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The combined action of chemical carcinogens on DNA repair in human cells

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Summary

Excision repair was studied in normal human and ataxia telangiectasia (AT) cells proficient in repair of UV and its mimetic chemicals, and in xeroderma pigmentosum group C (XP C) cells (deficient in repair of UV and its mimetics), after treatment with several combinations of chemical carcinogens, by the photolysis of bromodeoxyuridine incorporated into parental DNA during repair. Results indicate that repair was additive in AT, and XP C cells treated with N-acetoxy-2-acetylaminofluorene (AAAF) plus ethyl methanesulfonate (EMS) or methyl methanesulfonate (MMS) indicating that there are different rate limiting steps for removal of both types of damage. Data on the combinations of 4-nitroquinoline 1-oxide (4NQO) plus MMS or EMS are difficult to interpret, but they do not indicate inhibition of DNA repair.

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Author notes

  1. Farid E. Ahmed

    Present address: Pharmacopathics Research Laboratories, 9705 North Washington Blvd., 20810, Laurel, MD, USA

Authors and Affiliations

  1. Biology Department, Brookhaven National Laboratory, 11973, Upton, NY, USA

    Farid E. Ahmed

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  1. Farid E. Ahmed
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Research carried out under the auspices of the U.S. Dept. of Energy

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Ahmed, F.E. The combined action of chemical carcinogens on DNA repair in human cells. Radiat Environ Biophys 18, 57–64 (1980). https://doi.org/10.1007/BF01324374

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  • DOI: https://doi.org/10.1007/BF01324374

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