Ritter M A
Biochim Biophys Acta. 1981 Jan 29;652(1):151-9. doi: 10.1016/0005-2787(81)90218-5.
Normal and ataxia telangiectasia fibroblast strains were labeled with 3H- or 125I-labelled iododeoxyuridine, were stored at -75 degrees C to accumulate damage, and were thawed for survival assays. X-ray survival of frozen, unlabeled cells was also determined. The ataxia telangiectasia strains were about twice as sensitive as normal (based upon survival curve slopes) when irradiated with X-rays or 3H decays under frozen conditions. Accumulated 125I decays, while about 13 times more toxic than 3H decays, also killed ataxia telangiectasia cells about twice as efficiently as normal cells. These results indicate that a large proportion of 125I-induced damage--at least 50%--is subject to repair in normal cells. In addition, they suggest that ataxia telangiectasia cells less capably repair a lesion that is induced in common by X-rays and 125I, but in larger porportion by the latter--probably a DNA double-strand break.