文摘
Summary
This study examined whether oxidative DNA damage and its repair system contribute to the occurrence of diabetes in an experimental rat model. The changed morphological findings of the 8-hydroxydeoxyguanosine (8-OHdG) and 8-oxoG-DNA glycosylase (OGG1) were examined in the pancreatic islets in streptozotocin-induced diabetic rats (60 mg/kg, i.p.). The patterns of immunolocalization were mainly observed in the periphery of the normal pancreatic islet: 8-OHdG in the nucleus and OGG1 in the cytoplasm. The altered immunolocalization of 8-OHdG and OGG1 were greatest in the first hours after streptozotocin injection, and then declined in parallel with the morphological observations of pancreatic beta cell destruction. These results suggested that increased oxidative DNA damage might play a role as the inducer of diabetes and that OGG1 may not successfully mediate DNA repair in streptozotocin-induced diabetic rat pancreas.
