ABSTRACT

I. INTRODUCTION Free radicals derived from molecular oxygen have been implicated in a variety of human diseases, ranging from atherosclerosis, to cancer, to neurodegenerative disorders (1-4). It is postulated that the pathophysiological sequelae of oxidant stress result partly from damage to tissue biomolecules. Understanding the role that oxidant stress plays in human disease has been hampered, however, by the lack of reliable methods to assess oxidant injury (5). The development of accurate methods for measuring oxidative stress in humans is essential to establish a means for quantifying the role of free radical injury in disease processes.