DOES LEAD PROVOKE THE PEROXIDATION PROCESS IN RAT-BRAIN SYNAPTOSOMES

Up to now there has been no information concerning the effect of lead on the peroxidation process in brain nerve endings. We have examined w hether lead acetate (in chronic and acute models of toxicity in vivo a nd in vitro) affected the level of free radicals in synaptosomes obtai ned from rat brain. Simultaneously, we have checked the effect of pero xidation of Pb2+ on brain homogenates and microsomal fraction. Our res ults indicated that the lead level in synaptosomal fraction obtained f rom lead-treated rats was much higher than in controls. We did not obs erve induction of spontaneous and Fe3+-dependent peroxidation either i n synaptosomes or in homogenates and brain microsomes after chronic an d acute lead administration to the rats. Lead itself also did not enha nce both processes when added in vitro to the control brain synaptosom es in micromolar concentrations. The lack of the lead effect on the pe roxidation process in subcellular fractions of brain was rather surpri sing, because lead is known to be the accelerator of Fe3+-dependent pe roxidation processes in liver. Additionally, livers from rats under th e same toxicity conditions were examined. We have found that lead did not provoke spontaneous peroxidation in liver, but contrary to brain f ractions, it drastically increased iron-dependent peroxidation in live r homogenates and microsomes. The lack of the effect of lead on induci ng peroxidation processes in brain is probably the consequence of the brain having stronger protective mechanisms against its toxicity than the liver.