Streffer C, Müller W U
Institut für Medizinische Strahlenbiologie, Universitätsklinikum Essen, Germany.
Int J Dev Biol. 1996 Feb;40(1):355-60.
Our studies have shown that, contrary to the opinion in most textbooks, it is possible to increase the number of malformed fetuses in one of our mouse strains (originally "Heiligenberger Stamm", meanwhile HLG/Zte) by radiation exposure of zygotes or of subsequent preimplantation stages. The malformation affected most pronouncedly is gastroschisis, a defect occurring at a frequency of 1 to 4% in the controls. The observed increase is strain specific (C57Bl mice or (HLGxC57Bl)F1 hybrids do not react in the same way), it is accompanied by an increased frequency of chromosomal aberrations in skin fibroblasts and of modified protein patterns in liver, kidney, and skin cells of day 19 fetuses. The most probable explanation seems to be the assumption that radiation exposure of preimplantation stages increases a defect with a genetic predisposition in a specific way and labelizes the genome of subsequent cell generations making these cells more susceptible for noxes acting on the fetus.
我们的研究表明，与大多数教科书的观点相反，通过对受精卵或随后的植入前阶段进行辐射照射，有可能增加我们一种小鼠品系（最初为“Heiligenberger Stamm”，现称HLG/Zte）中畸形胎儿的数量。受影响最明显的畸形是腹裂，在对照组中出现的频率为1%至4%。观察到的增加是品系特异性的（C57Bl小鼠或(HLGxC57Bl)F1杂种不会有相同反应），同时，第19天胎儿的皮肤成纤维细胞中的染色体畸变频率以及肝脏、肾脏和皮肤细胞中的蛋白质模式改变频率也会增加。最可能的解释似乎是这样一种假设，即植入前阶段的辐射照射以特定方式增加了具有遗传易感性的缺陷，并标记了后续细胞世代的基因组，使这些细胞更容易受到作用于胎儿的有害物质的影响。
