Titlebook: Biological Reactive Intermediates—II; Chemical Mechanisms Robert Snyder,David J. Jollow,Stephen L. Longacre Book 1982 The Editor(s) (if ap

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Development of a Novel Method for Measuring Covalent Binding and Its Application to Investigations ot interactions have been suggested to be involved in hepatic, renal, pulmonary and bone marrow toxicity as well as carcinogenicity (Mitchell et al., 1976; Mitchell et al., 1977; Hinson, 1980; Gillette et al., 1974; Boyd, 1980; Irons et al., 1980; Miller, 1970). More recently it has become apparent t

Salivary-Gland

Biotransformation of Bromobenzene to Reactive Metabolites by Isolated Hepatocytes(Koch-Weser et al., 1953; Reid et al., 1971). Metabolic activation of bromobenzene to reactive intermediate(s) by the cytochrome P-450-linked monooxygenase system is required for this agent to produce liver damage which, in turn, is preceded by depletion of hepatic glutathione (GSH) (Jollow et al.,

Diatribe

Urinary Metabolites of Benzene in the Mousecaused by a metabolite of benzene. Our understanding of the metabolism of benzene derives largely from the reports of R.T. Williams and his co-workers (Porteus and Williams, 1949a, 1949b; Parke and Williams, 1952, 1953a, 1953b), who were the first to systematically identify benzene metabolites in ra

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Fortschritte der Urologie und Nephrologie of conjugated phenolic metabolites of benzene. Upon acid hydrolysis of the conjugates, phenol was found to account for 24% of the dose while other metabolites included catechol (2.2%), hydroquinone (4.8%), and hydroxyhydroquinone (0.3%). 1-Phenylmercapturic acid (0.5%) and trans-trans-muconic (1.3%) acid were also recovered in the urine.

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