摘要
目的 研究贫铀 (DU)对细胞存活的影响和诱发基因突变的作用 ,并初步探讨其可能的机制。方法 用包含单条人类 11号染色体 (Hchr 11)的人 中国仓鼠卵巢杂交细胞 (AL 细胞 )为靶 ,观察DU作用细胞的低密度接种效率 ;用CD59表面抗原抗体及其补体筛选突变细胞克隆 ,研究DU诱发的Hchr 11基因突变率。结果 DU可明显降低细胞存活率 ,并使Hchr 11基因突变率显著增高 ;二甲基亚砜 (DMSO)、Ca2 + 和Na2 SeO3对DU诱发的细胞增殖死亡和基因突变有较好的保护效果。结论 DU对细胞存活的影响和基因突变作用可能与其诱发产生活性氧自由基及其与Ca2 + 的交换有关。
Objective To investigate the effects of depleted uranium(DU)on cell survival and mutagenicity,and explore primarily its possible mechanism.Methods The human\|hamster hybrid cells (A\-L cells) including a single human chromosome 11(Hchr 11)were used for target cells.Cell survival rate was measured by counting the number of clone which grew in the condition of low density planting.DU induced mutagenicities on Hchr 11 were assayed through screening mutants in presence of anti\|CD 59 surface antigen antibody and serum complement.Results DU decreased obviously cell survival,and increased remarkably mutagenicities of Hchr 11.However,there were resultful protection of DMSO,Ca 2+ and Na\-2SeO\-3 on DU\|induced cell proliferation death and mutagenicity.Conclusion Free radicals such as reactive oxygen species(ROS)produced by DU and the exchange of DU with intracellular Ca 2+ were likely to involve DU\|induced cell proliferation death and mutagenicity.
出处
《卫生毒理学杂志》
CSCD
北大核心
2002年第3期146-149,共4页
Journal of Health Toxicology
基金
全军十五指令性课题资助项目 (0 1L0 61 )
关键词
贫铀
细胞存活
影响
基因突变
Depleted uranium
Human\|hamster hybrid cell(A\-L cells)
Cell survival
Human chromosome 11
Mutagenicity