Acute liver injury by vinyl chloride: involvement of endoplasmic reticulum in phenobarbital-pretreated rats. | Zendy

Edward S. Reynolds | Zendy; Rudolph J. Jaeger | Zendy; Sheldon D. Murphy | Zendy

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Acute liver injury by vinyl chloride: involvement of endoplasmic reticulum in phenobarbital-pretreated rats.

Author(s) -

Edward S. Reynolds,

Rudolph J. Jaeger,

Sheldon D. Murphy

Publication year - 1975

Publication title -

environmental health perspectives

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.257

H-Index - 282

eISSN - 1552-9924

pISSN - 0091-6765

DOI - 10.1289/ehp.7511227

Subject(s) - endoplasmic reticulum , vacuolization , vinyl chloride , phenobarbital , chemistry , reticulum , metabolite , biochemistry , biology , endocrinology , organic chemistry , copolymer , polymer

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.

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