Titlebook: Biological Reactive Intermediates III; Mechanisms of Action James J. Kocsis,David J. Jollow,Robert Snyder Book 1986 The Editor(s) (if appli

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https://doi.org/10.1007/978-3-642-77776-9 aromatic hydrocarbons are carcinogenic, and that the cytochrome P450-dependent mixed function oxidase system preferentially catalyzes the formation of the optical isomer with the highest carcinogenic activity (3).

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Role of Thiols in Protection Against Biological Reactive Intermediatesly serve a protective function. Hence, it is obvious that the formation of toxic metabolites cannot be attributed to any single enzyme or enzyme system, and that the balance between metabolic activation and inactivation is absolutely critical in deciding whether exposure to a potentially toxic compound will result in toxicity, or not.

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Role of Parenchymal Versus Non-Parenchymal Cells on the Control of Biologically Reactive Intermediat activities than did the PC. Furthermore, the NPC were capable of forming biologically reactive intermediates which caused cyto- and genotoxicity. From these data we conclude that the NPC provide a distinct contribution to hepatic metabolism of xenobiotics.

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Significance of Covalent Binding of Chemically Reactive Metabolites of Foreign Compounds to Proteinswever, many foreign compounds have been shown to be transformed to chemically reactive metabolites that combine with proteins and lipids. Indeed, even carcinogens that presumably evoke mutagenic changes in DNA almost invariably also become covalently bound to proteins.

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Expression and Sequence Analysis of Rat Liver Glutathione S-Transferase Genesnous compounds such as bilirubin and heme (1–3). The enzymes are comprised of binary combinations of at least six major subunits, Yα, Ya, Ybl, Yb2, Yc and Yn, which can be separated by onedimensional SDS-polyacrylamide gel electrophoresis (4–6).