Sipilä I, Simell O, O'Donnell J J
J Clin Invest. 1981 Jun;67(6):1805-7. doi: 10.1172/jci110222.
Deficient activity of L-ornithine:2-oxoacid aminotransferase is associated with gyrate atrophy of the choroid and retina with hyperornithinemia, an autosomal recessive disease leading to blindness. Liver tissue from two patients contained trace activity of the enzyme. The Michaelis (Km) value of the mutant enzyme for ornithine was 200 mM, 50-fold higher than normal, but increasing the concentrations of alpha-oxoglutarate and pyridoxal 5'-phosphate to 10 times those giving maximal activity of the normal enzyme had no effect on the mutant enzyme. Substrate inhibition of the mutant could not be demonstrated at 1,000 mM ornithine concentration, whereas ornithine concentrations above 70 mM inhibited the normal enzyme. The data suggest that the abnormal L-ornithine:2-oxoacid aminotransferase in the two patients studied has an altered binding site for ornithine.
L-鸟氨酸:2-氧代酸氨基转移酶活性缺乏与伴有高鸟氨酸血症的脉络膜和视网膜回旋状萎缩相关,这是一种导致失明的常染色体隐性疾病。两名患者的肝脏组织中该酶的活性极低。突变酶对鸟氨酸的米氏(Km)值为200 mM,比正常情况高50倍,但将α-酮戊二酸和磷酸吡哆醛5'-磷酸的浓度提高至正常酶最大活性时浓度的10倍,对突变酶没有影响。在1000 mM鸟氨酸浓度下未观察到突变酶的底物抑制现象,而鸟氨酸浓度高于70 mM时会抑制正常酶。数据表明,所研究的两名患者体内异常的L-鸟氨酸:2-氧代酸氨基转移酶的鸟氨酸结合位点发生了改变。