Oxygen toxicity and chromosomal breakage in ataxia telangiectasia.
Toxic effects of ionizing radiation and elevated O2 levels (hyperoxia) are both thought to be mediated by oxidizing free radicals. In view of the reported hypersensitivity of ataxia telangiectasia (A-T) cells to the clastogenic effect of ionizing radiation, the chromosomal sensitivity of A-T cells to hyperoxic culture conditions was investigated in unirradiated and G0-irradiated A-T lymphocyte cultures. Unlike Fanconi's anaemia lymphocytes, which tend to respond to oxygen, especially after treatment with mitomycin C, both non-irradiated and G0-irradiated A-T lymphocytes failed to show an effect. We conclude that the excessive spontaneous and radiation-induced chromosomal breakage in A-T does not result from a deficiency in the cellular defences against the clastogenic effect of hyperoxia.
D001260:Ataxia Telangiectasia / Q000235:genetics*; D001761:Bleomycin / Q000633:toxicity; D002869:Chromosome Aberrations; D002875:Chromosomes / Q000187:drug effects*; D004249:DNA Damage; D005609:Free Radicals; D006801:Humans; D009153:Mutagens; D010100:Oxygen / Q000633:toxicity*; D010269:Paraquat; D013308:Streptonigrin / Q000633:toxicity
D005609:Free Radicals; D009153:Mutagens; D001761:Bleomycin; D013308:Streptonigrin; D010269:Paraquat; D010100:Oxygen