Sinelshchikova T A, Lvova G N, Shoniya N N, Zasukhina G D
Laboratory of Genetic Mechanisms of Repair, N.I. Vavilov Institute of General Genetics, U.S.S.R. Academy of Sciences, Moscow.
Mutat Res. 1987 Nov;184(3):265-70. doi: 10.1016/0167-8817(87)90025-3.
Fibroblasts obtained from biopsied material and lymphocytes from patients with homocystinuria were studied for repair activity using the criterion of repair of DNA breaks induced by 4-nitroquinoline 1-oxide and gamma-irradiation and criteria of reactivation and induced mutagenesis of vaccinia virus. Lymphocytes showed defective DNA repair for all these criteria. In fibroblast cultures, the inhibition of cell-repair activity for the gamma-type was retained. The number of spontaneous and gamma-induced virus mutations increased as passaging of fibroblasts proceeded.
从活检材料中获取的成纤维细胞以及同型胱氨酸尿症患者的淋巴细胞，通过4-硝基喹啉1-氧化物和γ射线诱导的DNA断裂修复标准以及痘苗病毒的复活和诱导诱变标准来研究其修复活性。对于所有这些标准，淋巴细胞均显示出DNA修复缺陷。在成纤维细胞培养中，γ型细胞修复活性的抑制作用仍然存在。随着成纤维细胞传代，自发和γ诱导的病毒突变数量增加。
