Abstract
In an attempt to assess possible functional consequences of chlorphentermine (CP) to pulmonary tissue, we investigated the effects of this drug on energy metabolism in slices and isolated mitochondria of control rat lungs. Oxygen consumption in 0.5-mm thick slices was inhibited in a concentration-dependent manner by 0.5 to 2.0 m m CP (max. depression = 91%). In isolated mitochondria, the respiratory control ratio (RCR) was decreased by 1.0 to 5.0 m m CP. In addition, the ADP-mediated respiratory burst (State III) and the subsequent recovery (State IV) were decreased at 2.5 and 5.0 m m CP. When mitochondria were isolated from lung slices preincubated with CP, RCR was again decreased by 1.0 to 5.0 m m CP. At 2.5 m m CP, oxidative phosphorylation was uncoupled. In addition, aerobic glucose metabolism in lung slices was impaired by CP concentrations above 2.0 m m. The metabolism of [6- 14C]- and [1- 14C]glucose was inhibited 95 and 70%, respectively, suggesting a preferential inhibition of glycolysis in comparison to the hexose monophosphate shunt. These data show that CP inhibits oxidative functions in lung preparations and suggest that CP has the potential for disrupting energy metabolism in the intact organ.
Published Version
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