Zinc lead-interaction in the rabbit.
Subacute lead poisoning was performed in a group of rabbits by dissolving lead acetate (5 g/l) in the drinking distilled water. Another group of rabbits was left to drink the same lead acetate solution containing 0.435 g/l acetate to study the effects of zinc on lead poisoning. A third group drinking 0.435 g/l zinc acetate solution alone was studied for comparison. Intake of zinc caused a relative decrease of blood, urine and faecal lead, significant activation of the lead-inhibited erythrocyte delta-aminolaevulinic acid dehydratase (ALAD) activity and a relative decrease of urinary delta-aminolaevulinic acid (ALA) level. The analysis of several tissues for lead indicated that zinc caused biotransformation of lead from blood to some other tissues, leading to excess storage in bone, kidney and liver and less extent in the lung, brain and muscle.
D000622:Aminolevulinic Acid / Q000652:urine; D000818:Animals; D001711:Biotransformation / Q000187:drug effects; D004347:Drug Interactions; D004912:Erythrocytes / Q000201:enzymology; D007854:Lead / Q000378:metabolism / Q000494:pharmacology*; D007855:Lead Poisoning / Q000378:metabolism*; D000623:Porphobilinogen Synthase / Q000097:blood; D011817:Rabbits; D014018:Tissue Distribution; D015032:Zinc / Q000494:pharmacology*
D007854:Lead; D000622:Aminolevulinic Acid; D000623:Porphobilinogen Synthase; D015032:Zinc