Oxidative stress in type 1 diabetes

被引：140

作者：

Haskins, K

Bradley, B

Powers, K

Fadok, V

Flores, S

Ling, XF

Pugazhenthi, S

Reusch, J

Kench, J

机构：

[1] Univ Colorado, Hlth Sci Ctr, Dept Immunol, Denver, CO 80206 USA

[2] Univ Colorado, Hlth Sci Ctr, Dept Pediat, Denver, CO 80206 USA

[3] Natl Jewish Med & Res Ctr, Denver, CO USA

[4] Univ Colorado, Hlth Sci Ctr, Webb Waring Inst Antioxidant Res, Denver, CO 80206 USA

[5] VA Med Ctr, Denver, CO USA

来源：

IMMUNOLOGY OF DIABETES II: PATHOGENESIS FROM MOUSE TO MAN | 2003年 / 1005卷

关键词：

oxidative stress; SOD mimetic; autoimmune diabetes;

D O I：

10.1196/annals.1288.006

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

We have been investigating the effects of preventing oxidative stress on pathogenesis and complications of type 1 diabetes in the NOD mouse model. Our studies have shown that damage caused by oxidative stress is higher in islets and vascular tissue of NOD mice than in nonautoimmune controls or a diabetes-resistant NOD mouse. In addition, phagocytic function and cytokine production by macrophages are aberrant in the NOD. We have demonstrated that treatment of prediabetic NOD mice for 2 weeks with a metalloporphyrin superoxide dismutase (SOD) mimetic results in marked reduction of oxidative stress in islets and vascular tissue and a reversal of macrophage defects.

引用

页码：43 / 54

页数：12

共 57 条

[1] Adenovirus-mediated catalase gene transfer reduces oxidant stress in human, porcine and rat pancreatic islets [J].