HEK 293细胞
氧化应激
细胞生物学
化学
线粒体
肾
活力测定
线粒体分裂
受体
内分泌学
生物化学
细胞
生物
作者
Biqi Han,Zhanjun Lv,Xue-Min Han,Siyu Li,Bing Han,Qingyue Yang,Xiaoqiao Wang,Pengfei Wu,Jiayi Li,Ning Deng,Zhigang Zhang
标识
DOI:10.1007/s12011-021-02766-3
摘要
Mercury is widely used in industry and has caused global environmental pollution. Inorganic mercury accumulates in the body causes damage to many organs, and the kidney is the most susceptible to the toxic effects of mercury. However, the underlying specific molecular mechanism of renal injury induced by inorganic mercury remains unclear at the cellular level. Therefore, in order to understand its molecular mechanism, we used in vitro method. We established experimental models by treating human embryonic kidney epithelial cell line (HEK-293 T) cells with HgCl2 (0, 1.25, 5, and 20 µmol/L). We found that HgCl2 can lead to a decrease in cell viability and oxidative stress of HEK-293 T, which may be mediated by upregulation mitochondrial fission. In addition, HgCl2 exposure resulted in the mitochondrial disorder of HEK-293 T cells, which was mediated by downregulating the expression of silent information regulator two ortholog 1 (Sirt1)/peroxisome proliferator–activated receptor coactivator-1α (PGC-1α) signaling pathway. In summary, our results suggest that HgCl2 induces HEK-293 T cell toxicity through promoting Sirt1/PGC-1α axis-mediated mitochondrial dynamics disorder and oxidative stress. Sirt1/PGC-1α may be an appealing pharmaceutical target curing HgCl2-induced kidney injury.
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