Sorokina S S, Zaichkina S I, Rozanova O M, Aptikaeva G F, Akhmadieva A Kh, Smirnova E N, Romanchenko S P, Vakhrusheva O A, Dyukina A R, Peleshko V N
Institute of Theoretical and Experimental Biophysics, Pushchino, Russia.
Radiat Prot Dosimetry. 2011 Feb;143(2-4):305-10. doi: 10.1093/rpd/ncq531. Epub 2010 Dec 24.
In the present work, the delayed effects of chronic high linear energy transfer (LET) radiation in polychromatic erythrocytes (PCEs) of mice bone marrow were investigated in vivo. Irradiation of the two-month-old SHK white mongrel random-bred male mice was performed in the radiation field behind the concrete shield of the accelerator of 70 GeV protons to accumulate doses of 0.005-0.16 Gy. The dependence of the biological response on dose, adaptive response (AR) and genomic instability (GI) in F(1) and F(2) generations from males irradiated with doses of 0.005 and 0.16 Gy and from males exposed to combined action of immunomodulator-bendazol hydrochloride (BH) and of 0.16 Gy irradiation, were examined using the micronucleus formation test. The data demonstrated that irradiation of mice with these doses lead to an increase in the level of cytogenetic damage and induces no AR. With analysis of the bone marrow radiosensitivity to 1.5 Gy of X rays and the capacity to AR it was found that the chronic high-LET irradiation of parents induced the GI at least two generations. The combined exposure to BH and the dose of 0.16 Gy induces no AR in F(0) generation but induces AR in F(1) and F(2) offspring.
在本研究中，对小鼠骨髓多色红细胞（PCEs）中慢性高传能线密度（LET）辐射的延迟效应进行了体内研究。对两个月大的SHK白色杂种随机繁殖雄性小鼠，在70 GeV质子加速器混凝土屏蔽后的辐射场中进行辐照，累积剂量为0.005 - 0.16 Gy。使用微核形成试验，研究了剂量为0.005和0.16 Gy的辐照雄性小鼠以及暴露于免疫调节剂盐酸苯达唑（BH）和0.16 Gy辐照联合作用下的雄性小鼠的F(1)和F(2)代中生物反应对剂量、适应性反应（AR）和基因组不稳定性（GI）的依赖性。数据表明，用这些剂量辐照小鼠会导致细胞遗传损伤水平增加，且不会诱导AR。通过分析骨髓对1.5 Gy X射线的放射敏感性和AR能力，发现亲代的慢性高LET辐照至少在两代中诱导了GI。BH与0.16 Gy剂量的联合暴露在F(0)代中不诱导AR，但在F(1)和F(2)代子代中诱导AR。
