摘要
研究了不同水平浓缩铀(235UO2F2)对淋巴细胞DNA损伤修复的作用及其机理。应用紫外线诱导的非程序DNA合成 (UDS) 检测,观察浓缩铀(235UO2F2)内污染对小鼠脾淋巴细胞DNA损伤修复的影响。结果表明, 浓缩铀摄入量为0.1—20μg/kg 体重时, 脾淋巴细胞紫外线诱导的UDS显著高于对照组 (p<0.05或p<0.01); 浓缩铀内污染12d时, 脾淋巴细胞未经紫外线照射的UDS显著增加 (p<0.05或p<0.01); PHA组脾淋巴细胞紫外线诱导的UDS显著低于未加PHA组。在一定剂量范围内,低剂量浓缩铀内污染对淋巴细胞DNA损伤修复功能具有明显的刺激作用,并且该剂量范围明显大于外照射;浓缩铀内污染对淋巴细胞DNA具有持续的损伤作用,继而诱发细胞DNA修复功能的增强;PHA刺激但未增殖的脾淋巴细胞DNA损伤修复功能明显减低。
The paper is to elucidate the effects of in vivo exposure to different levels of 235UO2F2 on DNA repair capability and the mechanism. The DNA repair capacity, as measured by UV-induced unscheduled DNA synthesis (UDS) of splenic lymphocytes from inbred BALB/c male mice, was observed after injection of different doses of 235UO2F2 into the caudal vein. UV-induced UDS of the splenic lymphocytes increased significantly (p<0.05 or p< 0.01) at doses of 0.1—20μg / kg body weight. Non-UV-induced UDS showed a significant increase (p<0.05 or p< 0.01) 12 days after 235UO2F2 injection. The UV-induced UDS in PHA activated but non-proliferating (hydroxyurea treated) lymphocytes were lower than those of lymphocytes unexposed to PHA at the same doses of 235UO2F2 (p<0.05 or p<0.01). Low doses of internally deposited 235UO2F2 have a continuous DNA damage effect on the mouse lymphocytes, so that a significant stimulative effect on DNA repair capability in the cells is induced. The stimulative effect occurs only in a limited dose range, and the dose range of internally deposited 235UO2F2 is larger than that of the external radiation. The DNA repair synthesis is significantly inhibited after UV-irradiation in PHA stimulated but non-proliferating lymphocytes.
出处
《辐射研究与辐射工艺学报》
CAS
CSCD
北大核心
2003年第2期139-142,共4页
Journal of Radiation Research and Radiation Processing
基金
中国核工业科学基金(Y7196Q6201)资助