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首页> 外文期刊>Journal of Theoretical Biology >Induction and repair rate of DNA damage: A unified model for describing effects of external and internal irradiation and contamination with heavy metals
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Induction and repair rate of DNA damage: A unified model for describing effects of external and internal irradiation and contamination with heavy metals

机译：DNA损伤的诱导和修复率：描述外部和内部辐射以及重金属污染的统一模型

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DNA is a key-target for genotoxic stress. Hence, the knowledge of induction and repair rate of DNA damage are crucial to describe and predict the impact of stress situations. Unfortunately, DNA damage induction and repair rates are generally assessed separately whereas they act either concomitantly or transiently in living organisms. Furthermore, the interplay of induction and repair raises the question whether DNA repair adapts to respond to different amounts of DNA damage. In a previous report, we proposed a stochastic interpretation of the repair rate of the major radiation-induced DNA damage. We provided evidence that the repair rate of individual DNA damage is time-independent whereas that of a population of DNA damage is time-dependent (Foray, N., Charvet, A.-M., Duchemin, D., Favaudon, V., Lavalette, D., 2005. The repair rate of radiation-induced DNA damage: a stochastic interpretation based on the gamma function. J. Theor. Biol. 236, 448-458). Here, to better describe situations in which DNA damage induction and repair occur together, our biostatistical model was modified by the introduction of a DNA damage induction parameter. Theoretical and experimental data were compared and discussed by taking concrete experimental situations: X-rays irradiation at different dose-rates, internal irradiation with radioactive compound, contamination with heavy metal and detection of DNA damage by immunofluorescence. By assuming that DNA repair rate is invariant whatever the amount of DNA damage, our model provides good prediction of experimental data suggesting its relevance for the description of complex situations of co-toxicities. (c) 2007 Elsevier Ltd. All rights reserved.
机译：DNA是遗传毒性压力的关键目标。因此，对DNA损伤的诱导和修复率的了解对于描述和预测压力情况的影响至关重要。不幸的是，DNA损伤的诱导和修复率通常是分别评估的，而它们在生物中同时或短暂地起作用。此外，诱导和修复的相互作用提出了一个问题，即DNA修复是否适应于应对不同量的DNA损伤。在以前的报告中，我们提出了对主要辐射诱导的DNA损伤修复率的随机解释。我们提供的证据表明，单个DNA损伤的修复率是时间依赖性的，而DNA损伤群体的修复率是时间依赖性的（Foray，N.，Charvet，A.-M.，Duchemin，D.，Favaudon，V. ，Lavalette，D.，2005。辐射诱导的DNA损伤的修复率：基于伽马函数的随机解释（J. Theor。Biol。236，448-458）。在这里，为了更好地描述DNA损伤诱导和修复同时发生的情况，我们通过引入DNA损伤诱导参数对我们的生物统计学模型进行了修改。通过具体的实验情况对理论和实验数据进行了比较和讨论：不同剂量率的X射线辐照，放射性化合物的内部辐照，重金属污染以及通过免疫荧光检测DNA损伤。通过假设DNA修复率是不变的，而不管DNA的破坏程度如何，我们的模型可以很好地预测实验数据，表明其对描述复杂的共毒性情况具有相关性。 （c）2007 Elsevier Ltd.保留所有权利。

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