Oxygen radical-mediated damage to brain tissue.

Abstract

The brain is the primary information-processing center of the body; its functioning in the most perfect state possible, within genetic constraints, is very important. Damage to brain most likely has more serious consequences than to other tissue because neuronal tissue is post-mitotic. Brain is a tissue having an abnormally high amount of 22:6 fatty acids,1 which due to the large number of carbon-carbon double bonds are easily peroxidized. Brain is not well endowed with the antioxidant protective enzymes superoxide dismutase, catalase or glutathione peroxidase, nor does it have high levels of vitamin E.1 It does, however, have higher levels of ascorbate,2 which can in certain circumstances act as a prooxidant. Brain, especially human brain, does contain high levels of iron,3 apparently stored as ferritin. Catalytic levels of iron, in combination with oxygen free radicals, appear to be extremely important in mediating oxidative damage to membranes.4 The administration of free iron directly into the brain has been shown to cause death of neurons, resulting in permanent epiletiform centers.5 The iron-induced damage to brain has been shown to be due to peroxidative events.5 Thus, all of the background information clearly indicates the need to understand the basic aspects of oxidative damage to nervous tissue.