期刊
CANCER LETTERS
卷 226, 期 1, 页码 1-15出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2004.10.021
关键词
nitric oxide; apoptosis; free radicals; carcinogenesis; oxidative stress
类别
资金
- NCI NIH HHS [CA26731] Funding Source: Medline
Unphysiologically high levels of nitric oxide (NO.) are mutagenic and may contribute to carcinogenesis. Proapoptotic and anitiapoptotic functions of NO. have been reported in various in vivo and in vitro experimental models. The complexity of biological responses induced is a consequence of the multiple chemical pathways through which NO. causes damage to critical cellular macromolecules. The extent and kinetics of apoptotic and other responses are highly dependent on steady-state NO. levels, cumulative total dose and cell type. Steady-state and total dose thresholds have been defined, both of which must be exceeded for the induction of apoptosis and other responses in human lymphoblastoid cells. DNA damage, protein modifications, p53 activation and mitochondrial respiratory inhibition contribute to NO.-mediated apoptosis via mitochondrial and Fas receptor pathways. Multifaceted cellular defense systems including glutathione, antioxidant enzymes and Nrf2-Keap1 signaling participate in protective responses to mitigate damage by toxic levels of NO.. (c) 2004 Elsevier Ireland Ltd. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据