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尿卟啉原I对大鼠肝脏匀浆中5-氨基酮戊酸代谢的刺激作用。

Stimulation of 5-aminolevulinic acid metabolism by uroporphyrinogen I in rat liver homogenate.

作者信息

Shivji A, Bernstein M

出版信息

Clin Biochem. 1985 Apr;18(2):88-91. doi: 10.1016/s0009-9120(85)80087-4.

Abstract

The effect of excess uroporphyrinogens I and III, coproporphyrinogen III, and the corresponding porphyrins, on the rate of 4-14C-5-aminolevulinic acid (ALA) metabolism was studied. Experiments were performed with mitochondria-free rat liver homogenates prepared from normal rats. The consumption of labelled 5-aminolevulinic acid was followed by measuring its level in aliquots removed at intervals. The pattern of porphyrinogen synthesis was examined by high pressure liquid chromatography. Only uroporphyrinogen I had an effect; it increased the rate of conversion of ALA and porphobilinogen (PBG) to porphyrinogens. Chromatographic analysis revealed increased synthesis of uroporphyrinogen and heptacarboxylic porphyrinogen. It is believed that this mechanism might explain the lack of ALA and PBG accumulation in erythropoietic porphyria and porphyria cutanea tarda, and the absence of acute porphyria attacks in these conditions.

摘要

研究了过量的尿卟啉原I和III、粪卟啉原III以及相应的卟啉对4-¹⁴C-5-氨基酮戊酸(ALA)代谢速率的影响。实验使用从正常大鼠制备的无线粒体大鼠肝脏匀浆进行。通过测量每隔一定时间取出的等分试样中标记的5-氨基酮戊酸的水平来跟踪其消耗情况。通过高压液相色谱法检查卟啉原合成模式。只有尿卟啉原I有影响;它增加了ALA和胆色素原(PBG)转化为卟啉原的速率。色谱分析显示尿卟啉原和七羧基卟啉原的合成增加。据信,这种机制可能解释了红细胞生成性卟啉病和迟发性皮肤卟啉病中ALA和PBG缺乏积累的原因,以及在这些情况下无急性卟啉病发作的原因。

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