Elder G H, Roberts A G
Department of Medical Biochemistry, University of Wales College of Medicine, Cardiff, England.
J Bioenerg Biomembr. 1995 Apr;27(2):207-14. doi: 10.1007/BF02110035.
Uroporphyrinogen decarboxylase (EC 4.1.1.37) catalyzes the decarboxylation of uroporphyrinogen III to coproporphyrinogen III. The amino acid sequences, kinetic properties, and physicochemical characteristics of enzymes from different sources (mammals, yeast, bacteria) are similar, but little is known about the structure/function relationships of uroporphyrinogen decarboxylases. Halogenated and other aromatic hydrocarbons cause hepatic uroporphyria by decreasing hepatic uroporphyrinogen decarboxylase activity. Two related human porphyrias, porphyria cutanea tarda and hepatoerythropoietic porphyria, also result from deficiency of this enzyme. The roles of inherited and acquired factors, including iron, in the pathogenesis of human and experimental uroporphyrias are reviewed.
尿卟啉原脱羧酶(EC 4.1.1.37)催化尿卟啉原III脱羧生成粪卟啉原III。来自不同来源(哺乳动物、酵母、细菌)的该酶的氨基酸序列、动力学特性和物理化学特征相似,但关于尿卟啉原脱羧酶的结构/功能关系却知之甚少。卤代烃和其他芳烃通过降低肝脏尿卟啉原脱羧酶活性而导致肝性卟啉病。两种相关的人类卟啉病,迟发性皮肤卟啉病和肝红细胞生成性卟啉病,也由该酶缺乏引起。本文综述了包括铁在内的遗传和后天因素在人类和实验性卟啉病发病机制中的作用。