Big Chemical Encyclopedia

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

Articles Figures Tables About

Urine, aromatic amines

R-NH-COOH), followed by decarboxylation to the aromatic amine, was an important pathway in humans. However, in contrast to loratadine, the carbamic acid metabolite appeared to be sufficiently stable to be detectable in fair amounts in human urine. It can be postulated that the aromatic nature of the amine accounts for the relative stability of its carbamic acid derivative. [Pg.409]

Bowman MC, Rushing CR. 1981. Trace-level determination of benzidine, 3,3 -dichlorobenzidine in animal chow wastewater and human urine. In Egan H, ed. Environmental carcinogens - selected methods of analysis. Volmne 4. Some aromatic amines and azo dyes in the general and industrial environment. Lyon, France International Agency for Research on Cancer, 159-174. [Pg.152]

Nony CR, Bowman MC, Cairns T, et al. 1980. Metabolism studies of an azo dye and pigment in the hamster based on analysis of urine for potentially carcinogenic aromatic amine metabolites. Anal Toxicol 4 132-140. [Pg.162]

It is plausible that analysis of urine samples may be used to monitor exposure to aromatic amines. In a model experiment, rats were treated with 2,4-diaminoanisole (2,4-DAA) and the urine analyzed for the amine and its most important metabolites (33). The results are shown in Table II. For the two doses used in this study, the major metabolite is 4-acetamido-2-aminoanisole, indicating that this compound may be used to monitor occupational exposure to 2,4-DAA. [Pg.377]

Azo-based dyes, known to be carcinogenic, contain easily hydrolyzed azo bonds. In the GI tract, these bonds are cleaved to yield the free aromatic amine(s) [20]. Azo reduction may also take place in the liver of humans and other mammals by reductase enzymes, but it is likely that hydrolysis in the GI tract is predominant [21]. The resultant aromatic amines are easily absorbed in the intestines. It was found that inclusion of sulfonate moieties on the aromatic amine feedstocks mitigates the toxicity, as illustrated with the azo dye Brilliant Black BN (Cl Food Black 1) in Figure 13.6. The sulfonate moieties are highly ionized in the GI tract and at environmental pHs (5-9), and their reduction products cannot penetrate the GI endothelial membranes following oral exposure. Consequently, the chemicals are poorly absorbed, and any portion that is absorbed is rapidly excreted in the urine [22, 23]. [Pg.358]

The first, unequivocal evidence for N-hydroxylation of an aromatic amine in vivo was obtained with 2-(acetamido)fluorene, which was detected in urine as its N-hydroxy derivative almost entirely in the form of a D-glucuronic acid conjugate (that could be cleaved by /3-d-glucosiduronase), to which structure 133 was assigned.362,383 Activation of chemical carcinogens (that are not themselves reactive, but are... [Pg.131]

Iodide in urine [39] and catecholamines [40,41] are example of analytes recently detected electrochemically and studied under IPC conditions. Pulsed amperometric detection on a gold electrode was used to detect etimicin [42] and gentamicin [43] in commercial samples, thus avoiding tedious pre-column derivatization. Heterocyclic aromatic amines in soup cubes [44] were determined by a coulometric electrode array detector, and the coulometric detection of a quinone-bearing drug candidate [45] allowed the study of electrochemical properties. [Pg.144]

Sulphate conjugates are formed with hydroxy compounds (e.g. alcohols and phenols) or aromatic amines. For example, morphine-3-(9-ethereal sulphate is a minor metabolite of morphine and N-phenylsulphamic acid is a metabolite of aniline. Sulphate conjugates are strong acids and are readily excreted in the urine they are of relatively little importance in drug metabolism. [Pg.291]

When given orally, 8% of the amaranth is absorbed from the intestinal tract. Intestinal flora have a reducing effect on amaranth, and azo reduction is also mediated by the hepatic monooxygenase system. Aromatic amine metabolites, including 1-amino-4-naphthalene sulfonic acid and l-amino-2-hydro-xy-3,6-naphthalene disulfonic acid, are excreted in the urine and bile. [Pg.2207]

Acetylation is an important route of metabolism for aromatic amines, sulphonamides, hydrazines and hydrazides and there is a wide variety of substrates. This metabolic reaction is one of two types of acylation reaction and involves an activated conjugating agent, acetyl CoA. It is hence a type 1 reaction. Acetylation is notable in that the product may be less water soluble than the parent compound. This fact gave rise to problems with sulphonamides when these were administered in high doses. The acetylated metabolites, being less soluble in urine, crystallized out in the kidney tubules, causing tubular necrosis (table 4,1). The enzymes which catalyse the acetylation reaction, acetyltransferases, are cytosolic and are found in the liver, in both hepatocytes and Kupffer cells, in the gastrointestinal mucosa and in white blood cells. The enzyme has been purified and its mechanism of action extensively studied and is now well understood. This involves first acetylation of the enzyme by acetyl CoA... [Pg.205]

Sharping, G., Dalene, M., and Brunmark, P., Liquid-chromatography and mass-spectrometry determination of aromatic-amines in hydrolyzed urine from workers exposed to thermal degradation products of pol3Tirethane, Chromatographia, 39, 619-623, 1994. [Pg.800]

Tissue-specific NAT expression can ajfect toxicity of environmental pollutants. NATl is ubiquitously expressed in human tissues, whereas NATl is found in liver and the GI tract. Both enzymes have a capacity to form N-hydroxy-acetylated metabolites from bicyclic aromatic hydrocarbons, a reaction that leads to the nonenzymatic release of the acetyl group and the generation of highly reactive nitrenium ions. Thus, N-hydroxy acetylation is thought to activate certain environmental toxicants. In contrast, direct N-acetylation of the environmentally generated bicyclic aromatic amines is stable and leads to detoxification. NATl fast acetylators efficiently metabolize and detoxify bicyclic aromatic amine through liver-dependent acetylation. Slow acetylators (NATl deficient) accumulate bicyclic aromatic amines, which are metabolized by CYPs to N-OH metabolites that are eliminated in the urine. In bladder epithelium, NATl efficiently catalyzes the N-hydroxy acetylation of bicyclic aromatic amines, a process that leads to deacetylation and the formation of the mutagenic nitrenium ion. Slow acetylators due to NATl deficiency are predisposed to bladder cancer if exposed to environmental bicyclic aromatic amines. [Pg.53]


See other pages where Urine, aromatic amines is mentioned: [Pg.273]    [Pg.54]    [Pg.1087]    [Pg.152]    [Pg.91]    [Pg.303]    [Pg.305]    [Pg.330]    [Pg.423]    [Pg.104]    [Pg.111]    [Pg.161]    [Pg.417]    [Pg.152]    [Pg.40]    [Pg.273]    [Pg.121]    [Pg.132]    [Pg.291]    [Pg.161]    [Pg.152]    [Pg.256]    [Pg.1236]    [Pg.1775]    [Pg.2096]    [Pg.648]    [Pg.650]    [Pg.660]    [Pg.839]    [Pg.842]    [Pg.844]    [Pg.848]    [Pg.283]    [Pg.683]    [Pg.322]    [Pg.337]    [Pg.551]    [Pg.462]   
See also in sourсe #XX -- [ Pg.423 , Pg.424 , Pg.425 ]




SEARCH



Aromatic amination

Aromatic amines

Aromatics amination

Urine aromatics

© 2024 chempedia.info