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PubMed1991

[The effect of the acetanilide herbicide Acetochlor on the cardiovascular system of white rats].

A study is performed on the long-term effect of the chloracetanilide herbicide "Acetochlor" in doses 21.0; 10.6: 5.5 and 2.6 mg/kg-1 in conditions of 6-month oral application and 2-month rehabilitation period on the metabolite processes and the balance of the connective-tissue components in the myocardium and aorta of male white rats. A complex of biochemical and histological methods are performed (activity of succinate dehidrogenase, lactate dehydrogenase, glucose-6-phosphate dehydrogenase, adenosin triphosphatase, cytochrome oxidase, fructoso-1,6-diphosphatase, level of the thiol groups, soluble globular, elastine, collagen fractions, insoluble collagen and elastine, general and sulphated glucosamino glycanes). The dose 21.0 mg/kg-1 leads to blocking of the thyol groups, inactivation of succinate dehydrogenase, cytochrome oxidase, adenosin triphosphatase, fructose-1,6-diphosphatase, glucose-6-phosphate dehydrogenase, activation of lactate dehydrogenase, decrease of the soluble globular, elastine, and collagen fractions and increase of the glucoseaminoglycanes in the heart muscle and aorta. The changes established in the heart muscle at 10,6 mg/kg-1 certify for stronger sensitivity of the organ of the aorta wall. The presence of single changes in the examined indices, their complete dying out after the rehabilitation period and absence of structural changes in the myocardium and aorta permit the dose of 5.5 mg/kg-1 to be accepted as not effective in the conditions of chronic experiment concerning the cardiovascular system.

Administration, Oral↗
PubMed1991

[Biochemical and histological changes after acute oral poisoning with the acetanilide herbicide acetochlor].

Changes in the liver of male rats were studied on the 1, 3, 5, 7, 10 and 14 days after a single oral application of 1/5 DL 50 of the chloracetanilic herbicide Acetochlor (DL50 = 1063 mg/kg-1). Two main periods in the action of acetochlor can be identified: between 1-2 days when the influence of the compound itself is predominant and between 5-7 days, when the toxic action of the slowly eliminated metabolites is most pronounced. These two periods provoke a biphasic activation/inhibition response of the liver. Remarkable is the compensatory effect of the cytochrome P-450 system responsible for the metabolism of acetochlor. The phase-specific changes were are followed by pathomorphological observations of liver tissue as well as by the time-course of the biochemical parameters studied in different liver fractions.

Administration, Oral↗
PubMed1994

Peroxidase-catalyzed oxidation of azo dyes: mechanism of disperse Yellow 3 degradation.

Disperse Yellow 3 [2-(4'-acetamidophenylazo)-4-methylphenol] (DY3) (I) is an important yellow dye used in industry and is also a carcinogen. Earlier we demonstrated that lignin-degrading cultures of white-rot basidiomycete Phanerochaete chrysosporium degrade DY3 to CO2. In this report, we have examined the degradation of DY3 and its naphthol analog, 1-(4'-acetamidophenylazo)-2-naphthol (NDY3) (II) by lignin peroxidase, horseradish peroxidase, and Mn(III)-malonate complex (a manganese peroxidase mimic). Lignin and manganese peroxidases are two extracellular peroxidase produced by ligninolytic cultures of P. chrysosporium and are involved in the degradation of lignin and various other environmental pollutants by this fungus. DY3 oxidation by peroxidases yields 4-methyl-1,2-benzoquinone (III), acetanilide (IV), and a dimer of DY3 (V) as products. NDY3 oxidation yields acetanilide (IV) and 1,2-naphthoquinone (VI). In deuterium incorporation experiments with DY3, 55-67% incorporation of deuterium from dioxane-d8 into acetanilide (IV) is observed. However, when D2O is the donor, deuterium is not incorporated into acetanilide (IV). Based on these results, a mechanism for azo dye degradation is proposed. The H2O2-oxidized forms of a peroxidase oxidize the phenolic ring of DY3, or its analogs, by two electrons to produce a carbonium ion, which is located on the carbon bearing the azo linkage. Water attacks the carbonium ion, producing an unstable intermediate which breaks down to generate 1,2-naphthoquinone (VI) or 4-methyl-1,2-benzoquinone (III) and 4-acetamido-phenyldiazene. O2, H2O2-oxidized peroxidase, or a metal ion, oxidize the phenyldiazene by one electron to produce a phenyldiazene radical, which cleaves homolytically to generate 4-acetamidophenyl radical and molecular nitrogen. The 4-acetamidophenyl radical then abstracts a hydrogen radical from the surroundings to produce acetanilide (IV). DY3 degradation by whole cultures of P. chrysosporium yields acetanilide as the major product. This suggests that lignin peroxidase and manganese peroxidase are involved in the in vivo metabolism of DY3 by P. chrysosporium.

Acetanilides↗
PubMed1979

Metabolism of 2-chloro-N-isopropylacetanilide (propachlor) in the rat.

Eleven urinary metabolites from [14C]propachlor were either identified or characterized by mass spectrometry. Those identified were 2-[S-(N-acetyl)cysteinyl]-N-isopropylacetanilide, 2-(methylsulfonyl)-acetanilide, 4'-hydroxy-2-(methylsulfonyl)-acetanilide, and 4'-hydroxyacetanilide. Those characterized were N-(1-hydroxyisopropyl)-2-(methylsulfonyl) acetanilide and its glucuronide, the glucuronides of 4'-hydroxy-N-isopropyl-2-(methylsulfonyl)acetanilide, N-(1-hydroxyisopropyl) aniline, 4'-hydroxy-2-(methylsulfonyl)acetanilide, and either N-(1-hydroxy-isopropyl) acetanilide or 2-hydroxy-N-isopropylacetanilide.

Acetanilides↗
PubMed1970

Herbicide transformation. II. Studies with an acylamidase of Fusarium solani.

Replacement cultures liberated 3,4-dichloroaniline (DCA) from 3,4-dichloropropionanilide (propanil). The kinetics of the conversion suggest a requirement for de novo enzyme synthesis, but the system was not influenced by chloramphenicol or puromycin. Enzyme activity was detected when acetanilide (K(m) = 0.195 mm) was used to replace propanil as substrate. Fungal acylamidase (E.C. 3.5.1., an aryl acylamine amidohydrolase) was concentrated by salt precipitation and characterized. The Fusarium solani acylamidase exhibited an optimum at pH 7.5 to 9.0 and was inactivated in 10 min at 50 C. The enzyme was not sensitive to methyl-carbamate or organophosphate insecticides, but the herbicide, Ramrod (N-isopropyl-2-chloroacetanilide), acted as a competitive inhibitor of acetanilide hydrolysis (K(i) = 0.167 mm). Hydrolysis rates were decreased by various para substitutions of acetanilide. Chloro substitution in the acyl moiety of acetanilide also reduced the rate of hydrolysis. 3,4-Dichloroacetanilide was less susceptible to enzyme action than acetanilide, but 3,4-dichloropropionanilide was hydrolyzed much more rapidly than propionanilide. The fungal acylamidase was highly specific for N-acetylarylamines. It did not catalyze hydrolysis of formanilide, butyranilide, dicryl, Karsil, fenuron, monuron, or isopropyl-N-phenylcarbamate. It appears to differ from acylamidases that have been isolated from rice, rat liver, chick kidney, and Neurospora.

Acetanilides↗
PubMed2000

Herbicides and herbicide degradates in shallow groundwater and the Cedar River near a municipal well field, Cedar Rapids, Iowa.

Water samples were collected near a Cedar Rapids, Iowa municipal well field from June 1998 to August 1998 and analyzed for selected triazine and acetanilide herbicides and degradates. The purpose of the study was to evaluate the occurrence of herbicides and herbicide degradates in the well field during a period following springtime application of herbicides to upstream cropland. The well field is in an alluvial aquifer adjacent to the Cedar River. Parent herbicide concentrations generally were greatest in June, and decreased in July and August. Atrazine was most frequently detected and occurred at the greatest concentrations; acetochlor, cyanazine and metolachlor also were detected, but at lesser concentrations than atrazine. Triazine degradate concentrations were relatively small (< 0.50 microg/l) and generally decreased from June to August. Although the rate of groundwater movement is relatively fast (approx. 1 m per day) in the alluvial aquifer near the Cedar River, deethylatrazine (DEA) to atrazine ratios in groundwater samples collected near the Cedar River indicate that atrazine and DEA probably are gradually transported into the alluvial aquifer from the Cedar River. Deisopropylatrazine (DIA) to DEA ratios in water samples indicate most DIA in the Cedar River and alluvial aquifer is produced by atrazine degradation, although some could be from cyanazine degradation. Acetanilide degradates were detected more frequently and at greater concentrations than their corresponding parent herbicides. Ethanesulfonic-acid (ESA) degradates comprised at least 80% of the total acetanilide-degradate concentrations in samples collected from the Cedar River and alluvial aquifer in June, July and August; oxanilic acid degradates comprised less than 20% of the total concentrations. ESA-degradate concentrations generally were smallest in June and greater in July and August. Acetanilide degradate concentrations in groundwater adjacent to the Cedar River indicate acetanilide degradates are transported into the alluvial aquifer in a manner similar to that indicated for atrazine and DEA.

Acetamides↗
PubMed1982

Drug-induced antinuclear antibodies in the guinea pig.

Antinuclear antibodies (ANA) development was studied in male guinea pigs in response to chronic treatment with procainamide, hydralazine, acetanilide or caffeine. Acetanilide and caffeine have not previously been associated with ANA induction. Fifty-one weanling Hartley guinea pigs were divided into five groups which received either procainamide, hydralazine, acetanilide, caffeine or saline sc for 55 weeks; drug dosage was 10 mg/kg initially and was increased incrementally to 40 mg/kg by 10 months except for hydralazine, which was increased to 20 mg/kg. Two weeks before initiation of treatment, 1 mg of the appropriate drug in 0.4 ml of buffered Freund's complete adjuvant (FCA-PBS) was administered intradermally. Controls received FCA-PBS only. Sera ANA were assayed at 6, 10 and 13 months. After 13 months of treatment, those sera which were ANA positive were assayed for anti-deoxyribonucleoprotein antibodies and were titered for ANA. Chi-square analyses were performed on results of the 10- and 13-month ANA screening results. ANA induction was significant at P = 0.05 only for the group receiving procainamide at both 10 and 13 months of treatment. When the cumulative results of all ANA screens were analyzed, ANA induction was significant for procainamide, acetanilide and caffeine. The test system did not prove to be promising for unambiguous identification of drugs with ANA-inducing potential, but may be useful for studies of mechanisms of ANA induction by chemicals.

Acetanilides↗
PubMed1993

Generalized cytochrome P450-mediated oxidation and oxygenation reactions in aromatic substrates with activated N-H, O-H, C-H, or S-H substituents.

1. The general mechanism of metabolic oxidation of substrates by cytochromes P450 (P450s) appears to consist of sequential one-electron oxidation steps rather than of a single concerted transfer of activated oxygen species from P450 to substrates. 2. In case of the acetanilides paracetamol (PAR), phenacetin (PHEN), and 4-chloro-acetanilide (4-CLAA), the first one-electron oxidation step consists of a hydrogen abstraction from the acetylamino nitrogen and/or from the other side-chain substituent on the aromatic ring. The substrate radicals thus formed delocalize their spin and the respective reactive centres of the substrate radical recombine with a P450 iron-bound hydroxyl radical to either yield oxygenated metabolites, or undergo a second hydrogen abstraction forming dehydrogenated products. By this mechanism, the formation of all known oxidative metabolites of PAR, PHEN, and 4-ClAA can be explained. Furthermore, this mechanism is consistent with all available experimental data on [18O]PAR/PHEN, [2H]PAR, and [14C]PHEN. 3. The oxidative metabolic reactions proposed for the acetanilides PAR, PHEN, and 4-ClAA are used to generalize P450-mediated oxidations of these and other acetanilides, such as analogues of PAR and 2-N-acetyl-aminofluorene. 4. A further generalization of the hydrogen abstraction, spin delocalization, radical recombination concept is derived for other aromatic substrates with abstractable hydrogen atoms, notably those with activated N-H, O-H, C-H, or S-H bonds directly attached to the aromatic nucleus.

Acetaminophen↗
PubMed1983

Selective induction of xenobiotic metabolizing esterases/amidases of liver by methaqualone consumption.

The present investigation reports the influence of po and ip methaqualone administration on the hydrolytic metabolism of acetylsalicylic acid, procaine, p-nitrophenylacetate, acetanilid, and butyrylcholine in the liver, kidney, and brain of male rats. Oral administration of methaqualone (60 mg/kg/day) to rats for 20 days caused 41.0, 46.5, and 55.0% stimulation of acetylsalicyclic acid esterase I, acetylsalicyclic acid esterase II, and acetanilid N-deacetylase, respectively, in the liver. Under such conditions, the activities of other esterases remained unaffected. The responses of tissue esterases to ip methaqualone treatment (40 mg/kg/day for 6 days) were similar to those observed after po methaqualone administration. Since a single po dose of methaqualone failed to produce any alteration in the rate of metabolism of acetylsalicylic acid, procaine, p-nitrophenylacetate, acetanilid, and butyrylcholine within 20 hr, it may be interpreted that the stimulation of acetylsalicylic acid and acetanilid metabolism is possibly due to selective enhanced de novo synthesis of the enzymes/isozymes necessary for the hydrolysis of the two drugs. The ability of the kidney and brain to metabolize the esters/amides was not modified by po or ip methaqualone pretreatment suggesting the possibility of noninducible forms of renal and neuronal esterases/amidases.

Amidohydrolases↗
PubMedDate not supplied

Further studies of metyrapone effects upon anilide hydroxylation.

The enhancing effect of metyrapone upon the p-hydroxylation of acetanilide has been confirmed with the use of a new gas-chromatographic method for the determination of acetaminophen. This effect has been shown not to be due to inhibition of hydrolysis of acetaminophen or interference with its determination, or to preferential formation of other phenolic metabolites. This effect of metyrapone is remarkably substrate-specific: phenol formation from the homologues of acetanilide, formanilide and propionanilide, and that from the sulfonamide analog of acetanilide, methanesulfonanilide, is inhibited by metyrapone over the concentration range in which acetanilide hydroxylation is enhanced. The same substrate specificity was observed when the modifier was acetophenone. alpha,alpha'-Dipyridyl, however, enhances phenol formation from all three carbonacylanilides, but does not affect that from methanesulfonanilide.

2,2'-Dipyridyl↗
PubMedDate not supplied

Use of the NIH shift to determine the relative contribution of competing pathways of aniline metabolism in the rat.

The retention of tritium in urinary p-aminophenol and p-hydroxyacetanilide was determined following the administration of p-3H-aniline or p-3H-acetanilide to rats. When p-3H-aniline (1.5 mmol/kg, ip) was given to rats, the retention of tritium in urinary p-aminophenol and p-hydroxyacetanilide was 15% and 38%, respectively. Similar results were obtained following the administration of p-3H-acetanilide (1.5 mmol/kg). However, when p-3H-acetanilide was given to rats which had been pretreated with bis-(p-nitrophenyl)phosphate to block the deacetylation capacity, urinary 3H-p-hydroxyacetanilide was recovered with 53% retention of tritium. The data indicate that, at the doses studied: the primary route of aniline metabolism is via sequential acetylation and hydroxylation, and deacetylation plays a significant role in the disposition of acetanilide.

Acetylation↗
PubMed1980

Ontogenetic expression of regulatory and structural gene products associated with the Ah locus. Comparison of rat, mouse, rabbit and Sigmoden hispedis.

The murine Ah complex represents a 'cluster' of genes controlling the induction of numerous cytochrome P-450-mediated monooxygenase 'activities' by polycyclic aromatic compounds. These forms of cytochrome represent structural gene products. A major regulatory gene product is a cytosolic receptor to which radiolabeled 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD) binds with very high affinity. Developmental differences in mouse, rat and rabbit liver have been previously reported, indicating that some form of temporal control exists during the induction of enzymes associated with the ah locus. The cytosolic receptor levels were determined by sucrose density gradient centrifugation after dextran-charcoal treatment. Hepatic receptor levels, beta-naphthoflavone-inducible and control aryl hydrocarbon hydroxylase (EC 1.14.14.2) and acetanilide 4-hydroxylase activities and total P-450 content were studied in the Sprague-Dawley rat, C57BL/6N mouse, New Zealand White rabbit and Sigmoden hispedis (cotton rat) as a function of age. 3-Methylcholanthrene-inducible and control aryl hydrocarbon hydroxylase and acetanilide 4-hydroxylase activities in nonhepatic tissues of the neonatal and adult rabbit were examined. beta-Naphthoflavone-inducible hepatic microsomal proteins detectable by sodium dodecyl sulfate-polyacrylamide gel electrophoresis were also studied in the four species. Taken altogether, the developmental data indicate that: the form of P-450 responsible for induced aryl hydrocarbon hydroxylase activity is not the same as that for induced acetanilide 4-hydroxylase, and neither one is the same as induced cytochrome P-448; the presence of the TCDD-specific cytosolic receptor per se (detected as a distinct high-specificity saturable peak on sucrose density gradients) does not guarantee the expression of inducible aryl hydrocarbon hydroxylase or acetanilide 4-hydroxylase activity; although interesting developmental differences exist among all four species examined, the TCDD-specific receptor is maximal between the neonatal and weaning period, is considerably decreased in the adult, and is suppressed even more during the latter half of pregnancy; in general, the times at which the cytosolic receptor is highest or lowest parallels quite closely the well-known increases in inducible drug-metabolizing enzymes that have been commonly observed in the rat, mouse and other laboratory animals, and more studies are necessary before we understand what the 'TCDD-specific binding peak' (as observed on the sucrose density gradients) actually represents.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1984

In vitro deacetylation studies of acetamidophenolic compounds in rat brain, liver and kidney.

The in vitro deacetylation of ortho-, meta- and para-substituted acetophenetidines and acetamidophenols including acetanilide by arylacylamidases in rat brain, liver and kidney was investigated. In general, deacetylation rates were highest in liver and kidney preparations, whereas brain exhibited lower enzyme activities. Acetophenetidines were more suitable N-deacetylation substrates in comparison to acetamidophenols, whereby o-substituted compounds were split more easily than their corresponding m- or p-analogues. Among the arylacylamides tested, o-acetophenetidine was the predominant substrate in all tissues. It was deacetylated by far more rapidly than phenacetin. The enzymic deacetylation of acetophenetidines in kidney and brain was inhibited by p-nitrophenylacetate revealing that N-acetylamides as well as O-acetyl esters undergo similar degradation by carboxylesterase-amidases. The organophosphorous diester bis(p-nitrophenyl)-phosphate which is known to be a rather selective inhibitor of acetanilide-cleaving hydrolases in rat liver suppressed the deacetylation of acetanilide in all tissues investigated. In contrast to acetanilide, the deacetylation of acetophenetidines was inhibited by bis(p-nitrophenyl)-phosphate in liver and kidney, but bis(p-nitrophenyl)-phosphate was by far less active against acetophenetidine hydrolases in brain.

Acetamides↗
PubMed1991

In vitro studies on the deacetylation-reacetylation of arylamides and the transacetylation of arylamines by human and rat whole blood.

Human and rat whole blood were shown to metabolize the aromatic amides acetanilide and phenacetin by deacetylation followed by reacetylation in vitro. Derivatives of the parent compounds labelled with deuterium in the N-acetyl group produced non-labelled material after incubation. The reaction was monitored by capillary gas chromatographic-mass spectrometric (GC-MS) analysis. There was no significant difference in the acetyl group exchange of these substrates using blood samples donated by non-diabetic volunteers or Type 2 diabetic patients (respective mean +/- SEM values = 4.0 +/- 0.2% and 4.2 +/- 0.3% for trideuteroacetanilide, 6.2 +/- 0.6% and 6.1 +/- 0.3% for trideuterophenacetin). Increasing the glucose concentration in the incubation medium by 50 mmol/L significantly (P less than 0.01) increased deacetylation-reacetylation of trideuteroacetanilide in each group (4.6 +/- 0.2% and 4.7 +/- 0.2% for non-diabetic and diabetic subjects, respectively). In rat blood the amount of deacetylation-reacetylation was much higher: 7.2 +/- 0.6% and 8.3 +/- 0.7% for trideuteroacetanilide and trideuterophenacetin, respectively. Induction of experimental diabetes using streptozotocin did not significantly change the extent of deacetylation-reacetylation of either deuterated substrate (10.1 +/- 2.1% and 9.5 +/- 1.1%). Elevation of the incubation glucose concentration by 50 mmol/L produced an increase in acetyl group exchange (for trideuteroacetanilide) in diabetic (14.3 +/- 2.2%) and non-diabetic (10.6 +/- 1.0%) rats. The donation of acetyl groups (transacetylation) was observed after incubation of blood samples from both diabetic and non-diabetic human subjects and rats with trideuterophenacetin and a molar excess of aniline. This reaction significantly (P less than 0.001) decreased the acetyl group exchange of trideuterophenacetin (these values were 4.5 +/- 0.4% and 3.4 +/- 0.6% using samples from non-diabetic human subjects and rats, respectively) and demonstrated the ability of whole blood to catalyse transacetylation (acetyl-CoA-independent acetylation). There was correlation between the amount of (unlabelled) acetanilide produced by acetylation with acetyl-CoA and the percentage present as trideuteroacetanilide. The proportion of trideuteroacetanilide was higher using rat blood (e.g. the values for non-diabetic subjects were 25.5 +/- 1.7% vs 8.5 +/- 0.3%; P less than 0.001) although the total amount of acetanilide produced was lower (0.54 +/- 0.14 nmol vs 1.82 +/- 0.23 nmol; P less than 0.05) than that observed using human blood.

Acetanilides↗
PubMed1981

Toxic-allergic syndrome caused by ingestion of rapeseed oil denatured with aniline.

In the past four months a new syndrome has caused more than 100 deaths in Spain. The most striking feature is a toxic-allergic pneumonopathy with respiratory distress and radiological evidence of interstitial (occasionally alveolar) exudation. Other features are fever, headache, nausea, muscular and abdominal pains, rash, hepatosplenomegaly, and eosinophilia; later, thrombotic phenomena and neurological disorders may appear. The epidemic has been traced to ingestion of rapeseed oil, denatured with aniline and containing acetanilide. The syndrome does not resemble intoxication with aniline or acetanilide, and is provisionally ascribed to "oleoanilide", a product formed by reaction of acetanilide with fatty acids.

Acetanilides↗
PubMed2006

Synthesis and characterization of N-acylaniline derivatives as potential chemical hybridizing agents (CHAs) for wheat (Triticum aestivum L.).

Induction of male sterility by deployment of chemical hybridizing agents (CHAs) are important in heterosis breeding of self-pollinated crops like wheat, wherein the male and female organs are in the same flower. Taking a lead from the earlier work on rice, a total of 25 N-acylanilines comprising of malonanilates, acetoacetanilides, and acetanilides (including halogenated acetanilides) were synthesized and screened as CHAs on three genotypes of wheat, viz., PBW 343, HD 2046, and HD 2733 at 1500 ppm in the winter of 2001-2002. The N-acylanilines containing variations at the acyl and aromatic domain were synthesized by condensation of substituted anilines with appropriate diesters, acid chlorides, or monoesters. The test compounds with highly electronegative groups such as F/Br at the para position of the aryl ring were identified as the most potent CHAs, causing higher induction of male sterility. A variation of N-substitution at the side chain generally furnished analogues like 4'-fluoroacetoacetanilide (7) and ethyl 4'-fluoromalonanilate (1), which induced 89.12 and 84.66% male sterility, respectively, in PBW 343. Among halogenated acetanilides, the increasing number of chlorine atoms in the side chain led to an increase in the activity of 4'-fluoro (23) and 4'-bromo (24) derivatives of trichoroacetanilides, which induced >87% male sterility. Quantitative structure-activity relationship (QSAR) models indicated the positive contributions of the field effect exemplified by the Swain-Lupton constant (Fp) and negative contributions of the Swain-Lupton resonance constant (R) for the aromatic substitution. The positive influences of parachor (P) for the acyl domain have been underlined. These leads will be significant in explaining the CHA fit in the macromolecular receptor site. The CHAs appeared to act by causing an imbalance in the acid-base equilibrium in pollen mother cells resulting in dissolution of the callose wall by premature callase secretion.

Acetanilides↗