SummaryRats were fed either a thiamine-deficient diet or diets con taining pyrithiamine or oxythiamine. When symptoms of thiamine deficiency appeared, the animals were injected intraperitoneally with [2-14C] pyruvate six to twelve minutes prior to sacrifice. Free glutamic and aspartic acids were isolated from liver and brain and degraded. The results indicate that, in thiamine-deficient or oxythiamine-treated rats, pyruvate metabolism in liver and brain is similar to that in normal animals. In contrast, pyrithiamine drastically decreases the oxidative decarboxyla tion of pyruvate by rat liver.Since the classical work of PETERS (1) using pigeons, thiamine deficiency has often been described as a well defined biochemical lesion. Lack of thiamine is supposed to diminish the organism's ability to decarboxylate pyruvate, and this impairment of pyruvate oxidation is thought by many to account for the physiolo gical changes, particularly polyneuritis, observed in thiamine deficiency.However, the results of a large number of diverse experiments (2-16) have led to serious questioning of the concept that thiamine deficiency results in a gross change in the ability of animal organs to decarboxylate pyruvate. The parameters measured include rates of pyruvate oxidation in vivo (2, 12) and in vitro (3-8), concentrations of blood pyruvate (6, 8) and brain thiamine (13, 14) and 14C labeling patterns in glutamic acid after administration of pyruvate-14C (15, 16). In many investigations, thiamine deficiency was induced by administration of the antime tabolites oxythiamine and pyrithiamine as well as by thiamine deprivation. Al though some treatments have resulted in decreased rates of pyruvate oxidation in vitro (3, 6), these do not necessarily correlate with increases in blood pyruvate and lactate concentrations (6), indicating that there is no clear evidence that the Present address: