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1.
Vopr Med Khim ; 43(3): 158-64, 1997.
Article in Russian | MEDLINE | ID: mdl-9273779

ABSTRACT

Experimentally induced lead poisoning especially under simultaneous iron deficit leads to the development of secondary thiamine insufficiency. Erythrocyte riboflavin content and erythrocyte glutathion reductase and aspartate aminotransferase activities have been demonstrated to be increased. Lead treatment is accompanied with the increase of urinary excretion of riboflavin, 4-pyridoxic acid and 1-vtthylnicotinamide in rats fed with adequate diet. Thus lead intoxication and iron deficiency influence vitamin B group metabolism.


Subject(s)
Iron Deficiencies , Lead Poisoning/metabolism , Vitamin B Complex/metabolism , Animals , Aspartate Aminotransferases/blood , Erythrocytes/drug effects , Erythrocytes/metabolism , Glutathione Reductase/blood , Lead Poisoning/complications , Male , Niacinamide/analogs & derivatives , Niacinamide/urine , Pyridoxic Acid/urine , Rats , Riboflavin/blood , Riboflavin/urine , Thiamine/blood , Thiamine/urine , Thiamine Deficiency/blood , Thiamine Deficiency/etiology , Thiamine Deficiency/urine
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