Lead (Pb) exerts prooxidative effects and causes oxidative damage to various tissues by altering their antioxidant system. In the experiments male CD rats (Charles River) were treated twice a week with lead acetate at the dose of 12.5 mg/kg body weight ip for 4 weeks with and without Sc co-administration of deferiprone [Lipomed, Switzerland] (LI) at the dose molar ratio to lead acetate 10:1. Pb induced the lipid peroxidation (LPO) in both, the liver and the brain. LI prevented this effect of lead in the liver but not in the brain. L] alone did not change the LPO in liver whereas in the brain an elevation of LPO occured. The level of reduced glutathione (GSH) in the liver was significantly elevated in all groups compared to the control, in the brain increased by L] treatment only. The activity of glutathione peroxidase (GSH-Px) in the liver was not influenced by Pb administration, however the combination of Pb+LI and LI alone decreased the activity of this enzyme. The liver, kidneys, lungs and the brain were analyzed for Pb and essential elements. Pb concentration in the liver, kidneys and brain was not changed by the LI treatment, however Pb level increased in lungs due to L] administration. In the liver and in the kidneys the concentration of most of the essential elements decreased due to Pb-acetate administration and were corrected by L] co-treatment in the liver, however in the kidneys remained unaffected. The level of calcium in the liver was enhanced due to Pb administration and this effect was more expressed by L] co-treatment. In the brain and lungs the changes in essential element concentration were minor.

Keywords: Toxicology; deferiprone