Abstract
The experiments were undertaken in order to investigate the mechanism by which ethanol inhibits the tricarboxylic acid cycle. Isolated livers were perfused with human erythrocytes suspended in an artificial “plasma”. Ethanol was added 45 min. after the start of the perfusions. In some experiments dinitrophenol was added after ethanol. The O2 consumption in the perfused rat liver was unaltered by the addition of ethanol to the medium, whereas the CO2 production fell considerably, resulting in a decrease in the RQ from 0.8 to 0.4. The addition of ethanol caused an increase in both lactate/pyruvate and hydroxybutyrate/acetoacetate ratios in the perfusion medium. When DNP was added to the perfusion medium, half an hour after the addition of ethanol, both the O2 uptake and CO2 production increased. The RQ increased from 0.4 to 0.6. The lactate/pyruvate ratio was increased by the addition of DNP because the amount of lactate liberated from the liver was increased, while the pyruvate concentration was almost unchanged. The addition of DNP caused a fall in the hydroxybutyrate/acetoacetate ratio from 2.2 to 0.6, and a net disappearance of ketone bodies was observed. An opposite change in the extra‐ and intramitochondrial NADH/NAD ratio was observed, favouring the hypothesis that they are really independent of each other. A correlation between the intramitochondrial NADH/NAD ratio and the tricarboxylic acid cycle inhibition was demonstrated.
Published Version
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