Possible involvement of NO-mediated oxidative stress in induction of rat forestomach damage and cell proliferation by combined treatment with catechol and sodium nitrite |
| |
Authors: | Ishii Yuji Umemura Takashi Kanki Keita Kuroiwa Yuichi Nishikawa Akiyoshi Ito Rie Saito Koichi Nakazawa Hiroyuki Hirose Masao |
| |
Institution: | Department of Analytical Chemistry, Hoshi University, 2-4-41 Ebara, Shinagawa-ku, Tokyo 142-8501, Japan. |
| |
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 Sodium nitrite Nitric oxide Hydroxyl radical Peroxynitrite 8-Hydroxydeoxyguanosine Oxidative stress Forestomach Electron spin resonance Carcinogenesis Nitrotyrosine |
本文献已被 ScienceDirect PubMed 等数据库收录! |
|