Involvement of cytochrome P4502E1 in the toxicity of dichloropropanol to rat hepatocyte cultures.
Toxicology
; 118(2-3): 171-9, 1997 Mar 28.
Article
en En
| MEDLINE
| ID: mdl-9129171
Hepatocytes were isolated and cultured from untreated rats and rats treated with isoniazid to induce cytochrome P4502E1. Isoniazid selectively increased p-nitrophenol hydroxylase activity in 2-h cultures, and increased the toxicity of both 1,3- and 2,3-dichloropropanol. Isoniazid also increased the rate and extent of glutathione depletion by the dichloropropanols. There was no effect of isoniazid on the toxicity of 1,3-dichloroacetone, precocene II or allyl alcohol. In addition, diethyldithiocarbamate selectively inhibited p-nitrophenol hydroxylase in 2-h cultures from untreated and isoniazid-treated rats, as well as abolishing toxicity of the dichloropropanols. In 24-h cultures from isoniazid-treated rats diethyldithiocarbamate inhibited high affinity MCOD activity by 55% and there was also a small but significant inhibition of precocene II toxicity. These results indicate that isoniazid-inducible P4502E1 can mediate the toxicity of dichloropropanol.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Clorhidrinas
/
Citocromo P-450 CYP2E1
/
Alfa-Clorhidrina
/
Hígado
/
Mutágenos
Límite:
Animals
Idioma:
En
Revista:
Toxicology
Año:
1997
Tipo del documento:
Article
Pais de publicación:
Irlanda