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Published on: April 26, 2018
UV-B induced thymocytes apoptosis blocked by dicyclodextrinyl ditelluride-A GPX mimic
Linlin Wang1, Shaowu Lv, Ganglin Yan
1Research Center for Analytical Instrumentation, Institute of Cyber-Systems and Control, State Key Laboratory of Industrial Control Technology, Zhejiang University, Hangzhou 310058, PR China; Key Laboratory for Molecular Enzymology and Enginnering of Ministry of Education, Jilin University, Changchun 130023, PR China.
Abstract:
Apoptosis is known to occur after ultraviolet-B (UV-B) radiation. It was found that UV-B could induce cell apoptosis and change cell cycle progression. After exposure to 100J/m(2) of UV-B, pre-G1 phase thymocytes were increased significantly and S phase thymocytes were decreased significantly. UV-B could also induce lipid peroxidation of thymocytes to have their MDA amount increased. These phenomena could be explained by production of reactive oxygen species (ROS), which were induced by UV-B radiation. In this study, we examined the protective effect of dicyclodextrinyl ditelluride (2-TeCD), the glutathione peroxidase (GPX, EC 1.11.1.9) mimics, on thymocytes apoptosis induced by UV-B radiation. The experimental results showed that 2-TeCD protects thymocytes from apoptosis. Moreover, 2-TeCD inhibits lipid peroxidation of thymocytes and displayed great antioxidant ability. Furthermore, 2-TeCD blocks the accumulation of wild-type-p53 (wt-p53) tumor-suppressor gene product caused by UV-B radiation.
