Title of article :
Possible involvement of NO-mediated oxidative stress in induction of rat forestomach damage and cell proliferation by combined treatment with catechol and sodium nitrite
Author/Authors :
Ishii، نويسنده , , Yuji and Umemura، نويسنده , , Takashi and Kanki، نويسنده , , Keita and Kuroiwa، نويسنده , , Yuichi and Nishikawa، نويسنده , , Akiyoshi and Ito، نويسنده , , Rie and Saito، نويسنده , , Koichi and Nakazawa، نويسنده , , Hiroyuki and Hirose، نويسنده , , Masao، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2006
Abstract :
To clarify the mechanisms underlying forestomach carcinogenesis in rats by co-treatment with catechol and sodium nitrite (NaNO2), we investigated the involvement of oxidative stress resulting from reaction of the two compounds. Since generation of semiquinone radical, hydroxyl radical (OH), and peroxynitrite (ONOO−) arose through the reaction of catechol with NO, we proposed that superoxide resulting from catechol oxidation reacted with excess NO, consequently yielding OH via ONOO−. Male F344 rats were co-treated with 0.2% catechol in the diet and 0.8% NaNO2 in the drinking water for 2 weeks. Prior to occurrence of histological evidence indicating epithelial injury and hyperplasia, 8-hydroxydeoxyguanosine levels in forestomach epithelium significantly increased from 12 h together with appearance of immunohistochemically nitrotyrosine-positive epithelial cells. There were no remarkable changes in rats given each chemical alone. We conclude that oxidative stress due to NO plays an important role in induction of forestomach epithelial damage, cell proliferation, and thus presumably forestomach carcinogenesis.
Keywords :
Catechol , Hydroxyl radical , peroxynitrite , 8-hydroxydeoxyguanosine , forestomach , oxidative stress , Electron spin resonanceCarcinogenesisNitrotyrosine , Nitric oxide , Sodium Nitrite
Journal title :
Archives of Biochemistry and Biophysics
Journal title :
Archives of Biochemistry and Biophysics