Pancreatic islet β-cell and oxidative stress:: The importance of glutathione peroxidase

被引:144
作者
Robertson, R. Paul [1 ]
Harmon, Jamie S. [1 ]
机构
[1] Univ Washington, Pacific NW Res Inst, Seattle, WA 98122 USA
来源
FEBS LETTERS | 2007年 / 581卷 / 19期
关键词
type; 2; diabetes; gluathione peroxidase; pancreatic; beta-cell;
D O I
10.1016/j.febslet.2007.03.087
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Pancreatic beta-cell function continuously deteriorates in type 2 diabetes despite optimal treatment regimens, which has been attributed to hyperglycemia itself via formation of excess levels of reactive oxygen species (ROS). Glutathione peroxidase GPx), by virtue of its ability to catabolize both H2O2 and lipid peroxides, is uniquely positioned to protect tissues from ROS. The level of this antioxidant in 0 cells is extremely low and overexpression of GPx in islets provides enhanced protection against oxidative stress. This suggests that GPx mimetics may represent a valuable ancillary treatment that could add a novel layer of protection for the P-cell. (c) 2007 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:3743 / 3748
页数:6
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