Titlebook: N-Oxidation of Drugs; Biochemistry, pharma P. Hlavica (Full Professor of Pharmacology and Tox Book 1991 Chapman & Hall 1991 Drogen.Oxidatio

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Moderate

Purification and characterization of rat hepatic acetyltransferaseome from occupational, environmental, dietary and pharmacological sources. Structurally these compounds are similar in that they all have, or can be metabolized to arylhydroxylamine derivatives. Biological experiments revealed that these metabolites were likely to be more closely related to the adve

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metabolism of ,-oxidese and minoxidil. In both these cases some of the major metabolites in man either retain the .-oxide group as such or form conjugates thereof (Thomas and Harpootlian, 1975; Johnson et al., 1983; Boxenbaum et al., 1977; also see Chapter 4).

SAGE

The Application of ,N-NMR in the Analysis of ,-Oxygenated amidines and guanidines2.1) and is thus not appropriate for high resolution studies. As a result of quadrupole relaxation, the line widths of the signals are very broad and relatively sharp resonance lines can be observed only in special cases.

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Mechanism, multiple forms and substrate specificities of flavin-containing mono-oxygenasesknown and the present discussion will be restricted to a subgroup of flavin-dependent mono-oxygenases that catalyse the oxidation of an exceptionally broad range of substrates . a mechanism distinctly different from all other mono-oxygenases or oxidases.

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Purification and characterization of rat hepatic acetyltransferaserse genotoxic properties of aromatic amines or nitroarenes than the parent compounds themselves. Although it was demonstrated that some of these potential metabolites could react with nucleic acid in acidic media (e.g. pH 5) (Kriek, 1965), many had only marginal reactivity at pH values that were likely to be encountered in physiological systems.

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Formation of aromatic amine free radicals by prostaglandin hydroperoxidase and peroxyl radicals: anaroxidase subsequently reduces the hydroperoxide to the corresponding alcohol, PGH.. PGH. is then converted into a variety of other prostanoid metabolites, including thromboxanes, prostacyclin, and PGs E. and F..

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