Energy metabolism in the liver of rats fed a diet contaminated with dithiocarbamates

Young male rats, Wistar CF strain, weighing about 100 g, were fed during 14 days with a well-balanced diet, but containing either 275 p.p.m. nabame, either 600 p.p.m. thirame or 3 600 p.p.m. zinebe. The animals given the non-contaminated diet were the controls. On the evening before the experiment, they were all fasted and some of them, forced to walk during 18 hours in a restraint wheel. On the morning of the experiment, some of the rats which have not been working were placed in a cold room at + 4 degrees C, and some others were given an i.p. injection of 2,6 g glucose per kg body weight. The animals were then killed, those that received the glucose treatment 30 mn after the injection, the cold-exposed rats 90 mn after the beginning of their exposure. The redox and energy potentials of the liver tissue were determined after the enzymatic assay of the following liver metabolites : lactate, pyruvate, beta-hydroxybutyrate, acetoacetate, ATP, ADP, AMP, inorganic phosphate. The thirame group rats had the smallest body weight and the lowest food intake. All the pesticides-exposed animals has a higher liver weight than predicted by their body weight. The pesticides-containing diets decreased liver lactate concentration and the lac/pyr ratio. Thirame was the more efficient and it partly impaired the glucose induced increase of the cytoplasmic redox potential, as estimated from the variation of the lac/pyr ratio. The pesticide-containing diets also lowered the liver concentrations of beta-hydroxybutyrate, acetoacetate, and their ratio. Last the pesticides, which but slightly modified the liver contents in adenine nucleotides and inorganic phosphate in the fasting state, increased the ATP fall following cold exposure and decreased the net ATP synthesis produced by glucose administration. The thirame diet was the more efficient in our experimental conditions, the zinebe diet the least one. It was concluded in our discussion that dietary dithiocarbamates either induced a hyperthyroidic status in the animal, or acted themselves as thyroxin-like compounds, because the liver metabolism was more directed towards heat production than towards that of chemical energy available for syntheses.