ROS, particularly superoxide, have been implicated to play a key role in neuronal cell death following cerebral ischemia (62-66). The superoxide anion radical (O2 -) is the product of a one electron reduction of oxygen and it is the precursor of most ROS, including the highly toxic and damaging hydroxyl ion and peroxynitrite (67-68). While ROS are suggested to mediate physiological processes at low concentrations, when they are over-produced in pathological situations they can be highly injurious to adjacent structures in cells and neurons, including lipid membranes, DNA, and proteins (63). It is well known that following the onset of either permanent or transient FCI, ROS increase significantly in the cerebral cortex and other brain regions (1, 62-66). Along these lines, it has been shown that there is a marked steady elevation of ROS in the penumbra (infarct border) of the parietal cortex during a 3h measurement period post ischemia in permanent cerebral ischemia (64).