Lack of induction of O6-methylguanine-DNA methyltransferase in mammalian cells treated with N-methyl-N'-nitro-N-nitrosoguanidine.
Lack of induction of O6-methylguanine-DNA methyltransferase in mammalian cells treated with N-methyl-N'-nitro-N-nitrosoguanidine.
复制标题
用 N-甲基-N-硝基-N-亚硝基胍处理的哺乳动物细胞中缺乏 O6-甲基鸟嘌呤-DNA 甲基转移酶的诱导。
DOI：
10.1093/carcin/5.2.277
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发表时间：
1984
期刊：
影响因子：
4.7
通讯作者：
Mitra,S
中科院分区：
文献类型：
--
作者：
Foote,RS;Mitra,S
使用含有 O6-甲基(8-3H)鸟嘌呤的合成 DNA 底物测定经多剂量 N-甲基-N'-硝基-N-亚硝基胍 (MNNG) 处理的 HeLa 细胞、中国仓鼠卵巢细胞和正常大鼠肾细胞提取物中 O6-甲基鸟嘌呤-DNA 甲基转移酶对诱变前碱基的去甲基化作用。在任何测试的细胞系中均未观察到甲基转移酶活性的诱导。通过在广泛的剂量水平范围内进行单次或多次 MNNG 处理，O6-甲基鸟嘌呤修复能力良好的细胞系 (Mex+) 中甲基转移酶的组成水平以剂量依赖性方式降低。基本活性水平的恢复需要 24 至 48 小时的潜伏期。修复缺陷（Mex−）细胞系缺乏组成型和诱导型甲基转移酶活性。
A synthetic DNA substrate containing O6-methyI(8-3H)guanine was used to assay demethylation of the premutagenic base by O6-methylguanine-DNA methyltransferase in extracts of HeLa cells, Chinese hamster ovary cells and normal rat kidney cells which had been treated with multiple doses of N-methyl-N' -nitro-N-nitrosoguanidine (MNNG). No induction of methyltransferase activity was observed in any of the cell lines tested. Constitutive levels of methyltransferase in cell lines proficient (Mex+) in O6-methylguanine repair were decreased in a dose-dependent fashion by either single or multiple treatments with MNNG over a broad range of dose levels. Recovery of constitutive levels of activity required 24-to 48-h incubation periods. Repair deficient (Mex−) cell lines lacked both constitutive and inducible methyltransferase activity.