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Deficient recovery from potentially lethal radiation damage in ataxia telangiectasia and xeroderma pigmentosum

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Abstract

THE enhanced survival that occurs when mammalian cells are maintained in a density-inhibited state for a short time after treatment with X rays, ultraviolet light or drugs has been termed potentially lethal damage repair (PLDR)1–3. It is analogous to liquid-holding recovery in bacteria and yeast, and has been studied using a variety of agents in different cell lines3–5 and in malignant tumours6,7. To investigate the relationship between this cellular recovery phenomenon and repair at the molecular level, we have examined PLDR in human diploid cell strains with known molecular repair defects. We report here that xeroderma pigmentosum (XP) skin fibroblasts show no PLDR following ultraviolet light irradiation, whereas ataxia telangiectasia (AT) skin fibroblasts are specifically deficient in PLDR following X-ray irradiation. The results suggest that, as in bacterial cells, this cellular recovery phenomenon does reflect molecular DNA repair—probably the excision repair pathway.

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Authors and Affiliations

  1. Laboratory of Radiobiology, Department of Physiology, Harvard University, School of Public Health, Joint Center for Radiation Therapy, Harvard Medical School, Boston, Massachusetts, 02115

    RALPH R. WEICHSELBAUM, JOHN NOVE & JOHN B. LITTLE

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  1. RALPH R. WEICHSELBAUM
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  2. JOHN NOVE
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  3. JOHN B. LITTLE
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WEICHSELBAUM, R., NOVE, J. & LITTLE, J. Deficient recovery from potentially lethal radiation damage in ataxia telangiectasia and xeroderma pigmentosum. Nature 271, 261–262 (1978). https://doi.org/10.1038/271261a0

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