Ku Yong Pyong, Jin Ming, Kim Kyung Hee, Ahn Young Jun, Yoon Sang Pil, You Ho Jin, Chang In Youb
Department of Surgery, Sun General Hospital, Daejun, Republic of Korea.
Acta Histochem. 2009;111(2):138-44. doi: 10.1016/j.acthis.2008.05.008. Epub 2008 Aug 3.
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.
本研究在实验性大鼠模型中检测了氧化性DNA损伤及其修复系统是否与糖尿病的发生有关。在链脲佐菌素诱导的糖尿病大鼠(腹腔注射60mg/kg)的胰岛中,检测了8-羟基脱氧鸟苷(8-OHdG)和8-氧代鸟嘌呤DNA糖基化酶(OGG1)形态学变化。免疫定位模式主要在正常胰岛的周边观察到:细胞核中的8-OHdG和细胞质中的OGG1。链脲佐菌素注射后的最初几个小时内,8-OHdG和OGG1的免疫定位改变最为明显,随后随着胰腺β细胞破坏的形态学观察结果而平行下降。这些结果表明,氧化性DNA损伤增加可能作为糖尿病的诱导因素发挥作用,并且OGG1可能无法成功介导链脲佐菌素诱导的糖尿病大鼠胰腺中的DNA修复。