Decreased DNA repair synthesis and defective colony-forming ability of ataxia telangiectasia fibroblast cell strains treated with N-methyl-N'-nitro-N-nitrosoguanidine.
Decreased DNA repair synthesis and defective colony-forming ability of ataxia telangiectasia fibroblast cell strains treated with N-methyl-N'-nitro-N-nitrosoguanidine.
复制标题
用 N-甲基-N-硝基-N-亚硝基胍处理的共济失调毛细血管扩张成纤维细胞株的 DNA 修复合成减少和集落形成能力缺陷。
作者：
D. Scudiero
对来自常染色体隐性遗传病共济失调毛细血管扩张症（AT）患者的6株人成纤维细胞和来自正常人的5株细胞进行了DNA修复合成和治疗后集落形成能力的测定。用苯甲酰化萘酰化二乙胺乙基纤维素法测定，所有11株细胞株经甲磺酸甲酯和紫外光处理后的DNA修复合成水平大致相同。4株AT细胞株经n -甲基-n′-硝基-n -亚硝基胍（MNNG）处理后，其修复能力为正常细胞株的27% ~ 41%。两株AT细胞株经MNNG处理后修复合成水平正常。经甲磺酸甲酯和紫外光处理后的菌落形成能力测定，所有被试AT菌株均存活正常。MNNG处理后，6株AT细胞株的存活率下降。MNNG浓度对[3H]胸腺嘧啶摄取的抑制作用在所有正常和AT细胞株中都是相似的。
DNA repair synthesis and posttreatment colony-forming ability were measured in six human fibroblast cell strains derived from patients with the autosomal recessive disorder, ataxia telangiectasia (AT), and five cell strains from normal individuals. All 11 cell strains showed approximately equal levels of DNA repair synthesis after methyl methanesulfonate and ultraviolet light treatments assayed by the benzoylated naphthoylated diethylaminoethyl-cellulose method. Four AT cell strains exhibited 27 to 41% of the repair shown by normal cell strains after treatment with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). Two AT cell strains had normal levels of repair synthesis after MNNG treatment. All the AT strains tested had normal survival after treatment with methyl methanesulfonate and ultraviolet light as assayed by posttreatment colony-forming ability. The six AT cell strains exhibited diminished survival after MNNG treatment. The inhibition of [3H]thymidine uptake as a function of MNNG concentration was similar for all the normal and AT cell strains tested.