The covalent binding of acetaminophen to protein. Evidence for cysteine residues as major sites of arylation in vitro
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Comments on “DNA-binding activities of compounds acting as enzyme inhibitors, ion channel blockers and receptor binders.”
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2016, Toxicology and Applied PharmacologyCitation Excerpt :To effectively use the mouse model, a few issues need to be considered (Fig. 2). First, the mechanism of toxicity depends on the formation of a reactive metabolite, N-acetyl-p-benzoquinone imine (NAPQI), by the cytochrome P450 (CYP) enzyme system (Dahlin et al., 1984; Mitchell et al., 1973a; Streeter et al., 1984), especially CYP2E1 (Lee et al., 1996; McClain et al., 1980; Sato and Lieber, 1981; Sato et al., 1981). NAPQI is detoxified by GSH (Albano et al., 1985; Corcoran and Wong, 1986; Mitchell et al., 1973b; Rosen et al., 1984), but can equally bind to cysteine sulfhydryl groups of proteins (Hoffmann et al., 1985; Jollow et al., 1973; Streeter et al., 1984).
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