Prevention of Oxidative Stress by Adenoviral Overexpression of Glutathione-Related Enzymes in Pancreatic Islets

: Chronic exposure to supraphysiologic glucose concentrations causes functional damage to cells and tissues, a process known as glucose toxicity. Recent research indicates that one important mechanism for glucose toxicity is oxidative stress. Glucose has been shown to form reactive oxygen species th...

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Bibliographic Details
Published in:Annals of the New York Academy of Sciences 2005-06, Vol.1043 (1), p.513-520
Main Authors: ROBERTSON, R.PAUL, TANAKA, YOSHITO, TAKAHASHI, HIROKI, TRAN, PHUONG OANH T., HARMON, JAMIE S.
Format: Article
Language:English
Subjects:
Adenoviridae - enzymology
Animals
antioxidant enzymes
Antioxidants
Beta
D-glyceraldehyde
Diabetes
Enzymes
Glucose
Glucose - pharmacology
Glutamate-Cysteine Ligase - metabolism
Glutathione Peroxidase - metabolism
Islets of Langerhans - drug effects
Islets of Langerhans - enzymology
Islets of Langerhans - virology
oxidative stress
Oxidative Stress - drug effects
Oxidative Stress - physiology
pancreatic islets
Reactive Oxygen Species - metabolism
Stress concentration
Stresses
Toxicity
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Summary:: Chronic exposure to supraphysiologic glucose concentrations causes functional damage to cells and tissues, a process known as glucose toxicity. Recent research indicates that one important mechanism for glucose toxicity is oxidative stress. Glucose has been shown to form reactive oxygen species through several metabolic pathways. The pancreatic islet is distinguished by its relatively low antioxidant enzyme content and activity, which render it especially susceptible to oxidative stress. Adenoviral overexpression of glutathione peroxidase as well as gamma‐glutamylcysteine ligase have been shown to protect the islet against oxidative stress. Antioxidants have been shown to brake the worsening of diabetes by improving beta cell function in animal models. These observations suggest that enhancing antioxidant defense mechanisms in pancreatic islets may be a valuable pharmacologic approach to managing diabetes.
ISSN:0077-8923
1749-6632
DOI:10.1196/annals.1333.058