Effect of lead poisoning on the thiamine status and function in liver and blood of rats.

Three groups of Sprague-Dawley rats were fed a thiamine deficient diet, which was supplemented by daily subcutaneous injections of a minimum requirement of thiamine, and treated with lead(II) acetate in different molar ratios to thiamine (1:1, 2:1, 10:1) for 5 and 9 months, respectively. The prolonged administration of lead(II) acetate decreases the thiamine level in lead-treated rats and diminishes the enzymatic activity of pyruvate dehydrogenase as well as that of transketolase. The thiamine level in the liver decreased by 30 to 40% compared with a reference group and the activity of the erythrocyte transketolase diminished by 5 to 40%. The level of the blood pyruvate increased by about 20% and the rate of the oxidative decarboxylation of pyruvate by liver mitochondria decreased.