Nylund Reetta, Lemola Elina, Hartwig Sonja, Lehr Stefan, Acheva Anna, Jahns Jutta, Hildebrandt Guido, Lindholm Carita
STUK - Radiation and Nuclear Safety Authority, Laippatie 4, PO Box 14, 00881 Helsinki, Finland
STUK - Radiation and Nuclear Safety Authority, Laippatie 4, PO Box 14, 00881 Helsinki, Finland.
J Radiat Res. 2014 Jul;55(4):674-82. doi: 10.1093/jrr/rru007. Epub 2014 Feb 24.
In studies reported in the 1960s and since, blood plasma from radiation-exposed individuals has been shown to induce chromosome damage when transferred into lymphocyte cultures of non-irradiated persons. This effect has been described to occur via clastogenic factors, whose nature is still mostly unknown. We have previously examined clastogenic factors from irradiated individuals by looking at plasma-induced DNA damage in reporter cells. Plasma was tested from ca. 30 locally exposed clinical patients receiving fractionated radiation treatment, as well as from three radiological accident victims exposed in 1994, albeit sampled 14 years post-accident. In the current work, proteome changes in the plasma from all subjects were examined with 2D gel electrophoresis-based proteomics techniques, in order to evaluate the level of protein expression with respect to the findings of a clastogenic factor effect. No differences were observed in protein expression due to local radiation exposure (pre- vs post-exposure). In contrast, plasma from the radiation accident victims showed alterations in the expression of 18 protein spots (in comparison with plasma from the control group). Among these, proteins such as haptoglobin, serotransferrin/transferrin, fibrinogen and ubiquitin-60S ribosomal protein L40 were observed, none of them likely to be clastogenic factors. In conclusion, the proteomics techniques applied were unable to identify changes in the proteome of the locally irradiated patients, whereas such differences were observed for the accident victims. However, association with the clastogenic effect or any specific clastogenic factor remains unresolved and thus further studies with more sensitive techniques are warranted.
在20世纪60年代及之后报道的研究中,已表明将受辐射个体的血浆转移至未受辐射者的淋巴细胞培养物中时,会诱导染色体损伤。据描述,这种效应是通过致断裂因子发生的,但其性质大多仍不清楚。我们之前通过观察报告细胞中血浆诱导的DNA损伤,研究了受辐射个体的致断裂因子。检测了约30名接受分次放射治疗的局部受照临床患者的血浆,以及1994年受照的三名放射事故受害者的血浆,不过是在事故发生14年后采集的样本。在当前工作中,使用基于二维凝胶电泳的蛋白质组学技术检测了所有受试者血浆中的蛋白质组变化,以便根据致断裂因子效应的研究结果评估蛋白质表达水平。未观察到因局部辐射暴露(暴露前与暴露后)导致的蛋白质表达差异。相比之下,放射事故受害者的血浆显示出18个蛋白点的表达发生了改变(与对照组血浆相比)。其中观察到了诸如触珠蛋白、血清转铁蛋白/转铁蛋白、纤维蛋白原和泛素-60S核糖体蛋白L40等蛋白质,但它们都不太可能是致断裂因子。总之,所应用的蛋白质组学技术无法识别局部受照患者蛋白质组的变化,而事故受害者则观察到了这种差异。然而,与致断裂效应或任何特定致断裂因子的关联仍未解决,因此有必要采用更灵敏的技术进行进一步研究。