Harmful Effects of Inorganic Mercury Exposure on Kidney Cells: Mitochondrial Dynamics Disorder and Excessive Oxidative Stress

• Published in: Biological trace element research Vol. 200; no. 4; pp. 1591 - 1597
• Main Authors: Han, Biqi, Lv, Zhanjun, Han, Xuemin, Li, Siyu, Han, Bing, Yang, Qingyue, Wang, Xiaoqiao, Wu, Pengfei, Li, Jiayi, Deng, Ning, Zhang, Zhigang
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.04.2022; Springer Nature B.V
• Subjects: Biochemistry; Biological stress; Biomedical and Life Sciences; Biotechnology; Body organs; cell lines; Cell viability; cytotoxicity; Damage accumulation; Dynamics; Epithelial cells; Epithelial Cells - metabolism; Epithelium; HEK293 Cells; Humans; In vitro methods and tests; industry; Kidney - metabolism; Kidneys; Life Sciences; Lymphocytes; Lymphocytes T; Mercuric chloride; Mercury; Mercury - metabolism; Mitochondria; Mitochondrial Diseases - metabolism; Mitochondrial Dynamics; Molecular modelling; Nutrition; Oncology; Organs; Oxidative Stress; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - metabolism; Pollution; Receptors; Signal transduction; SIRT1 protein; Sirtuin 1 - metabolism; T-lymphocytes; Toxicity; trace elements; Sirt1/PGC-1α; HgCl; Mitochondrial dynamics dysfunction; Kidney cell; ROS; HgCl2
• ISSN: 0163-4984; 1559-0720; 1559-0720
• DOI: 10.1007/s12011-021-02766-3

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 HgCl 2 (0, 1.25, 5, and 20 µmol/L). We found that HgCl 2 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, HgCl 2 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 HgCl 2 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 HgCl 2 -induced kidney injury.