Cell Death, Chromosome Damage and Mitotic Delay in Normal Human, Ataxia Telangiectasia and Retinoblastoma Fibroblasts after X-irradiation

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Abstract
Human fibroblasts with reported differential sensitivity to ionizing radiation (i.e., normal donors and patients with ataxia telangiectasia and retinoblastoma) support the hypothesis that chromosome aberrations contribute much more to lethality than spindle defects. A positive correlation was observed between chromosome aberration frequencies and cell killing and no induced spindle defects. The hypothesis that DNA lesions are less effectively repaired in the sensitive cells and give rise to more G2 mitotic delay and chromosome aberrations is not substantiated since X-ray sensitive fibroblasts from the ataxia patient suffered less mitotic delay than cells from normal donors. A common lesion for mitotic delay and chromosome aberrations can still be assumed by adopting the hypothesis of Painter and Young that the defect in ataxia cells is not in repair but in a failure of DNA damage to initiate mitotic delay. Retinoblastoma cells were of normal radiation sensitivity (cell killing and aberrations).
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