We have previously described chromosomal instability in cells of a human-hamster hybrid cell line after exposure to X rays. Chromosomal instability in these cells is characterized by the appearance of novel chromosomal rearrangements multiple generations after exposure to ionizing radiation. To identify the cellular target(s) for radiation-induced chromosomal instability, cells were treated with125 I-labeled compounds and frozen. Radioactive decays from125 I cause damage to the cell primarily at the site of their decay, and freezing the cells allows damage to accumulate in the absence of other cellular processes. We found that the decay of <tex-math>${}^{125}{\rm I}\text{-iododeoxyuridine}$</tex-math>, which is incorporated into the DNA, caused chromosomal instability. While cell killing and first-division chromosomal rearrangements increased with increasing numbers of125 I decays, the frequency of chromosomal instability was independent of dose. Chromosomal instability could also be induced from incorporation of <tex-math>${}^{125}{\rm I}\text{-iododeoxyuridine}$</tex-math> without freezing the cells for accumulation of decays. This indicates that DNA double-strand breaks in frozen cells resulting from125 I decays failed to lead to instability. Incorporation of an125 I-labeled protein (<tex-math>${}^{125}{\rm I}\text{-succinyl-concanavalin}$</tex-math> A), which was internalized into the cell and/or bound to the plasma membrane, neither caused chromosomal instability nor potentiated chromosomal instability induced by <tex-math>${}^{125}{\rm I}\text{-iododeoxyuridine}$</tex-math>. These results show that the target for radiation-induced chromosomal instability in these cells is the nucleus.

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