The influence of chronic administration of thioacetamide on levels of ALT, AST and GLDH in serum and markers of oxidative stress in the liver and kidneys of female Wistar rats
Abstract
Background. Thioacetamide (TAA), a well known inducer of hepatic fibrosis, has been often used in experimental acute and chronic hepatotoxicity models.
Reactive oxygen species play an important role in TAA-induced liver damage. Aims.
To study the time course of activities of ALT, AST and GLDH in serum and markers of oxidative stress in the liver and kidneys of rats after chronic TAA administration. Methods.
Female Wistar rats were treated with TAA (intraperitoneally, 200 mg/kg body weight) for 12 weeks, the controls received saline. Animals were sacrificed 4, 12 or 16 weeks after the treatment discontinuation.
Lipid peroxidation (LP), reduced glutathione (GSH) and activities of glutathione peroxidase (GPx), glutathione reductase (GR) and katalase (CAT) were estimated in the liver and kidneys. ALT, AST and GLDH were measured in serum.
Results. Significant increases in serum ALT and GLDH persisted for 16 weeks ater the treatment, while serum AST was increased only in animals sacrificed 4 weeks after the treatment cessation.
No increase in LP or decrease in GSH was observed in the liver. Furthermore, a decrease in LP and an increase in GR activity appeared in the 16th week.
Significant decreases in the activities of catalase and GPx (which persisted in animals sacrificed 12 and 16 weeks after the treatment, respectively) were the only markers of hepatic oxidative damage. In kidneys, LP was significantly increased 4 and 12 weeks after the TAA treatment which implies the importance of oxidative stress in the renal damage that develops as a consequence of liver cirrhosis.