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Oxygen toxicity and chromosomal breakage in ataxia telangiectasia.

作者信息

Joenje H, Nieuwint A W, Taylor A M, Harnden D G

出版信息

Carcinogenesis. 1987 Feb;8(2):341-4. doi: 10.1093/carcin/8.2.341.

DOI:10.1093/carcin/8.2.341
PMID:2433071
Abstract

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.

摘要

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引用本文的文献

1
Ionizing radiation-induced mutagenesis.电离辐射诱导的诱变作用。
Br J Cancer. 1988 Jan;57(1):6-18. doi: 10.1038/bjc.1988.2.
2
Active oxygen in neuromuscular disorders.神经肌肉疾病中的活性氧
Mol Cell Biochem. 1988 Dec;84(2):199-216. doi: 10.1007/BF00421055.