Arsenic Induces Thioredoxin 1 and Apoptosis in Human Liver HHL-5 Cells |
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| Authors: | Yuanyuan Li Yuanyuan Zhang Yanhui Gao Wei Zhang Xiaohui Cui Junqiu Liu Yudan Wei |
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| Affiliation: | 1.Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Key Laboratory of Etiologic Epidemiology of Education Bureau of Heilongjiang Province and Ministry of Health,Harbin Medical University,Harbin,China;2.Department of Community Medicine,Mercer University School of Medicine,Macon,USA;3.Advanced Institute for Medical Sciences,Dalian Medical University,Dalian,China |
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| Abstract: | To further characterize the mechanisms underlying liver toxicity induced by arsenic, we examined in this study the effect of arsenic on thioredoxin (Trx) and the apoptotic signaling pathways in human liver HHL-5 cells. The cells were treated with 0, 2, 5, and 10 μM of sodium arsenite for 24 h, and the changes of Trx1 and thioredoxin reductase (TrxR1) as well as intracellular ROS and apoptosis were examined. A concentration-dependent increase in mRNA and protein levels of Trx1 and TrxR1 was observed in arsenic-treated cells. Intracellular ROS levels and apoptosis were also significantly increased in a concentration-dependent manner. In line with this, protein levels of Bax and cytochrome C were increased and Bcl-2 was decreased by arsenic treatments. Increases in caspase 3 activity were observed. These results indicate that Trx is involved in arsenic-induced liver cell injury, probably through the apoptotic signaling pathway. However, further studies are needed to elucidate on these findings. |
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