Biochemical mechanisms of toxic cell injury.
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.
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
D001969:Bromobenzenes; D005609:Free Radicals; D008054:Lipid Peroxides; D000082:Acetaminophen; C032036:bromobenzene; D006899:Mixed Function Oxygenases; D010100:Oxygen