Preface

Several biochemical and physiological characteristics of the brain make it especially vulnerable to free radical-induced damage. Such features include the large lipid content of myefin and the high rate of oxidative metabolism of central nerve tissue. This intense aerobic activity occurs in the presence of relatively low levels of potentially protective enzymes such as superoxide dismutase and cataiase. It has become increasingly apparent that the basis of many neurological disorders may in part involve excess oxidative activity. Generation of increased amounts of oxidative free radicals within the central nervous system may be a relatively common occurence, and this can exacerbate various kinds of neural insult. It has been estimated that around 2% of the oxygen consumed by mitochondria is incompletely utilized and appears as reactive oxygen species. This proportion may be elevated when the efficient functioning of the electron transport system is compromised. Any pathological event involving disruption of membrane structure or mitochondriai function has thus the potential for induction of free radicals. A lesion to the extensive cerebral capillary network carries an attendant risk of iron catalysis of oxygen radical generation which may further intensify free radical production. An imbalance of cellular redox status in favor of greater oxidative activity can lead to several kinds of macromolecular damage, such as disruption of genomic function by alterations to DNA, or impairment of membrane properties by attack on proteins or lipids. Lipid peroxidative events are especially hazardous, since iipoperoxy radicals can initiate oxidative chain reactions. This issue of the Zntern~i~onu~ Journal zyxwvutsrqponmlkjihgfedcbaZYXWVUTSRQPONMLKJIHGFEDCBA of ~e e~o~~entfff neuroscience is devoted to the evaluation of the origins and consequences of excess rates of generation of reactive oxygen species within the nervous system. Several papers also discuss therapeutic approaches with the potential for mitigation of oxidativefy induced damage. This volume documents the growing body of evidence implicating a role for oxidative radicals in a broad range of neuropathofogicaf events. While many important aspects of this topic are not to be dealt with here due to space limitations, it is hoped that this collection of viewpoints will illustrate current directions and future goals of research in this area.