Pyrogallol-induced hepatotoxicity in rats: a model to evaluate antioxidant hepatoprotective agents.

Various hepatic disorders and hepatotoxic agents are associated with increased free radical generation. In the present study, the free radical generator pyrogallol (100 mg/kg i.p.) caused significant hepatic damage. The serum enzymes asparatate aminotransaminase (AST) and alanine aminotransaminase (ALT) increased to 357 +/- 30.7 IU/I and 147.8 +/- 28.4 IU/I, respectively in the pyrogallol-treated group compared with 208.4 +/- 4.1 IU/I and 84.5 +/- 19.5 IU/I, respectively in the control rats. Compared with control rats, the liver tissue in the pyrogallol-treated group showed an increased level of malondialdehyde (MDA) as well as glutathione (GSH). The infiltration of white blood cells into the liver tissue, as seen histologically, further substantiated liver damage. Pretreatment with a standard hepatoprotective drug (silymarin, 100 mg/kg i.p.) afforded significant protection against pyrogallol hepatotoxicity, as evidenced by amelioration of the raised serum markers of hepatic function, markers of oxidative stress and normal liver histology. Thus, pyrogallol-induced hepatotoxicity could be used as an appropriate model to evaluate hepatoprotective agents that have an antioxidant property.