Suppression by ethanol of acetate and hexanoate oxidation studied by nonrecirculating liver perfusion

The relationship between the effect of ethanol on the redox state and the tricarboxylic acid cycle has been studied by perfusion of hemoglobin-free medium through the liver without recirculation. The production of ¹⁴CO₂ from 1-¹⁴C-acetate was suppressed 63 % by ethanol and that from 1-¹⁴C-hexanoate by 54 % in normal livers. These suppressions were much weaker in livers from hyperthyroid rats and stronger in those from hypothyroid rats. Conditions where the ethanol-induced elevation of the lactate/pyruvate ratio was decreased led to less suppression of substrate oxidation by ethanol.