Big Chemical Encyclopedia

Chemical substances, components, reactions, process design ...

Articles Figures Tables About

Aniline metabolism

Aminopyrine, 234 Aminotetradine, 265 2-Aminothiazole, 247 2-Aminothiazole synthesis, 126 Amisotetradine, 266 Amobarbital, 268 Amopyroquine, 342 Amoxycillin, 414 Amphetamine, 37, 70 Ampicillin, 413 Amprolium, 264 Amytriptylene, 141, 404 Anabolic effects, 169 Androgens, discovery, 155 Androstanolone, 173 Androstenedione, 158, 176 Anesthesia, parenteral, 56 Angst, 363 Anileridine, 300 Aniline, metabolism. 111 Anisindandione, 147 Anovlar , 186 Antagonists, 20, 65 Antazoline, 242 Antibodies, 41... [Pg.477]

The carcinogenicity of af la toxin is reduced by protein deficiency, presumably because of reduced metabolic activation to the epoxide intermediate, which may be the ultimate carcinogen, which binds to DNA (Fig. 5.14). A deficiency in dietary fatty acids also decreases the activity of the microsomal enzymes. Thus, ethylmorphine, hexobarbital, and aniline metabolism are decreased, possibly because lipid is required for cytochromes P-450. Thus, a deficiency of essential fatty acids leads to a decline in both cytochromes P-450 levels and activity in vivo. [Pg.161]

Evidence suggests that endosulfan can induce microsomal enzyme activity. Increased liver microsomal cytochrome P-450 activity was observed in male and female rats after single and multiple administrations of endosulfan (Siddiqui et al. 1987a Tyagi et al. 1984). Increased enzyme activity was observed in hepatic and extrahepatic tissues. Based on the increase in aminopyrine-A-demethylase and aniline hydroxylase activity, endosulfan has been shown to be a nonspecific inducer of drug metabolism (Agarwal et al. 1978). [Pg.132]

It has become clear that benzoate occupies a central position in the anaerobic degradation of both phenols and alkylated arenes such as toluene and xylenes, and that carboxylation, hydroxylation, and reductive dehydroxylation are important reactions for phenols that are discussed in Part 4 of this chapter. The simplest examples include alkylated benzenes, products from the carboxylation of napthalene and phenanthrene (Zhang and Young 1997), the decarboxylation of o-, m-, and p-phthalate under denitrifying conditions (Nozawa and Maruyama 1988), and the metabolism of phenols and anilines by carboxylation. Further illustrative examples include the following ... [Pg.436]

The degradation of 3- and 4-chloroaniline may require the presence of either aniline or glucose (references in Zeyer et al. 1985), while the metabolism of methylanilines required the addition of ethanol as additional carbon source (Fuchs et al. 1991). [Pg.490]

The complexity of the metabolism of alachlor, acetochlor, butachlor, and propachlor has led to the development of degradation methods capable of hydrolyzing the crop and animal product residues to readily quantitated degradation products. Alachlor and acetochlor metabolites can be hydrolyzed to two major classes of hydrolysis products, one which contains aniline with unsubstituted alkyl groups at the 2- and 6-positions, and the other which contains aniline with hydroxylation in the ring-attached ethyl group. For alachlor and acetochlor, the nonhydroxylated metabolites are hydrolyzed in base to 2,6-diethylaniline (DBA) and 2-ethyl-6-methylaniline (EMA), respectively, and hy-droxylated metabolites are hydrolyzed in base to 2-ethyl-6-(l-hydroxyethyl)aniline (HEEA) and 2-(l-hydroxyethyl)-6-methylaniline (HEMA), respectively. Butachlor is metabolized primarily to nonhydroxylated metabolites, which are hydrolyzed to DEA. Propachlor metabolites are hydrolyzed mainly to A-isopropylaniline (NIPA). The base hydrolysis products for each parent herbicide are shown in Eigure 1. Limited interference studies have been conducted with other herbicides such as metolachlor to confirm that its residues are not hydrolyzed to the EMA under the conditions used to determine acetochlor residues. Nonhydroxylated metabolites of alachlor and butachlor are both hydrolyzed to the same aniline, DEA, but these herbicides are not used on the same crops. [Pg.347]

The major metabolic pathways of flutolanil in plants are para-hydroxylation of the aniline ring and hydr-oxylation of the isopropoxy side chain. For potatoes, flutolanil anddesisopropyl-flutolanil (M-4) are selected as the target analytes. For rice plant, other metabolites containing 2-(trifluoromethyl)benzanilide moiety are also selected as the target analytes. For soil and water samples, flutolanil is selected as the only target analyte. [Pg.1199]

The presence of chemically reactive structural features in potential drug candidates, especially when caused by metabolism, has been linked to idiosyncratic toxicity [56,57] although in most cases this is hard to prove unambiguously, and there is no evidence that idiosyncratic toxicity is correlated with specific physical properties per se. The best strategy for the medicinal chemist is avoidance of the liabilities associated with inherently chemically reactive or metabolically activated functional groups [58]. For reactive metabolites, protein covalent-binding screens [59] and genetic toxicity tests (Ames) of putative metabolites, for example, embedded anilines, can be employed in risky chemical series. [Pg.401]

Aniline is rapidly and extensively metabolized following oral administration. In the pig and sheep, approximately 30% of a 50-mg/kg dose of 14C-labeled aniline was excreted in the urine, as measured by 14C activity, within 3 h after administration, whereas approximately 50% of the dose was excreted in rats. Within 24 h, more than half the administered dose was excreted by pigs and sheep and 96% of the dose was excreted by rats. Fecal radioactivity was low. A-acetylated metabolites accounted for most of the excretion—/V-acetyl-/>-aminophenyl glucuronide being the primary metabolite in sheep and pig urine and /V-acetyl-/>-aminophenyl sulfate being the primary metabolite in the rat (Kao et al. 1978). Biologic monitoring of workers exposed to aniline showed that /i-aminophenol constituted 15-55% of the parent compound in the urine the o- and ra-isomers were also formed (Piotrowski 1984). [Pg.53]

Kao, J., J.Faulkner, and J.W.Bridges. 1978. Metabolism of aniline in rats, pigs, and sheep. Drug Metab. Dispos. 6 549-555. [Pg.67]

Cravedi, J.P., C. Gillet, and G. Monod. 1995. In vivo metabolism of pentachlorophenol and aniline in Arctic charr (Salvelinus alpinus L.) larvae. Bull. Environ. Contam. Toxicol. 54 711-716. [Pg.1227]

In 1958, Kiese and coworkers for the first time detected nitrosobenzene in the blood of dogs after aniline administration, and it was his group who discovered V-oxygenation and the site of action in v/vo13-16. Finally, Kiese initiated17 and extended the research in the metabolic fate of nitrosobenzene in erythrocytes10 and encouraged one of the authors... [Pg.1000]

To acquire information on the intrinsic metabolic activity of aquatic organisms, liver of carp (Cyprinus carpio Linnaeus), rainbow trout (Salmo gairdneri) and freshwater snail (Cipango-paludina japonica Martens) was dissected out, homogenized in 0.1M phosphate buffer, pH 7.5, and centrifuged at 105,000 g for 60 min to obtain the microsome-equivalent (described as the microsomal fraction hereafter) fraction. The protein content of microsomal and submicrosomal (supernatant fractions by Lowry s method, microsomal P-450 content ( ), activity of aniline hydroxylase (4) and aminopyrine N-demethylase (5) were determined. [Pg.3]

Zok, S., Gorge, G., Kalsch, W., and Nagel, R. Bioconcentration, metabolism and toxicity of substituted anilines inthezebrafish (Brachydanio rerid), Sci. Total Environ., 109/110 411-421, 1991. [Pg.1746]

Peak methemoglobin levels may occur some hours after exposure, and it has been postulated that metabolic transformation of aniline to phenylhydroxylamine is necessary for the production of methemoglobin. Liquid aniline is mildly irritating to the eyes and may cause corneal damage. ... [Pg.50]

Limited information is available on the metabolism of 1,2-diphenylhydrazine. Two of the known metabolites, aniline and benzidine, may contribute to the toxicity and/or carcinogenicity of the substance. [Pg.284]


See other pages where Aniline metabolism is mentioned: [Pg.173]    [Pg.215]    [Pg.260]    [Pg.150]    [Pg.173]    [Pg.215]    [Pg.260]    [Pg.150]    [Pg.494]    [Pg.111]    [Pg.330]    [Pg.181]    [Pg.143]    [Pg.356]    [Pg.61]    [Pg.449]    [Pg.521]    [Pg.347]    [Pg.529]    [Pg.356]    [Pg.50]    [Pg.53]    [Pg.550]    [Pg.610]    [Pg.1018]    [Pg.124]    [Pg.124]    [Pg.5]    [Pg.155]    [Pg.683]    [Pg.160]    [Pg.106]    [Pg.32]    [Pg.32]    [Pg.44]    [Pg.86]    [Pg.301]   
See also in sourсe #XX -- [ Pg.111 ]




SEARCH



Drug metabolism aniline

© 2024 chempedia.info