Neuroprotective effect of an antioxidant in ischemic brain injury: involvement of neuronal apoptosis.

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.

• Authors: Miki Fujimura, Teiji Tominaga, Pak H Chan
• Journal: Neurocritical care (Neurocrit Care) Vol. 2 Issue 1 Pg. 59-66 ( 2005) ISSN: 1541-6933 [Print] United States
• PMID: 16174972 (Publication Type: Journal Article, Review)

Chemical References

• Antioxidants
• Reactive Oxygen Species
• SOD1 protein, human
• Cytochromes c
• Sod1 protein, mouse
• Superoxide Dismutase
• Superoxide Dismutase-1

Topics

• Animals
• Antioxidants (physiology)
• Apoptosis (physiology)
• Cytochromes c (metabolism)
• Cytosol (physiology)
• Humans
• Ischemic Attack, Transient (prevention & control)
• Mice
• Mice, Knockout
• Neurons (physiology)
• Oxidative Stress (physiology)
• Reactive Oxygen Species (metabolism)
• Signal Transduction (physiology)
• Superoxide Dismutase (physiology)
• Superoxide Dismutase-1