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 energy metabolism in nerve endings of the brains of adult rats exposed to 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 the synaptosomal fraction exhibited its significant accumulation under applied conditions. Oxygen consumption increased in synaptosomes from Pb-treated rats whereas the activity of cytochrome c oxidase did not change. The intrasynaptosomal levels of ATP and CrP were significantly elevated, as was the activity of creatine kinase, suggesting the activation of the CrP/CK system. On the other hand, the activity of the synaptosomal Na+,K(+)-ATP-ase decreased. We suggest that under acute Pb toxicity conditions the mobilization of CrP/CK system may take place to protect the cell against the effects of decreased Na+,K(+)-ATP-ase activity.