Abstract
In lead poisoning porphobilinogen (PBG) excretion may be increased. Presently, there is no explanation for this effect of lead. These studies show that lead inhibits erythrocytic uroporphyrinogen (URO) 1 synthetase activity in hemolysate preparations but has little effect on the hepatic enzyme. Lead chloride concentrations as low as 5 × 10 −6 M produced a significant inhibition of activity in human hemolysates, and 10 −4 M lead chloride produced 92 and 58% inhibition of URO 1 synthetase activity in human and rat hemolysates, respectively. However, lead chloride in concentrations up to 10 −4 M was unable to effect appreciable inhibition of activity in rat or human liver preparations. These results suggest that the source of PBG excretion following lead poisoning may be from erythropoietic tissue.
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