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Ann N Y Acad Sci. 2010 Aug;1203:138-45. doi: 10.1111/j.1749-6632.2010.05563.x.

Oxidative/nitrosative stresses trigger type I diabetes: preventable in streptozotocin rats and detectable in human disease.

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1
Department of Biochemistry and Molecular Biology/Physiology-Pharmacology, West Virginia University Medical School, West Virginia, USA. kvandyke@hsc.wvu.edu

Abstract

Recently we demonstrated that streptozotocin (STZ) diabetes (type I) in rats is preventable using a simultaneous equimolar injection of carboxy-PTIO (c-PTIO). Both changes in blood sugar and cataracts are prevented. This apparently occurs because the nitric oxide (NO) (from STZ) generated in the beta cells is oxidized to nitrite by c-PTIO preventing diabetes. STZ generates NO producing a NO-based toxin. The toxin damages DNA by nicking and activates poly-ADP-ribose causing necrosis and triggering inflammation. Is there evidence that O/N stress occurs in early human type I diabetes? We studied 40 children with or without early type I diabetes and observed that urate is decreased 25% in all these diabetic children each over the age of 3 years. Urate is a major portion of blood-antioxidant load. Surely this decrease in urate indicates ongoing O/N stress. Does O/N stress initiate disease? STZ studies in rats indicates that this is correct.

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