Spitkovskiĭ D M, Ermakov A V, Gorin A I, Pospekhova N I, Sorokinna T A, Talyzina T A
Radiats Biol Radioecol. 1994 Jan-Feb;34(1):23-31.
Effects of X-ray low doses (0.5-25 cGy) with following UV light (254 nm, 20 J/m2) on human peripheral blood lymphocytes were studied. Reparation response registered by unscheduled DNA synthesis (UDS) activity was demonstrated to be the most intensive after action of X-rays in dose ranges 2-3 cGy and 15-20 cGy, and least intensive after 10 cGy. In those cells where UV light was followed by X-rays, dose ranges 2-3 cGy and 15-20 cGy cause essential decrease of UDS as compared with UV-light action only. The most intensive UDS was in those UV-irradiated lymphocytes which where previously exposed to 10 cGy of X-rays. At the same time 10 cGy cause minimal reparation response without UV light. Possible mechanisms of discovered phenomena are discussed. In particular, reaction on 2-3 cGy might be a reorganization of genome for adaptive response or an evolution reserve cells response. From 10 cGy the reason of reaction might be a reparation, induced by radiation.
研究了后续接受紫外线（254纳米，20焦耳/平方米）照射的X射线低剂量（0.5 - 25厘戈瑞）对人外周血淋巴细胞的影响。通过非程序性DNA合成（UDS）活性记录的修复反应显示，在2 - 3厘戈瑞和15 - 20厘戈瑞剂量范围内的X射线作用后最为强烈，而在10厘戈瑞后最不强烈。在那些先接受紫外线照射后再接受X射线照射的细胞中，与仅紫外线作用相比，2 - 3厘戈瑞和15 - 20厘戈瑞剂量范围导致UDS显著降低。UDS最强烈的情况出现在那些先前接受过10厘戈瑞X射线照射的紫外线照射淋巴细胞中。同时，10厘戈瑞在无紫外线照射时引起的修复反应最小。文中讨论了所发现现象的可能机制。特别是，对2 - 3厘戈瑞的反应可能是基因组为适应性反应进行的重组或细胞进化储备反应。从10厘戈瑞起，反应的原因可能是辐射诱导的修复。
