Acute liver injury by vinyl chloride: involvement of endoplasmic reticulum in phenobarbital-pretreated rats.
A single 6-hr exposure to vinyl chloride monomer (5%) produces extensive vacuolization of centrolobular liver parenchyma and focal midzonal necrosis in the hepatic lobuole in phenobarbital-pretreated rats. Ultrastructurally, vacuolization consists of dilation of cysternae of rough endoplasmic reticulum and in the same cells smooth endoplasmic reticulum coalesces into discreet aggregates resembling denatured membranes. The findings support the hypothesis that vinyl chloride is hepatotoxic because it is converted into a toxic metabolite by components of the mixed function oxidase system of liver endoplasmic reticulum.
D000818:Animals; D056486:Chemical and Drug Induced Liver Injury / Q000209:etiology*; D004721:Endoplasmic Reticulum / Q000187:drug effects*; D004781:Environmental Exposure; D008099:Liver / Q000187:drug effects / Q000648:ultrastructure*; D008297:Male; D009336:Necrosis; D010634:Phenobarbital / Q000494:pharmacology*; D051381:Rats; D014617:Vacuoles / Q000187:drug effects; D014752:Vinyl Chloride / Q000633:toxicity*; D014753:Vinyl Compounds / Q000633:toxicity*
D014753:Vinyl Compounds; D014752:Vinyl Chloride; D010634:Phenobarbital