title: Biochemical mechanisms of toxic cell injury.
abstract: The recent studies of the toxicity of the well known hepatotoxins bromobenzene and acetaminophen have suggested an alternative to covalent binding as the mechanism coupling mixed-function oxidation to lethal cell injury. Formation of activated oxygen species and the loss of GSH as a result of its conjugation with the electrophilic products of toxin metabolism may overwhelm cellular defenses and induce oxidative damage to cellular membranes and resulting necrosis.
mesh_terms: D000082:Acetaminophen / Q000633:toxicity*; D000818:Animals; D001969:Bromobenzenes / Q000633:toxicity*; D002470:Cell Survival / Q000187:drug effects*; D005609:Free Radicals; D008054:Lipid Peroxides / Q000378:metabolism; D008099:Liver / Q000166:cytology / Q000187:drug effects*; D006899:Mixed Function Oxygenases / Q000378:metabolism; D010100:Oxygen / Q000633:toxicity
chemical_list: D001969:Bromobenzenes; D005609:Free Radicals; D008054:Lipid Peroxides; D000082:Acetaminophen; C032036:bromobenzene; D006899:Mixed Function Oxygenases; D010100:Oxygen