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.
D000818:Animals; D004912:Erythrocytes / Q000201:enzymology; D005260:Female; D007855:Lead Poisoning / Q000378:metabolism*; D008099:Liver / Q000378:metabolism*; D008297:Male; D008930:Mitochondria, Liver / Q000378:metabolism; D011773:Pyruvates / Q000097:blood / Q000378:metabolism; D051381:Rats; D013832:Thiamine Deficiency / Q000378:metabolism*; D013835:Thiamine Pyrophosphate / Q000097:blood / Q000378:metabolism*; D014174:Transketolase / Q000097:blood
D011773:Pyruvates; D014174:Transketolase; D013835:Thiamine Pyrophosphate