The damage mechanism of uranium(VI) to HK-2 cells

被引:2
|
作者
Qiang, Shirong [1 ]
Guo, Kunling [2 ]
Zhang, Dan [2 ]
Sun, Wei [2 ]
Wang, Zihuan [1 ]
Huang, Sujie [3 ]
Li, Ping [4 ]
Fan, Qiaohui [4 ]
机构
[1] Lanzhou Univ, Inst Physiol, Sch Basic Med Sci, Key Lab Preclin Study New Drugs Gansu Prov, Lanzhou 730000, Peoples R China
[2] Lanzhou Univ, Sch Publ Hlth, Lanzhou 730000, Peoples R China
[3] Zhangzhou Inst Technol, Zhangzhou 350600, Peoples R China
[4] Chinese Acad Sci, Northwest Inst Ecoenvironm & Resources, Lanzhou 730000, Peoples R China
基金
中国国家自然科学基金;
关键词
Uranium; HK-2; cells; DNA damage; Oxidative stress; Apoptosis; DEPLETED URANIUM; OXIDATIVE STRESS; NATURAL URANIUM; URANYL ACETATE; TOXICITY; RATS;
D O I
10.1007/s10967-023-08843-2
中图分类号
O65 [分析化学];
学科分类号
070302 ; 081704 ;
摘要
As one of the typical actinide elements, the chemical and radioactive toxicities of uranium have attracted more attention. In this work, the toxicity mechanism of uranium-238 in HK-2 cells was studied in detail using in vitro approach. The results confirmed that exposure to uranium solution significantly reduced the viability of HK-2 cells. Flow cytometry and double fluorescence AO/PI staining suggested that apoptosis was the main cause of the death of HK-2 cells. Moreover, reactive oxygen species and mitochondrial membrane potential tests further demonstrated that HK-2 cells underwent apoptosis under the combined action of oxidative stress and mitochondrial damage. The tails in the comet assay and the abnormal nuclear morphology in DAPI staining confirmed the genotoxicity of uranium to HK-2 cells. In conclusion, uranium mainly causes apoptosis and genotoxicity after exposure, and the main mechanisms of apoptosis are mainly related to oxidative stress, mitochondrial damage, and DNA damage.
引用
收藏
页码:1277 / 1285
页数:9
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