作者
Miguel A Perez-Pinzon, Kunjan R Dave, Ami P Raval
发表日期
2005/9/1
来源
Antioxidants & redox signaling
卷号
7
期号
9-10
页码范围
1150-1157
出版商
Mary Ann Liebert, Inc.
简介
It is now understood that the mechanisms leading to neuronal cell death after cerebral ischemia are highly complex. A well established fact in this field is that neurons continue to die over days and months after ischemia, and that reperfusion following cerebral ischemia contributes substantially to ischemic injury. It is now well accepted that central to ischemic/reperfusion-induced injury is what occurs to mitochondria hours to days following the ischemic insult. For many years, it has been established that reactive oxygen species (ROS) and reactive nitrogen species (RNS) promote lipid, protein, and DNA oxidation that affects normal cell physiology and eventually leads to neuronal demise. In addition to oxidation of neuronal molecules by ROS and RNS, a novel pathway for molecular modifications has risen from the concept that ROS can activate specific signal transduction pathways that, depending on the insult …
引用总数
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MA Perez-Pinzon, KR Dave, AP Raval - Antioxidants & redox signaling, 2005