Disease relevance of Acetanilid

• Pseudomonas aeruginosa mutants resistant to urea inhibition of growth on acetanilide [1].
• Acetanilide pharmacokinetics in kwashiorkor [2].
• The acute effects of ethanol on acetanilide disposition in normal subjects, and in patients with liver disease [3].
• Research strategies for design and development of NSAIDs: clue to balance potency and toxicity of acetanilide compounds [4].

High impact information on Acetanilid

• Urine samples were collected before and after work (i.e., pre-shift and post-shift, respectively) and stored at -70 degrees C. Base hydrolysis was used to convert acetanilide and N-acetyl-o-toluidine, metabolites of aniline and o-toluidine present in the urine, to the parent compounds [5].
• Enzymatic analysis of the cell homogenates in vitro and of the dividing cells in situ showed very high acetanilide hydroxylase activity and very low aryl hydrocarbon hydroxylase activity, a diagnostic feature of the cytochrome P3-450 [6].
• The antibody inhibits microsomal acetanilide hydroxylation (80%) [7].
• When reconstituted, this cytochrome catalyzes acetanilide hydroxylation at a higher rate than microsomes or the minor fraction [7].
• Reaction thermodynamics have been calculated for an oxene model for cytochrome P-450 oxidations of four related arylamines: aniline, p-hydroxyaniline, acetanilide, and acetaminophen, by both radical and nonradical mechanisms, using a semiempirical molecular orbital method (modified neglect of differential overlap) [8].

Chemical compound and disease context of Acetanilid

• Adaptation to phenylacetamide as a growth substrate by an acetanilide-utilizing mutant of Pseudomonas aeruginosa [9].
• Hydroxyurea inhibited growth of Pseudomonas aeruginosa strain AI 3 on media containing either acetanilide (N-phenyl acetamide) or acetamide as sole carbon sources [10].
• Three widely used xenobiotics pentachlorophenol (PCP), 2,4-dichlorophenoxyacetic acid (2,4-D) and 2-chloro-2,6-diethyl-N-(butoxymethyl) acetanilide (Butachlor) are evaluated for acute toxicity and stress behavior on freshwater fish (Heteropneustes fossilis, Clarias batrachus, Channa punctatus) and mosquito larvae (Culex pipiens fatigans) [11].
• Quantitative analysis of rat activity in the home cage by infrared monitoring. Application to the acute toxicity testing of acetanilide and phenylmercuric acetate [12].
• Most of the antipyretic analgesics such as acetanilide and phenacetin are no longer used in therapy because of their toxicity [13].

Biological context of Acetanilid

• There was correlation between the amount of (unlabelled) acetanilide produced by acetylation with acetyl-CoA and the percentage present as trideuteroacetanilide [14].
• The ability of the maize isoenzyme GST I to detoxify from the acetanilide herbicide alachlor was investigated by steady-state kinetics and site-directed mutagenesis studies [15].
• It is concluded that the chosen pharmacokinetic approach corrects for the NIH-shift and the results adequately reflect changes in acetanilide hydroxylation related to enzyme induction or inhibition and to liver pathology [16].
• We have determined blocking of DNA replication by various other N-acetylarylamine and arylamine deoxyguanosine adducts [17].
• The activities of four additional enzymes having no known association with the oxidative stress response--benzo[a]pyrene hydroxylase (CYP1A1, cytochrome P(1)450), acetanilide 4-hydroxylase (CYP1A2, cytochrome P(3)450), lactate dehydrogenase (LDH), and NADPH-cytochrome c reductase--are not significantly different among the three genotypes [18].

Anatomical context of Acetanilid

• Comparison of aryl hydrocarbon hydroxylase and acetanilide 4-hydroxylase induction by polycyclic aromatic compounds in human and mouse cell lines [19].
• Alteration of RL2 was determined by measuring acetanilide-hydrolyzing activity, by quantifying the protein amount using the single radial immunodiffusion method, and by activity staining following electrophoresis of liver microsomes [20].
• The product expressed in COS cells migrates in native gels in the region of ES-3 and is similarly active on acetanilide [21].
• 1. Hydrolysis of acetanilide by the nematode Ascaris lumbricoides var suum occurred in the cytosol of the intestinal epithelium and to a lesser degree in the cytosol of the reproductive organs [22].
• Sodium fluoride at a dose level of 5.0 mg/kg enhanced aminopyrine N-demethylase and NADPH cytochrome c reductase activities and cytochrome P450 and cytochrome b5 levels in rat liver, kidney, lung, intestine and testis, whereas acetanilide hydroxylase activity remained unchanged in kidney and lung and was increased in liver, intestine and testis [23].

Associations of Acetanilid with other chemical compounds

• Three cytochrome P-450IA1-catalyzed activities, 7-ethoxyresorufin O-deethylase, 7-ethoxycoumarin, O-deethylase, and aryl hydrocarbon hydroxylase, were measurable in human lung microsomes, but the cytochrome P-450IA2-dependent activity acetanilide 4-hydroxylase was not [24].
• Two compounds, acetanilide and antipyrine, for which the in vivo evidence was against an association between their metabolism and that of debrisoquine, were weak, noncompetitive inhibitors of debrisoquine 4-hydroxylase activity [25].
• Finally, the palmitoyl carnitine-cleaving esterase splits phenacetin and acetanilide [26].
• In comparison with controls, isoniazid pretreatment of rats significantly increased the sp. act. of acetanilide 4-hydroxylase and the in vitro [14C]acetylhydrazine-derived covalent binding to hepatic microsomes but significantly decreased the sp. act. of benzo[a]pyrene hydroxylase and testosterone 16 alpha-hydroxylase [27].
• 2 In normal subjects, ethanol produced a dose-dependent increase in acetanilide half-life, and a decrease in acetenilide clearance [3].

Gene context of Acetanilid

• CYP1A2 was more active than CYP1A1 for acetanilide hydroxylation and activation of aflatoxin B1 (AFB1) [28].
• In contrast, hydroxylated flavonoids increased the 7-methoxyresorufin O-demethylation and acetanilide 4-hydroxylation activities of cDNA-expressed human CYP1A2 and in human liver microsomes [29].
• The Ah locus in the C57BL/6N mouse regulates at least two cytochrome P-450 gene products, termed in the mouse P1-450 and P3-450; these two enzymes are so named because each is responsible for the highest turnover number for the substrates benzo[a]pyrene and acetanilide, respectively [30].
• The strain AI3 is able to use acetanilide as a carbon source through a mutation (T103I) in the amiE gene that encodes an aliphatic amidase (EC 3.5.1.4) [31].
• 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 [32].

Analytical, diagnostic and therapeutic context of Acetanilid

• Results obtained in the molluscan system may thus provide insight into the ionic, biophysical and physicochemical mechanisms underlying acetanilide-induced analgesia [33].
• After ovariectomy, deacylating activities increased (up to 1.6 times) except for those of 2-FAA and acetanilide [34].
• Separation of acetanilide and its hydroxylated metabolites and quantitative determination of "acetanilide 4-hydroxylase activity" by high-pressure liquid chromatography [35].
• For assessing genotoxicity of pentachlorophenol (PCP), 2,4-dichlorophenoxyacetic acid (2,4-D) and 2-chloro-2,6-diethyl-N-(butoxymethyl) acetanilide (butachlor), 50% effective concentration (EC(50)), c-mitosis, stickiness, chromosome breaks and mitotic index (MI) were used as endpoints of genotoxicity [36].
• 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 [37].

References