Evidence for an adaptive DNA repair pathway in CHO and human skin fibroblast cell lines.
作者： Leona Samson , Jeffrey L. Schwartz
DOI: 10.1038/287861A0
关键词: Cell culture 、 Biology 、 DNA Repair Pathway 、 Escherichia coli 、 Molecular biology 、 Cell biology 、 DNA Alkylation 、 Sister chromatid exchange 、 Mutation 、 Mutagen 、 Chinese hamster ovary cell
摘要: When Escherichia coli is chronically exposed to very low, nontoxic doses of a monofunctional alkylating agent (notably N-methyl-N′-nitro-nitrosoguanidine, MNNG), the adaptive DNA repair pathway induced which enables bacteria resist killing and mutagenic effects further alkylation damage1–3. Mutation resistance in adapted achieved, at least partly, by greatly increased capacity cells eliminate minor product O6-methyl-guanine4–6, has been strongly implicated as premu-tagenic7,8 precarcinogenic9. We now show that chronic treatment Chinese hamster ovary (CHO) SV40-transformed human skin fibroblast (GM637) cell line with non-toxic levels MNNG renders resistant induction sister chromatid exchange (SCE) damage. CHO also become (GM637 have not yet tested). Having ruled out explanations such changes cycle distribution, mutagen permeability detoxification, we conclude probably achieved becoming more efficient repairing alleviation damage, analogous response E. coli1.
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