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碘 - 125在共济失调毛细血管扩张症成纤维细胞中的放射毒性。

The radiotoxicity of iodine-125 in ataxia telangiectasia fibroblasts.

作者信息

Ritter M A

出版信息

Biochim Biophys Acta. 1981 Jan 29;652(1):151-9. doi: 10.1016/0005-2787(81)90218-5.

Abstract

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.

摘要

将正常和成共济失调性毛细血管扩张症的成纤维细胞株用³H或¹²⁵I标记的碘脱氧尿苷进行标记,保存在-75℃以积累损伤,然后解冻进行存活分析。还测定了冷冻、未标记细胞的X射线存活率。在冷冻条件下用X射线或³H衰变照射时,共济失调性毛细血管扩张症细胞株的敏感性约为正常细胞株的两倍(基于存活曲线斜率)。积累的¹²⁵I衰变虽然毒性比³H衰变大约13倍,但杀死共济失调性毛细血管扩张症细胞的效率也约为正常细胞的两倍。这些结果表明,在正常细胞中,很大一部分¹²⁵I诱导的损伤——至少50%——是可以修复的。此外,它们表明共济失调性毛细血管扩张症细胞修复由X射线和¹²⁵I共同诱导的损伤的能力较弱,但由后者诱导的损伤比例更大——可能是DNA双链断裂。

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