UV-B induced thymocytes apoptosis blocked by dicyclodextrinyl ditelluride-A GPX mimic

Linlin Wang; Shaowu Lv; Ganglin Yan; Guimin Luo; Ying Mu

doi:10.1016/j.etap.2010.03.003

UV-B induced thymocytes apoptosis blocked by dicyclodextrinyl ditelluride-A GPX mimic

Environ Toxicol Pharmacol. 2010 Jul;30(1):1-4. doi: 10.1016/j.etap.2010.03.003. Epub 2010 Mar 19.

Authors

Linlin Wang¹, Shaowu Lv, Ganglin Yan, Guimin Luo, Ying Mu

Affiliation

¹ Research 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.

PMID: 21787621
DOI: 10.1016/j.etap.2010.03.003

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.