An investigation of the effects of chronic emetine poisoning on certain oxidative processes in rat heart and liver was conducted. Conventional manometric techniques were employed to study the respiration of the tissue preparations in the presence of various citric acid cycle intermediates. In addition, the effect of chronic emetine poisoning on nicotinamide adenine dinucleotide levels in rat myocardium was studied utilizing a spectrophotometric assay. In animals chronically poisoned by emetine, the oxygen uptake by heart homogenates respiring in the presence of citrate, malate, or a-ketoglutarate was lower than that obtained with homogenates prepared from sham-injected control animals. With succinate as the substrate, however, this effect was not observed. Liver homogenates prepared from emetinepoisoned rats did not show an impaired ability to oxidize any of-the substrates, including succinate, which were employed in the experiments with heart homogenates. Since succinate is not considered to be a prime substrate in the synthesis of high-energy phos hate intermediates by heart muscle, it is possible that the inhibition of the oxi&tion of certain metabolites, other than succinate, which have a greater potential for the synthesis of these energy rich compounds, may contribute to the apparent hypersensitivity of this organ to emetine. A considerable amount of experimental evidence indicates that in the oxidation of citrate, malate, or aketoglutarate electron transport involves the nicotinamide adenine nucleotides. With succinate, however, the electrons enter the transport system at the flavin nucleotide step. Under the conditions of this experiment, no changes were noted in nicotinamide adenine dinucleotide levels in heart homogenates prepared from emetine-poisoned rats when compared to sham-injected control animals.