Free Radicals and Gastric Mucosal Injury

Abstract

Free radicals in excess high amounts, irrespective of radical and/or nonradical reactive species, are very reactive in nature and impose detrimental influence on living organisms through damaging all major cellular constituents including membrane, cytoplasmic proteins, and even nuclear DNAs, resulting in oxidative stress, whereas nitric oxide (NO), superoxide anion, and related reactive oxygen species (ROS) in low or modest amounts play an important role as regulatory mediators in signaling processes through which many of the ROS-mediated responses, paradoxically, can protect the cells against oxidative stress and maintain redox homeostasis. Compared to primitive organisms, vertebrates have evolved the use of NO and ROS also as signaling molecules for several physiological functions, which are generated by tightly regulated enzymes including NO synthase and NADPH oxidase isoforms, respectively. Simply stated, the problem is provoked by blazed ROS productions far beyond the quenching capacity of cells, by which free radicals are implicated in the pathogenesis of several gastrointestinal diseases, cancer, diabetes mellitus, atherosclerosis, neurodegenerative diseases, rheumatoid arthritis, ischemia and reperfusion injury, and other diverse diseases in addition to senescence. The implication of free radicals in gastric mucosal injuries will be the main focus of the current chapter. The offending systems like NADPH oxidase and NO synthase and defending systems of glutathione and heat shock protein related to gastric mucosal injury will be introduced.