Effect of Lead Poisoning on the Thiamine Status and Function in Liver and Blood of Rats.

Abstract

Three groups of Sprague-Dawley rats were fed a thiamine deficient diet which was supplemented by daily s.c. 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 mo., respectively. The prolonged administration of lead(II) acetate decreases the thiamine level in Pb-treated rats and diminishes the enzymatic activity of pyruvate dehydrogenase and that of transketolase. The thiamine level in the liver decreased by 30-40% compared with a reference group and the activity of the erythrocyte transketolase diminished by 5-40%. The level of the blood pyruvate increased by about 20% and the rate of oxidative decarboxylation of pyruvate by liver mitochondria decreased.