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首页> 外文期刊>International Journal of Environmental Research and Public Health >Response to Baverstock, K. Comments on Rithidech, K.N.; et al. Lack of Genomic Instability in Bone Marrow Cells of SCID Mice Exposed Whole-Body to Low-Dose Radiation. Int. J. Environ. Res. Public Health 2013, 10, 1356–1377.
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Response to Baverstock, K. Comments on Rithidech, K.N.; et al. Lack of Genomic Instability in Bone Marrow Cells of SCID Mice Exposed Whole-Body to Low-Dose Radiation. Int. J. Environ. Res. Public Health 2013, 10, 1356–1377.

机译：对Baverstock，K.的回应。对Rithidech，K.N.的评论;等。 SCID小鼠骨髓细胞缺乏基因组不稳定性，使全身暴露于低剂量辐射。诠释J.环境。 Res。公共卫生2013，10，1356-1377。

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摘要

We thank Dr. Baverstock [1] for his interest in reading our article and his time in writing his comments for our work [2]. We, however, respectfully disagree with his statement that we made “two category errors” associated with the assessment of the occurrence of “genomic instability” by determining the frequencies of delayed- or late-occurring chromosomal damage. Our disagreement is based upon the well-known fact that radiation-induced genomic instability (or delayed/late-occurring damage) can be manifested in many ways. These include late-occurring chromosomal damage, or mutations, or gene expression, or gene amplifications, or transformation, or microsatellite instability, or cell killing [3–9]. Such phenomena have been detected many cell generations after irradiation. We agree that genomic instability may well be the consequence of epigenetic changes. Another mechanism mentioned by Dr. Bavertock as being probably unlikely is the reversibility of damage. This potential may not be discarded off-hand, as Dr. Baverstock prefers to do. There is much reproducible evidence of adaptive protection that depending on absorbed dose precisely may reverse early damage, and damage appearing late may be due to some form of residual damage letting the cell become genetically unstable. In other words, the argument by Dr. Baverstock regarding upward or downward causation appears to be rather speculative and far from being settled.
机译：感谢Baverstock博士[1]感兴趣的阅读我们的文章以及他为我们的工作写评论的时间[2]。但是，我们完全不同意他的说法，即我们通过确定延迟或晚期发生的染色体损伤的频率，在评估“基因组不稳定性”时犯了“两类错误”。我们的分歧是基于众所周知的事实，即辐射诱发的基因组不稳定性（或延迟的/迟发的损害）可以通过多种方式表现出来。这些包括后期发生的染色体损伤，突变，基因表达，基因扩增，转化，微卫星不稳定性或细胞杀伤[3-9]。在辐射后许多细胞世代中已经检测到这种现象。我们同意，基因组不稳定性很可能是表观遗传变化的结果。巴弗托克博士提到的另一种不太可能的机制是损害的可逆性。这种潜力可能不会像Baverstock博士更喜欢的那样被立即丢弃。有许多可复制的适应性保护证据，确切地说，取决于吸收的剂量可以逆转早期损伤，而晚期出现的损伤可能是由于某种形式的残留损伤导致细胞变得遗传不稳定。换句话说，Baverstock博士关于向上或向下因果关系的论点似乎是投机性的，远未解决。

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