Abstract
The production of reactive oxygen species (ROS) has been implicated in reperfusion injury after cerebral ischemia, and antioxidant enzymes are believed to be among the major mechanisms by which the cells counteract the deleterious effect of ROS after cerebral ischemia. ROS also mediate the mitochondrial signaling pathway that may lead to apoptosis following cerebral ischemia. The recent development and availability of transgenic and knockout mutant rodents that either overexpress or are deficient in antioxidant genes have provided powerful tools for dissecting the molecular and cellular mechanisms of signaling pathways, direct oxidative damage, or both that are involved in ischemic brain injury. This article focuses on the contribution of ROS or an antioxidant system to the molecular pathway of postischemic apoptosis following transient focal cerebral ischemia by using transgenic mice that overexpress the cytosolic antioxidant copper/zinc superoxide dismutase.
Original language | English |
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Pages (from-to) | 59-66 |
Number of pages | 8 |
Journal | Neurocritical Care |
Volume | 2 |
Issue number | 1 |
DOIs | |
Publication status | Published - 2005 |
Keywords
- Apoptosis
- DNA damage
- Focal cerebral ischemia
- Reperfusion injury
- Superoxide dismutase
ASJC Scopus subject areas
- Clinical Neurology
- Critical Care and Intensive Care Medicine