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Oxidative Stress in Type 1 Diabetes
KATHRYN HASKINSa,
BRENDA BRADLEYa,
KATHERINE POWERSa,
VALERIE FADOKb,
SONIA FLORESc,
XIAOFENG LINGc,
SUBBIAH PUGAZHENTHId,
JANE REUSCHd AND
JENNIFER KENCHa
aDepartment of Immunology and bDepartment of Pediatrics, University of Colorado Health Sciences Center, and National Jewish Medical and Research Center, Denver, Colorado, USA
cWebb Waring Institute for Antioxidant Research, University of Colorado Health Sciences Center, Denver, Colorado, USA
dVA Medical Center, Denver, Colorado, USA
Address for correspondence: Kathryn Haskins, Department of Immunology, University of Colorado Health Sciences Center, and National Jewish Medical and Research Center, 1400 Jackson Street, K823, Denver, CO 80206. Voice: 303-270-2093; fax: 303-270-2325.
katie.haskins{at}uchsc.edu
Ann. N.Y. Acad. Sci. 1005: 43-54 (2003).
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.
Key Words: oxidative stress • SOD mimetic • autoimmune diabetes
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