Willers I, Held K R, Singh S, Goedde H W
Clin Genet. 1977 Mar;11(3):193-200. doi: 10.1111/j.1399-0004.1977.tb01299.x.
Incorporation of hypoxanthine, resistance to 8-azaguanine and activation by lyophilisation have been studied in cultured human fibroblasts. Cells from one family where there was a boy with Lesch-Nyham syndrome, from two families with variant H-PRT mutations and three cell strains from patients with the Lesch-Nyham syndrome were investigated. Cells from patients with the Lesch-Nyham syndrome showed almost no hypoxanthine incorporation and resistance to concentrations of 8-azaguanine up to 10(-3) M, whereas cells of patients with partial H-PRT deficiency demonstrated variant patterns of hypoxanthine uptake and partial resistance to 8-azaguanine. Lyophilisation of fibroblast sediment from patients with the Lesch-Nyhan syndrome and patients with variant H-PRT mutations showed activation of the deficient or partially deficient H-PRT enzyme. No such activation was observed in healthy controls. Activation of lyophilised fibroblast extract from patients and controls was not obtained. These results suggest that H-PRT could be associated with the cell membranes.
在培养的人成纤维细胞中,对次黄嘌呤的掺入、对8-氮杂鸟嘌呤的抗性以及冻干激活作用进行了研究。研究了来自一个有患莱施-尼汉综合征男孩的家庭的细胞、来自两个有变异型次黄嘌呤-鸟嘌呤磷酸核糖转移酶(H-PRT)突变的家庭的细胞以及来自三名莱施-尼汉综合征患者的三个细胞株。莱施-尼汉综合征患者的细胞几乎不掺入次黄嘌呤,并且对高达10^(-3) M浓度的8-氮杂鸟嘌呤具有抗性,而部分H-PRT缺乏患者的细胞则表现出次黄嘌呤摄取的变异模式以及对8-氮杂鸟嘌呤的部分抗性。对莱施-尼汉综合征患者和有变异型H-PRT突变患者的成纤维细胞沉淀物进行冻干显示,缺陷或部分缺陷的H-PRT酶被激活。在健康对照中未观察到这种激活。患者和对照的冻干成纤维细胞提取物未获得激活。这些结果表明H-PRT可能与细胞膜相关。