The cause of increased radiosensitivity in ataxia-telangiectasia (AT) cells may be a defect in their ability to respond to DNA damage rather than a defect in their ability to repair it. Doses of x-radiation that markedly inhibited the rate of DNA synthesis in normal human cells caused almost no inhibition in AT cells and thus less delay during which x-ray damage could be repaired. The radioresistance of DNA synthesis in AT cells was primarily due to a much smaller inhibition of replicon initiation than in normal cells; the AT cells were also more resistant to damage that inhibited chain elongation. AT cells have been reported to undergo less radiation-induced mitotic delay than normal cells, which may cause them to move from G2 phase into mitosis before repair is complete and may result in the increased incidence of chromatid aberrations observed by others. Therefore, AT cells fail to go through those delays that allow normal cells to repair DNA damage before it can be expressed.

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