Prevention of oxidative stress by adenoviral overexpression of glutathione-related enzymes in pancreatic islets

Ann N Y Acad Sci. 2005 Jun;1043:513-20. doi: 10.1196/annals.1333.058.


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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adenoviridae / enzymology*
  • Animals
  • Glucose / pharmacology
  • Glutamate-Cysteine Ligase / metabolism*
  • Glutathione Peroxidase / metabolism*
  • Islets of Langerhans / drug effects
  • Islets of Langerhans / enzymology*
  • Islets of Langerhans / virology
  • Oxidative Stress / drug effects
  • Oxidative Stress / physiology*
  • Reactive Oxygen Species / metabolism


  • Reactive Oxygen Species
  • Glutathione Peroxidase
  • Glutamate-Cysteine Ligase
  • Glucose