ACUTE LEAD TOXICITY AND ENERGY-METABOLISM IN RAT-BRAIN SYNAPTOSOMES

Although the neurotoxic effects of lead (Pb) are well documented, the subcellular mechanisms of its action in the central nervous system are not fully understood. The present work examined some parameters of en ergy metabolism in nerve endings of the brains of adult rats exposed t o Pb. We applied the model of acute Pb toxicity in vivo, imitating the acute action of lead observed in occupationally exposed workers or in occasional incidents of poisoning. The measurement of Pb levels in th e synaptosomal fraction exhibited its significant accumulation under a pplied conditions. Oxygen consumption increased in synaptosomes from P b-treated rats whereas the activity of cytochrome c oxidase did not ch ange. The intrasynaptosomal levels of ATP and CrP were significantly e levated, as was the activity of creatine kinase, suggesting the activa tion of the CrP/CK system. On the other hand, the activity of the syna ptosomal Na+,K+-ATP-ase decreased. We suggest that under acute Pb toxi city conditions the mobiliaztion of CrP/CK system may take place to pr otect the cell against the effects of decreased Na+,K+-ATP-ase activit y.