title: The molecular mechanism of protecting cells against oxidative stress by 2-selenium-bridged beta-cyclodextrin with glutathione peroxidase activity.
abstract: Ultraviolet B (UVB) induces apoptosis and lipid peroxidation of NIH3T3 cells by producing reactive oxygen species (ROS). Glutathione peroxidase (GPX) is one of the most important antioxidant enzymes in organism and it can scavenge ROS. 2-selenium-bridged beta-cyclodextrin (2-SeCD) is a GPX mimic generated in our lab. Its GPX activity is 7.4 U/mumol, which is 7.5 times as much as that of ebselen. In this paper, we have established a cell damage system using UVB radiation. Using this system, we have determined antioxidant effect of 2-SeCD by comparison of malondialdehyde (MDA) and H(2)O(2) contents in NIH3T3 cells before and after UVB radiation. Experimental results indicate that 2-SeCD can inhibit lipid peroxidation and protect the cells from the damage generated by UVB radiation. To evaluate the molecular mechanism of this protection, we determined the effect of 2-SeCD on the expression of p53 and Bcl-2 in NIH3T3 cells. The results showed that 2-SeCD inhibits the increase of p53 expression level and the decrease of expression of Bcl-2 induced by UVB radiation. Thus, we have concluded that protection of NIH3T3 cells against oxidative stress by 2-SeCD was carried out by regulation of the expression of Bcl-2 and p53.
authors.affiliation: Key Laboratory for Molecular Enzymology and Engineering of the Ministry of Education, Jilin University, Changchun, P.R. China.
authors.forename: Ye
authors.initials: Y
authors.lastname: Sun
authors.forename: Ying
authors.initials: Y
authors.lastname: Mu
authors.forename: Shumei
authors.initials: S
authors.lastname: Ma
authors.forename: Pingsheng
authors.initials: P
authors.lastname: Gong
authors.forename: Ganglin
authors.initials: G
authors.lastname: Yan
authors.forename: Jiuqiu
authors.initials: J
authors.lastname: Liu
authors.forename: Jiacong
authors.initials: J
authors.lastname: Shen
authors.forename: Guimin
authors.initials: G
authors.lastname: Luo
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D002470:Cell Survival / Q000187:drug effects; D004249:DNA Damage; D005786:Gene Expression Regulation / Q000187:drug effects / Q000528:radiation effects; D006861:Hydrogen Peroxide / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D051379:Mice; D041681:NIH 3T3 Cells / Q000187:drug effects* / Q000528:radiation effects; D016566:Organoselenium Compounds / Q000494:pharmacology*; D018384:Oxidative Stress; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis / Q000235:genetics; D011837:Radiation-Protective Agents / Q000494:pharmacology; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis / Q000235:genetics; D014466:Ultraviolet Rays; D047392:beta-Cyclodextrins / Q000494:pharmacology*
chemical_list: C500959:2-selenium-bridged beta-cyclodextrin; D000975:Antioxidants; D016566:Organoselenium Compounds; D019253:Proto-Oncogene Proteins c-bcl-2; D011837:Radiation-Protective Agents; D016159:Tumor Suppressor Protein p53; D047392:beta-Cyclodextrins; D006861:Hydrogen Peroxide