Measurements of the concentration of pyruvate and related compounds in the rat liver and blood in carbontetrachloride intoxication revealed the follwing: (1) Main histological changes of rat liver produced by subcutaneous injection of carbontetrachloride twice a week were centrolobural fatty infiltration in the first week, slight reaction of mesenchymal cells and fibrosis of portal triad in the second week, progression of the fibrosis in the fourth week, formation of pseudoacinus in the sixth week, and appearance of nodural cirrhosis from the eighth to twelfth week. (2) The pyruvate concentration in the liver paralleled with that in the blood (r=1.24, p<0.05). The pyruvate concentration increased in acute stage of carbontetrachloride intoxication (the first week), reaching the maximum in the sixth week, when the marked fibrosis was observed in the liver histology. There after the pyruvate level decreased in the eighth and tenth weeks and increased again in the twelfth week. (3) The pyruvate-oxidizing activity of rat liver mitochondrial fraction (QO(2)) decreased approximately half in the acute stage (the first week) of carbontetrachloride intoxication and below one tenth in most cases after the eighth week. Since a significant negative correlation between the pyruvate concentration and the QO(2) value was found until the fourtn week, the increase in the liver and blood pyruvate might be caused mainly by the disturbance of pyruvate oxidation in the rat liver mitochondria. (4) The negative correlation between the pyruvate and QO(2) became weak after the sixth week of carbontetrachloride intoxication. In the latter stages the lactate concentration of liver increased more than that in the acute stage. Consequently, the lactate/pyruvate ratio and hence the total pyruvate lactate pool of the liver increased more. For the explanation of the increased lactate level and the lactate/pyruvate ratio, it is considerable that a local hypoxia may develop as a result of the disturbance in liver circulation caused by a repetition of degeneration and regeneration of liver cells, and the hypoxia would accelerate glycolysis in the liver and at the same time decrease the oxidation of DPNH as well as that of pyruvate. The increase of pyruvate level and the decrease of lactate/pyruvate ratio in the twelfth week, when liver injury advanced progressively, could be accounted for by the extreme disturbance of oxidation and by a suppression of glycolysis which would exist in the latter stage. Although the metabolism of pyruvate in the liver tissue is easily influenced by hypoxia, as suggested by the changes in lactate/pyruvate ratio and total pyruvate-lactate pool size, the pyruvate level in the blood does not seem to reflect these metabolic changes of the liver sensitively enough. (5) Blood sugar levels decreased in accordance with the advance of liver injury. The decrease of blood sugar may be caused by a disturbance of reguratory mechanism of blood sugar by the liver.