Differential inhibition of erythrocyte and hepatic uroporphyrinogen I synthetase activity by lead.
Differential inhibition of erythrocyte and hepatic uroporphyrinogen I synthetase activity by lead.
复制标题
铅对红细胞和肝尿卟啉原 I 合成酶活性的差异抑制。
DOI：
10.1016/0024-3205(74)90076-9
复制
发表时间：
1974
期刊：
影响因子：
6.1
通讯作者：
T. R. Tephly
中科院分区：
文献类型：
--
作者：
Walter N. Piper;T. R. Tephly
在铅中毒时，胆红素原(PBG)的排泄可能增加。目前，还没有关于铅的这种效应的解释。这些研究表明，铅对溶血制剂中的红细胞尿卟啉原(URO)1合成酶活性有抑制作用，但对肝酶几乎没有影响。低浓度的氯化铅(5×10−6M)对人溶血产物的活性有明显的抑制作用，10−4M的氯化铅对人和大鼠溶血产物的URO 1合成酶活性分别有92%和58%的抑制作用。然而，浓度达10−4M的氯化铅对大鼠或人肝制剂的活性没有明显的抑制作用。这些结果提示，铅中毒后PBG的排泄可能来源于红细胞组织。
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 × 10−6M produced a significant inhibition of activity in human hemolysates, and 10−4M 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 10−4M 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.