Evidence for an adaptive DNA repair pathway in CHO and human skin fibroblast cell lines

Abstract
Chronic treatment of a Chinese hamster ovary (CHO) and a SV40-transfomred human skin fibroblast (GM637) cell line with non-toxic levels of MNNG [N-methyl-N''-nitro N-nitrosoguanidine] renders the cells resistant to the induction of sister chromatid exchange (SCE) by further alkylation damage. CHO cells also become resistant to killing. GM637 cells have not yet been tested. Having ruled out explanations such as changes in cell cycle distribution, mutagen permeability and mutagen detoxification, resistance is probably achieved by the cells becoming more efficient at repairing alkylation damage, analogous to the adaptive response of Escherichia coli.