Nishida Y, Kamatani N, Tanimoto K, Akaoka I
Agents Actions. 1979 Dec;9(5-6):549-52. doi: 10.1007/BF01968126.
Allopurinol-riboside competitively inhibits the action of purine nucleoside phosphorylase on inosine in vitro with a Ki of 277 mumol. After simple incubation of allopurinol-riboside with PNP, allopurinol was not formed. Lymphocyte blastogensis induced by PHA and Con A was significantly suppressed by allopurinol-riboside in a concentration-dependent manner. When LPS was used as a mitogen, the inhibition of allopurinol-riboside on lymphocyte proliferation was less marked. Humoral immunity was not suppressed by allopurinol-riboside. In contrast, cellular immunity was significantly suppressed by allopurinol-riboside in vivo. These results suggested that allopurinol-riboside is a drug which produces a model of PNP deficiency, and that it may be a useful inhibitor of cellular immunity.
别嘌呤醇-核糖苷在体外能竞争性抑制嘌呤核苷磷酸化酶对肌苷的作用，其抑制常数（Ki）为277 μmol。别嘌呤醇-核糖苷与嘌呤核苷磷酸化酶简单孵育后，不会形成别嘌呤醇。别嘌呤醇-核糖苷能以浓度依赖的方式显著抑制由植物血凝素（PHA）和刀豆蛋白A（Con A）诱导的淋巴细胞增殖。当使用脂多糖（LPS）作为促有丝分裂原时，别嘌呤醇-核糖苷对淋巴细胞增殖的抑制作用不太明显。别嘌呤醇-核糖苷不会抑制体液免疫。相反，在体内别嘌呤醇-核糖苷能显著抑制细胞免疫。这些结果表明，别嘌呤醇-核糖苷是一种能产生嘌呤核苷磷酸化酶缺乏模型的药物，并且它可能是一种有用的细胞免疫抑制剂。
