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Acute Liver Injury by Vinyl Chloride: Involvement of Endoplasmic Reticulum in Phenobarbital-pretreated Rats

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Date 1975 Jun 1
PMID 1175561
Citations 3
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Abstract

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.

Citing Articles

Effects of vinyl chloride exposures to rats pretreated with phenobarbital.

DREW R, Harper C, Gupta B, Talley F Environ Health Perspect. 1975; 11:235-42.

PMID: 1175562 PMC: 1475173. DOI: 10.1289/ehp.7511235.


Chemistry and toxicity of flame retardants for plastics.

Liepins R, PEARCE E Environ Health Perspect. 1976; 17:55-63.

PMID: 1026419 PMC: 1475265. DOI: 10.1289/ehp.761755.


Hepatotoxicity of vinyl chloride and 1,1-dichloroethylene. Role of mixed function oxidase system.

Reynolds E, Moslen M, Szabo S, Jaeger R, Murphy S Am J Pathol. 1975; 81(1):219-36.

PMID: 241261 PMC: 2032287.

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