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 t...

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Bibliographic Details
Published in:Carcinogenesis (New York) 1987-02, Vol.8 (2), p.341-344
Main Authors: Joenje, Hans, Nieiwint, W.M. Aggie, Taylor, A. Malcolm R., Harnden, David G.
Format: Article
Language:English
Subjects:
Ataxia Telangiectasia - genetics
Biological and medical sciences
Bleomycin - toxicity
Chromosome Aberrations
Chromosome fragility (bloom syndrome, ataxia telangiectasia, fanconi anemia, x-linked mental retardation...)
Chromosomes - drug effects
DNA Damage
Free Radicals
Humans
Medical genetics
Medical sciences
Mutagens
Oxygen - toxicity
Paraquat
Streptonigrin - toxicity
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Summary: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 nonirradiated 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.
ISSN:0143-3334
1460-2180
DOI:10.1093/carcin/8.2.341