Effects of chronic emetine treatment on mitochondrial function.

Emetine has long been recognized as a cardiotoxic drug, but its mechanism remains unknown. Since many studies reported an effect of emetine on cardiac metabolism, permanent damage to the heart could result from such treatment. To investigate this action of emetine in relation to the cardiotoxicity seen after a therapeutic regimen, New Zealand albino rabbits were given 2 mg/kg/day ip of emetine for 9 days. Heart and liver mitochondrial metabolism was assessed polarographically using pyruvate, pyruvate plus malate, or succinate as the substrate. Heart mitochondrial metabolism was reduced in emetine-treated rabbits in comparison to the normal controls. However, the metabolic activity of the pair-fed control group was equally reduced. Only the liver mitochondrial metabolism of the pair-fed control group was reduced in relation to the normal controls, while the liver mitochondrial metabolism of emetine-treated rabbits remained unchanged. These data indicated that the reduction in heart mitochondrial metabolism resulted from the inanition induced by the chronic emetine treatment and not from a primary effect of the drug.