Xanthine oxidase-derived reactive oxygen species contribute to the development of D-galactosamine-induced liver injury in rats.
Free Radic Res
; 41(2): 135-44, 2007 Feb.
Article
en En
| MEDLINE
| ID: mdl-17364939
ABSTRACT
We examined whether xanthine oxidase (XO)-derived reactive oxygen species (ROS) contribute to the development of D-galactosamine (D-GaIN)-induced liver injury in rats. In rats treated with D-GaIN (500 mg/kg), liver injury appeared 6 h after treatment and developed until 24 h. Hepatic XO and myeloperoxidase activities increased 12 and 6 h, respectively, after D-GalN treatment and continued to increase until 24 h. D-GalN-treated rats had increased hepatic lipid peroxide (LPO) content and decreased hepatic reduced glutathione (GSH) and ascorbic acid contents and superoxide dismutase (SOD), catalase and Se-glutathione peroxidase (Se-GSHpx) activities at 24 h, but not 6 h, after treatment. Allopurinol (10, 25 or 50 mg/kg) administered at 6 h after D-GalN treatment attenuated not only the advanced liver injury and increased hepatic XO activity but also all other changes observed at 24 h after the treatment dose-dependently. These results suggest that XO-derived ROS contribute to the development of D-GaIN-induced liver injury in rats.
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Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Xantina Oxidasa
/
Especies Reactivas de Oxígeno
/
Enfermedad Hepática Inducida por Sustancias y Drogas
/
Galactosamina
/
Hígado
/
Antioxidantes
Tipo de estudio:
Etiology_studies
Límite:
Animals
Idioma:
En
Revista:
Free Radic Res
Asunto de la revista:
BIOQUIMICA
Año:
2007
Tipo del documento:
Article
País de afiliación:
Japón