Zaichkina S I, Rozanova O M, Aptikaeva G F, Achmadieva A Ch, Klokov D Y
Institute of Theoretical and Experimental Biophysics, Pushchino, Russia.
Nonlinearity Biol Toxicol Med. 2004 Jul;2(3):213-21. doi: 10.1080/15401420490519861.
The percentage of cells with chromosome aberrations or micronuclei induced by low doses of acute (dose rate of 47 cGy/min) or chronic (dose rate of 0.01 cGy/min) gamma-irradiation was studied in vitro in Chinese hamster fibroblasts, human lymphocytes, and Vicia faba seeds and seedlings. The sensitivity of the indicated biological entities to low doses was greater than expected based on linear extrapolation from higher doses. The dose-response curves for cytogenetic damage that were obtained were nonlinear when evaluated over the full range of the doses used. At very low doses, the dose-response curves appeared linear, followed by a plateau region at intermediate doses. At high doses the dose response curves again appeared linear with a slope different from that for the low-dose region. There was no statistically significant difference between the yields of cells with micronuclei induced by low doses of acute versus chronic irradiation. Similar data were obtained both for human lymphocyte culture and for roots and seeds of Vicia faba. Our experiments revealed that the dose range over which the plateau occurs depends on the type of cells irradiated. We have also shown that the modifying effects of the repair inhibitor caffeine and the radioprotector mercaptoethylenamine (MEA) are absent at low doses of gamma irradiation and that caffeine increased the number of cells with cytogenetic damage when evaluated over the plateau region. In the presence of MEA, the upper end of the plateau region was extended from just above 1 Gy to about 2 Gy. We therefore provide direct evidence that a plateau exists in the dose-response curve for the indicated radiation-induced stochastic effects. Furthermore, our results suggest that, for low linear energy transfer radiation, the induction of DNA repair occurs only after a threshold level of cytogenetic damage and that the higher yield of cytogenetic damage per unit dose at low radiation doses is attributable to an insignificant contribution or the absence of DNA repair processes.
在中国仓鼠成纤维细胞、人淋巴细胞以及蚕豆种子和幼苗中,对低剂量急性(剂量率为47 cGy/分钟)或慢性(剂量率为0.01 cGy/分钟)γ射线照射诱导的染色体畸变或微核细胞百分比进行了体外研究。这些生物实体对低剂量的敏感性高于基于高剂量线性外推所预期的值。在所使用的整个剂量范围内评估时,所获得的细胞遗传损伤剂量 - 反应曲线是非线性的。在非常低的剂量下,剂量 - 反应曲线呈线性,随后在中等剂量时有一个平台区。在高剂量时,剂量反应曲线再次呈线性,但其斜率与低剂量区不同。低剂量急性照射与慢性照射诱导的微核细胞产率之间无统计学显著差异。在人淋巴细胞培养以及蚕豆的根和种子中均获得了类似的数据。我们的实验表明,出现平台区的剂量范围取决于所照射的细胞类型。我们还表明,在低剂量γ射线照射时,修复抑制剂咖啡因和辐射防护剂巯基乙胺(MEA)没有修饰作用,并且在平台区评估时,咖啡因增加了细胞遗传损伤细胞的数量。在MEA存在的情况下,平台区的上限从略高于1 Gy扩展到约2 Gy。因此,我们提供了直接证据表明在所指示的辐射诱导随机效应的剂量 - 反应曲线中存在一个平台区。此外,我们的结果表明,对于低线性能量传递辐射,DNA修复的诱导仅在细胞遗传损伤达到阈值水平后才发生,并且低辐射剂量下每单位剂量更高的细胞遗传损伤产率归因于DNA修复过程的贡献微不足道或不存在。