ABSTRACT
The biomedical literature contains multiple claims that “ free radicals” and other “ reactive species” are involved in different human diseases. They have been implicated in over 100 disorders, ranging from rheumatoid arthritis, hem orrhagic shock, and ulcerative colitis to gastrointestinal damage by Helico bacter pylori and acquired immunodeficiency syndrome (reviewed in Refs. 1-4). Indeed, their importance in diabetes is widely proposed (5,6). This wide range of disorders implies that free radicals are not something esoteric but that their increased formation accompanies tissue injury in most or all human diseases (1-8), for the reasons summarized in Figure 1. Sometimes they make a significant contribution to the disease pathology; at other times they may not (7,8). Reasons for such differences are summarized in Figure 2. Establish ing the real importance of reactive oxygen, nitrogen, and chlorine species (ROS/RNS/RCS) requires specific assays for their formation and the damage that they do in vivo. The lack of such assays in the past has impeded progress in our understanding of the role played by reactive species in normal physiol ogy and in human disease. Thus, as summarized in Table 1, demonstrating that reactive species are important in diabetes (or indeed any other disease) involves much more than a mere demonstration of their formation. Table 2 lists some of the reactive species to be considered.
