Free radicals have recently been implicated in a number of biochemical and chemical reactions in the body. Lipid peroxidation induced by free radical reaction is believed to be one of the major causes of cell damage and injuries in cell membranes. In recent years, reports have appeared citing the contribution of free radicals and active oxygen species in the etiology of various digestive diseases. For example, gastric mucosal injuries and the increases in thiobarbituric acid-reactive substances in the gastric mucosa induced by ischemia or ischemia/reperfusion were significantly inhibited by treatment with superoxide dismutase and catalase. It has been suggested that superoxide radical or hydroxyl radical may be the major oxygen radicals contributing to ischemia or ischemia/reperfusion injury in the stomach, small intestine, and liver. There reactive species can attack and damage important biological molecules. Within cellular membranes, hydroxyl radical can initiate a free radical chain reaction known as lipid peroxidation, in which polyunsaturated fatty acids are broken down into water soluble products and toxic lipid peroxides are produced with the consequent destruction of membrane integrity. The major source of active oxygen species produced after ischemia or ischemia/reperfusion seems to be the enzymatic xanthine oxidase and activated polymorphonuclear leukocytes (PMN). In the large intestine which has little activity in xanthine oxidase, PMNs are a more important source of active oxygen species and play a role in the pathogenesis of the inflammatory bowel diseases. The above information suggests that oxygen-derived free radicals are involved in the fundamental mechanism of tissue injury in various disorders of the digestive system.