Acetaminophen (AAP), a widely used analgesic drug, can damage various organs when taken in large doses. In this study, we investigate whether AAP causes cell damage by altering the early signaling pathways associated with cell death and survival. AAP caused
A model system for the detection of reactive metabolites, using glutathione depletion after microsomal activation, has been described previously. We developed a battery of complementary test systems using rat liver microsomes for metabolism and aqueous glutathione solutions, human erythrocytes or
The Journal of biological chemistry, 264(17), 9814-9819 (1989-06-15)
Acetaminophen (250 mg/kg) administered intraperitoneally to fasted, phenobarbital-induced mice produced hepatotoxicity. No hepatotoxicity was observed after the administration of the regioisomer 3'-hydroxyacetanilide (600 mg/kg). Similar levels of covalent binding to liver homogenates occurred in mice receiving either acetaminophen or 3'-hydroxyacetanilide
Identification of hepatic protein targets of the reactive metabolites of the non-hepatotoxic regioisomer of acetaminophen, 3'-hydroxyacetanilide, in the mouse in vivo using two-dimensional gel electrophoresis and mass spectrometry.
Y Qiu et al.
Advances in experimental medicine and biology, 500, 663-673 (2002-01-05)
Chemical research in toxicology, 2(1), 41-45 (1989-01-01)
3'-Hydroxyacetanilide (AMAP) is a nonhepatotoxic regioisomer of acetaminophen (APAP) that nonetheless does form reactive metabolites which bind to hepatic proteins. Because differences in the nature of reactive metabolites formed from AMAP and APAP may explain differences in their propensity to
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