ABSTRACT
The biomedical literature continues to resound with suggestions that “free radicals” and other “reactive species” are involved in different human diseases. They have been implicated in over 100 disorders, ranging from scleroderma and hemorrhagic shock to cardiomyopathy and cystic fibrosis to gastrointestinal ischemia, AIDS, hearing loss (1-7) and even male pattern baldness (8). The various chapters that follow provide further illustrations. This wide range of disorders implies that free radicals are not something esoteric, but that their increased formation accompanies tissue injury in most, if not all, human diseases (9). Reasons for this are summarized in Figure 1. Sometimes free radicals make a significant contribution to disease pathology; at other times they may not, as Figure 2 illustrates. A major task of researchers in this field is to distinguish between these scenarios so as to be able to create useful therapies: there is no therapeutic advantage to inhibiting free radical damage when it is merely an accompaniment to tissue injury. As Table 1 summarizes, demonstrating that free radicals are important in any disease involves much more than a mere demonstration of their formation in increased amounts. The same comment applies to nitric oxide, cytokines, leukotrienes, and any of the other potential mediators of tissue injury.
