)H:quinone oxidoreductase as the major NADPH-dependent activity. In ADH− deermice, both NADH- and NADPH-dependent p-nitrosophenol reduction are essentially dicumarol-sensitive (NAD(P)H: quinone oxidoreductase-dependent). Because the toxic expression of C-nitroso compounds is mediated by hydroxylamine intermediates, the present data indicate the importance of considering the role of ADH in the toxic sequelae of nitro and nitroso arenes.

Metabolism of 2-Nitrosofluorene andp-Nitrosophenol by Horse Liver Alcohol Dehydrogenase (HLADH)

Abstract Reductive metabolism of C-nitroso substrates to their corresponding hydroxyl amines is thought to be requisite to the activation of these compounds to mutagenic products. We have studied 2-nitrosofluorene (2-NOF) and p-nitrosophenol (p-NSP) as aldehyde substrate analogs for HLADH. The direct product of 2-NOF reduction is N-hydroxy-2-aminofluorene (N-OH-2-AF), which undergoes further reduction to 2-aminofluorene (2-AF) and rearrangement to 1- and 3-hydroxy-2-aminofluorene (1- and 3-OH-2-AF). The formation of these products is inhibited by pyrazole, indicating the involvement of active-site zinc ion in the role of a Lewis acid. It is suggested that the rearrangement reaction occurs via elimination of the hydroxyl group from the N-OH-2-AF and hydrolysis of the fluorenyl nitrenium-derived carbocations to yield the hydroxy 2-AF products. HLADH-dependent metabolism of p-NSP results in formation of p-aminophenol, which appears to proceed at pH above 6 via a spectral intermediate at ∽255 nm, but does not at pH below 6. It is suggested that the reduction of p-NSP proceeds via two-step reduction involving concomitant dehydration of p-hydroxylaminophenol to p-benzoquinoneimine. At pH above 6 the reduction of p-benzoquinoneimine to p-aminophenol is rate-limiting.

The role of p-aminophenol in acetaminophen-induced nephrotoxicity: Effect of bis( p-nitrophenyl) phosphate on acetaminophen and p-aminophenol nephrotoxicity and metabolism in Fischer 344 rats

Acetaminophen (APAP) produces proximal tubular necrosis in Fischer 344 (F344) rats. Recently, p-aminophenol (PAP), a known potent nephrotoxicant, was identified as a metabolite of APAP in F344 rats. The purpose of this study was to determine if PAP formation is a requisite step in APAP-induced nephrotoxicity. Therefore, the effect of bis( p-nitrophenyl) phosphate (BNPP), an acylamidase inhibitor, on APAP and PAP nephrotoxicity and metabolism was determined. BNPP (1 to 8 m m) reduced APAP deacetylation and covalent binding in F344 renal cortical homogenates in a concentration-dependent manner. Pretreatment of animals with BNPP prior to APAP or PAP administration resulted in marked reduction of APAP (900 mg/kg) nephrotoxicity but not PAP nephrotoxicity. This result was not due to altered disposition of either APAP or acetylated metabolites in plasma or renal cortical and hepatic tissue. Rather, BNPP pretreatment reduced the fraction of APAP excreted as PAP by 64 and 75% after APAP doses of 750 and 900 mg/kg. BNPP did not alter the excretion of APAP or any of its non-deacetylated metabolites nor did BNPP alter excretion of PAP or its metabolites after PAP doses of 150 and 300 mg/kg. Therefore, the BNPP-induced reduction in APAP-induced nephrotoxicity appears to be due to inhibition of APAP deacetylation. It is concluded that PAP formation, in vivo, accounts, at least in part, for APAP-induced renal tubular necrosis.

Metabolism and nephrotoxicity of phenacetin and sulfanilamide.

The mechanisms of renal damage produced by sulfanilamide and phenacetin were studied. N-Hydroxyphenacetin, 4-hydroxylaminobenzenesulfonamide (4-HABSA) and p-aminophenol were established to be nephrotoxic metabolites. As well as N-hydroxylase activity of sulfanilamide, that of phenacetin in kidney microsomes of rats was increased about 4 times by pretreatment with 3, 4, 5, 3', 4'-pentachlorobiphenyl (PenCB) which is a potent inducer of cytochrome P-448. Parallel to this enzyme induction, pretreatment with PenCB enhanced the nephrotoxicity of phenacetin and sulfanilamide in rats. On the other hand, the formation of p-aminophenol from phenacetin was also confirmed in rat kidney in vitro. These results suggested that 4-HABSA, N-hydroxyphenacetin and p-aminophenol formed in kidney play an important role in the renal damage produced by sulfanilamide and phenacetin.

Nephrotoxicity of p-aminophenol, a metabolite of acetaminophen, in the Fischer 344 rat

Acetaminophen (APAP) produces proximal tubular necrosis in the Fischer 344 rat. APAP is deacetylated to p-aminophenol (PAP) in the hamster, and PAP has been reported to be a potent specific cortical nephrotoxicant in the rat. However, the role of PAP in APAP nephrotoxicity has not been defined. Therefore, it was of interest to quantify PAP formation after APAP administration and to correlate PAP formation with renal injury produced by APAP in the Fischer 344 rat. Urinary PAP excretion, measured as an index of PAP formation, increased with increasing doses of APAP. In addition, APAP was metabolized to PAP in isolated perfused kidneys. PAP at doses as low as 100 mg/kg produced significant renal toxicity (elevation in blood urea nitrogen and reduction in accumulation of p-aminohippurate by thin renal cortical slices). Ortho- and meta-aminophenol were not nephrotoxic. Pretreatment with polybrominated biphenyls or β-naphthoflavone, inducers of mixed function oxidases, protected against nephrotoxicity of PAP, possibly as a result of enhanced hepatic biotransformation of the parent compound. These studies indicate that PAP is a potent, selective nephrotoxicant that can be generated from APAP by the kidney and may be responsible for the renal necrosis subsequent to APAP administration.