Abstract
Mitochondria isolated from livers of mice fed the copper-chelating agent, cuprizone, showed a decrease in state 3 respiration, respiratory control ratios and ADP/O or P/O ratios. This inhibition of state 3 respiration was not relieved by the addition of dinitrophenol (DNP). These inhibitory effects apparently involved all three sites of mitochondrial-coupled oxidative phosphorylation as well as possibly having an effect on substrate-level oxidative phosphorylation. Cuprizone produced a greater degree of inhibition of phosphorylation than of oxidation and therefore has the characteristics of an inhibitor uncoupler. Liver mitochondria isolated from control mice or from normal rats were unaffected by treatment in vitro with cuprizone. In contrast to liver mitochondria, mitochondria isolated from the hearts of mice fed cuprizone show no defects in oxidative phosphorylation.
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