Abstract
Several of the physiological and biochemical defects observed in the liver, kidney, and erythropoietic tissue of lead poisoned animals have been associated with altered mitochondrial structure and function (1-3). These observations suggested a direct effect of lead on the functional integrity of mitochondria. Reticulocytes incubated with 100 μM lead acetate (PbAc) for 3 hr were found to have a significant inhibition in O2 uptake. Exposure of actively respiring reticulocyte mitochondria to the same concentration of lead caused an immediate drop in oxidative activity (4, 5). Our preliminary studies with beef heart mitochondria indicated that the presence of inorganic phosphate in the incubation medium interfered with the interaction of lead with the mitochondrial membrane (6, 7). These findings, and the scarcity of information on the specific effects of lead on mitochondrial respiration, prompted an investigation of the dose-response relationship between lead concentration and mitochondrial oxidative phosph...
Published Version
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