Lead (Pb2+) is a widespread pollutant and potent central neurotoxin. We have studied its effect on energetic metabolism of cerebellar granule cells (CGC) in pre- and postnatally intoxicated rats. Pregnant Wistar rats received 0.1% lead acetate in water. CGC were prepared from 8-day-old born rats according to a standard procedure. Pb2+concentration was measured in blood and in cerebellum homogenates by AAS. Intracellular Pb2+ concentrations in CGC was studied by fl uorescent microscopy, in neurons loaded with the Ca2+-sensitive indicator Oregon Green. Intracellular Pb2+ was evaluated from the fl uorescence intensity and estimate in μM range. Pb-induced decrease in Adenylate Energy Charge (by 10%) and ATP concentration (by 35%) in cerebellum homogenates (HPLC method) was observed at Pb concentrations in whole blood (7.05 ± 2.05 μg/dL).The function of mitochondria of neurons of Pb-treated and control rats were evaluated using: Mitotracker Green FM and JC-1. We observed active mitochondria stained green with Mitotracker in cytoplasm of CGC from control and Pb-treated rats. Incubation of cultured CGC from rats of control groups with the mitochondrial probe JC-1 produced red-orange fl uorescence showing mitochondria with high membrane potential ΔΨ. The green fl uorescence dependent on mitochondria with low ΔΨ was visible in cytoplasm of cells in Pb-treated rats. Pre- and postnatal low-level exposure to lead caused disruption of mitochondria energetic status in neurons.
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