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 reticu...

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Detalles Bibliográficos
Autores principales: Reynolds, E S, Jaeger, R J, Murphy, S D
Formato: Texto
Lenguaje:English
Publicado: 1975
Materias:
Research Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1475197/
https://www.ncbi.nlm.nih.gov/pubmed/1175561
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author Reynolds, E S
Jaeger, R J
Murphy, S D
author_facet Reynolds, E S
Jaeger, R J
Murphy, S D
author_sort Reynolds, E S
collection PubMed
description 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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spelling pubmed-14751972006-06-09 Acute liver injury by vinyl chloride: involvement of endoplasmic reticulum in phenobarbital-pretreated rats. Reynolds, E S Jaeger, R J Murphy, S D Environ Health Perspect Research Article 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. 1975-06 /pmc/articles/PMC1475197/ /pubmed/1175561 Text en
spellingShingle Research Article
Reynolds, E S
Jaeger, R J
Murphy, S D
Acute liver injury by vinyl chloride: involvement of endoplasmic reticulum in phenobarbital-pretreated rats.
title Acute liver injury by vinyl chloride: involvement of endoplasmic reticulum in phenobarbital-pretreated rats.
title_full Acute liver injury by vinyl chloride: involvement of endoplasmic reticulum in phenobarbital-pretreated rats.
title_fullStr Acute liver injury by vinyl chloride: involvement of endoplasmic reticulum in phenobarbital-pretreated rats.
title_full_unstemmed Acute liver injury by vinyl chloride: involvement of endoplasmic reticulum in phenobarbital-pretreated rats.
title_short Acute liver injury by vinyl chloride: involvement of endoplasmic reticulum in phenobarbital-pretreated rats.
title_sort acute liver injury by vinyl chloride: involvement of endoplasmic reticulum in phenobarbital-pretreated rats.
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1475197/
https://www.ncbi.nlm.nih.gov/pubmed/1175561
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AT jaegerrj acuteliverinjurybyvinylchlorideinvolvementofendoplasmicreticuluminphenobarbitalpretreatedrats
AT murphysd acuteliverinjurybyvinylchlorideinvolvementofendoplasmicreticuluminphenobarbitalpretreatedrats

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