PREVENTION OF PRASEODYMIUM-INDUCED HEPATOTOXICITY BY SILYBIN

In rats, the hepatotoxicity of praseodymium nitrate was prevented by treatment with silybin, the main component of silymarin, a compound isolated from Silybum marianum. A single dose (100 mg/kg) of silybin, given 1 h before or up to 8 h after praseodymium, almost normalized the serum activities of glutamic pyruvic and oxaloacetic transaminases, sorbitol and glutamic dehydrogenases, as well as the content of hepatic triglycerides. When administered 17 or 24 h after the rare earth metal, the protective action of silybin was no longer significant. The hepatocytic changes elicited by praseodymium (endoplasmic reticulum fragmentation and dilatation, massive smooth endoplasmic reticulum proliferation and lipid droplet accumulation) were also prevented by silybin. In correlation with the biochemical parameters, the morphologic alterations were not influenced by silybin when administered 17 or 24 h after praseodymium.