遗传性黄嘌呤氧化酶缺乏症中吡嗪酰胺和别嘌醇的代谢
Metabolism of pyrazinamide and allopurinol in hereditary xanthine oxidase deficiency.
作者信息
Yamamoto T, Higashino K, Kono N, Kawachi M, Nanahoshi M, Takahashi S, Suda M, Hada T
机构信息
The Third Department of Internal Medicine, Hyogo College of Medicine, Japan.
出版信息
Clin Chim Acta. 1989 Feb 28;180(2):169-75. doi: 10.1016/0009-8981(89)90348-3.
The metabolism of pyrazinamide and allopurinol was studied in three xanthinuric patients from two families with hereditary xanthinuria to determine whether both substrates were oxidized only by xanthine oxidase or by other oxidases as well. One xanthinuric patient could neither metabolize pyrazinamide into 5-hydroxypyrazinamide nor allopurinol into oxypurinol. Two xanthinuric patients could metabolize both pyrazinamide into 5-hydroxypyrazinamide and allopurinol into oxypurinol but could not oxidize pyrazinoic acid to 5-hydroxypyrazinoic acid. These findings suggest that xanthinuria comprises at least two subgroups.
在来自两个患有遗传性黄嘌呤尿症家族的三名黄嘌呤尿症患者中研究了吡嗪酰胺和别嘌呤醇的代谢，以确定这两种底物是否仅由黄嘌呤氧化酶氧化，还是也由其他氧化酶氧化。一名黄嘌呤尿症患者既不能将吡嗪酰胺代谢为5-羟基吡嗪酰胺，也不能将别嘌呤醇代谢为氧嘌呤醇。两名黄嘌呤尿症患者既能将吡嗪酰胺代谢为5-羟基吡嗪酰胺，又能将别嘌呤醇代谢为氧嘌呤醇，但不能将吡嗪酸氧化为5-羟基吡嗪酸。这些发现表明，黄嘌呤尿症至少包括两个亚组。
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