抄録
The increased excretion of δ-aminolevulinic acid and coproporphyrin III in the urine in human plumbism is we11 documented. However, two questions on porphyrin metabolism in lead poisoning remain unansweres, i. g.
a) By what mechanism is coproporphyrin excreted in large amount in severe lead poisoning, despite the fact of the complete inhibition of δ-aminolevulinic acid dehydratase activity in red cell by lead?
b) Increased excretion of porphobilinogen is a prominent sequel of lead poisoning in the rabbit, but this phenomenon is not so prominent in other species including the human. Is this due to the difference of species or the amount of lead administered?
This paper describes the experiment on the excretions of δ-aminolevulinic acid, porphobilinogen, and coproporphyrin that are measured simultaneously in rats poisoned with different amounts of lead.
The following results were obtained.
1) Lead poisoned rats (A and B) were prepared by administering lead (5μmoles/kg) 40 and 50 times subcutaneously over the period of 52 and 58 days, respectively. Rats (C and D) were treated by lead (100μmoles/kg) 9 times over the period of 30 days. Porphyrins and precursors were determined continuously for 67 and 95 days (A and B) and for 60 days (C and D), respectively.
2) In cases A and B, δ-aminolevulinic acid was elevated remarkably in the urine with the increase of lead administration. Coproporphyrin was increased slightly but porphobilinogen was not increase.
3) In cases C and D, the proportions of heme precursors excreted as δ-aminolevulinic acid and coproporphyrin are remarkably increased with the slight increase of porphobilinogen. Thus, the appearance of porphobilinogen in lead poisoning is due to the large amount of lead administered.
4) δ-aminolevulinic acid dehydratase activity in red cells determined at the end of the experiments was found to be completely inhibited in both groups.
5) These results support Sho, s experiment (Jap. J. Hygiene, 29, 379 (1974)) δ-aminolevulinic acid synthetase activity is stimulated in lead poisoning, thus excessive δ-aminolevulinic acid seems to overcome the blocking of δ-aminolevulinic acid dehydratase resulting in the increased formation of coproporphyrin in lead poisoning
