Abstract
Oxidative phosphorylation was measured polarographically before and after adding lead acetate to cerebral and cerebellar mitochondria isolated from two week old and adult rats. With glutamate and malate as substrates, lead acetate (0.25 mM) produced a transient increase in respiration followed by complete inhibition of ADP-dependent respiration. The inhibition was not relieved by dinitrophenol or by freezing and thawing the mitochondria. NADH-supported respiration, in frozen and thawed mitochondria, was not affected by these low concentrations suggesting that lead acts on substrate transport or dehydrogenases. With succinate as substrate, inorganic lead produced an increased respiratory rate, approaching State 3, and no respiratory inhibition. The enhanced respiration was inhibited by oligomycin. There were no differences in lead effects associated with age, two weeks vs adult, or with brain region, cerebral vs cerebellar. We conclude that there is an energy-dependent transport of inorganic lead in brain mitochondria. Low concentrations of lead inhibit oxidative phosphorylation with NAD-linked substrates but not with succinate. These in vitro lead effects are similar to those seen in cerebellar mitochondria from lead-treated immature rats (Holtzman and Hsu, Pediat. Res. 10:70-75, 1976). However, this in-vitro mitochondrial effect does not show the age and regional specificity seen in lead encephalopathy in the rat and the human.
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Holtzman, D., Hsu, J. & Mortell, P. EFFECTS OF INORGANIC LEAD ON ISOLATED RAT BRAIN MITOCHONDRIAL RESPIRATION. Pediatr Res 11, 407 (1977). https://doi.org/10.1203/00006450-197704000-00227
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DOI: https://doi.org/10.1203/00006450-197704000-00227