Formaldehyde-induced cytotoxicity and sister-chromatid exchanges in human lymphocyte cultures |
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Authors: | R A Kreiger V F Garry |
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Affiliation: | 1. Department of Fundamental Radiology, Osaka University Medical School, Osaka 530 Japan;2. Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709 U.S.A. |
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Abstract: | The role of the error-prone misrepair pathway in mutagenesis was examined for a series of mutagens in umuC+ and umuC36 strains of Escherichia coli. Mutagenesis by ENU, MNU, MNNG and EMS was independent of the umuC+ gene function, while mutagenesis by MMS, 4NQO, γ-rays and UV was largely umuC+-dependent. Residual mutagenesis following UV-treatment of a umuC? strain showed the same mutational specificity seen in the umuC+ strain. In contrast, the umuC mutation altered specificity substantially in an excision-repair-defective strain that showed a UV-spectrum strikingly different from that seen in an excision-repair-proficient strain. Only one of nine trpE frameshift mutations examined was reverted by UV-light and its reversion was umuC-dependent. In comparison, the dependence of frameshift mutagenesis following ICR 191 treatment was site-specific, suggesting at least two mechanisms of frameshift mutagenesis, one dependent upon misrepair, the other not.The results, together with those of previous reports (Kato and Nakano, 1981; Shinoura et al., 1983), suggest that the umuC+ gene exerts it's mutator activity via misrepair of DNA lesions provoking the induction of all types of mutational events, though following UV-irradiation mainly transition events are recovered. |
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Keywords: | dose producing 37% survival EMS ethyl methanesulfonate ENU MMS methyl methanesulfonate MNNG MMN 4NQO Address all correspondence to: Takesi Kato, Department of Fundamental Radiology, Osaka University Medical School, Osaka 530 (Japan). |
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