Role of metabolism in 1-bromopropane-induced hepatotoxicity in mice.
J Toxicol Environ Health A
; 73(21-22): 1431-40, 2010.
Article
en En
| MEDLINE
| ID: mdl-20954070
ABSTRACT
A possible role of metabolism in 1-bromopropane (1-BP)-induced hepatotoxicity was investigated in male ICR mice. The depletion of glutathione (GSH) by formation of GSH conjugates was associated with increased hepatotoxicity in 1-BP-treated mice. The formation of S-propyl and 2-hydroxypropyl GSH conjugates were identified in the liver following 1-BP treatment. In addition, the formation of reactive metabolites of 1-BP by certain cytochrome P-450 (CYP) may be involved in 1-BP-induced hepatotoxicity. The decreased content of hepatic GSH produced by 1-BP was associated not only with increased activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) but also with elevated levels of hepatic thiobarbituric acid-reactive substance (TBARS) in mice where metabolic enzymes were induced by pretreatment with phenobarbital. In addition, the hepatotoxicity induced by 1-BP was prevented by pretreatment with SKF-525A. Taken together, the formation of reactive metabolites by CYP and depletion of GSH may play important roles in hepatotoxicity induced by 1-BP.
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Enfermedad Hepática Inducida por Sustancias y Drogas
/
Hígado
Tipo de estudio:
Etiology_studies
Límite:
Animals
Idioma:
En
Revista:
J Toxicol Environ Health A
Asunto de la revista:
SAUDE AMBIENTAL
/
TOXICOLOGIA
Año:
2010
Tipo del documento:
Article