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目的 阐明贫铀 (depleteduranium ,DU)对人肾小管上皮细胞 (humankidneycell,HKC)的急性毒性作用及损伤部位 ,为救治提供依据。方法 将 0 0 63～ 0 5 0 0mg ml的DU溶液作用于HKC ,研究细胞超微结构、存活率的变化 ,多种酶含量的改变及HGPRT基因突变的频率。结果 0 0 63～ 0 5 0 0mg ml浓度的DU可引起HKC细胞结构改变 ,存活率显著下降 ;溶酶体酶NAG含量随DU浓度的增加而增加 ;其他酶含量也发生变化 ;HGPRT基因突变的发生率显著高于正常对照组 ,并呈二项式相关关系。加入苯乙酸、亚硒酸钠使上述指标变化不大。结论 DU可引起细胞活力降低 ,损伤细胞膜、线粒体、溶酶体等 ,使细胞抗氧化能力下降 ;HGPRT基因突变率与DU浓度之间呈相关关系 ;加入恶性转化的抑制剂亚硒酸钠和苯乙酸 ,不会显著增加DU的毒性作用
Objective To elucidate the acute toxic effects of depleted uranium (DU) on human renal tubular epithelial cells (HKC) and provide the basis for treatment. Methods The DU solution of 0 0 63 ~ 0 0 0 0 mg ml was applied to HKC to study the changes of cell ultrastructure, the change of survival rate, the change of various enzyme contents and the frequency of HGPRT gene mutation. Results The concentration of DU from 0 0 63 to 0 0 0 mg ml caused a structural change in HKC cells and the survival rate decreased significantly. The lysosomal enzyme NAG content increased with the increase of DU concentration, and the content of other enzymes also changed. The mutation of HGPRT gene The incidence was significantly higher than the normal control group, and showed a binomial correlation. Adding phenylacetic acid, sodium selenite to make the above indicators changed little. Conclusions DU can decrease cell viability, impair cell membrane, mitochondria, lysosome and so on, and decrease the anti-oxidative capacity of cells. The mutation rate of HGPRT gene is correlated with the concentration of DU, and the inhibitors of malignant transformation such as sodium selenite and benzene Acetic acid does not significantly increase the toxicity of DU