The Ion Channels Involved in Oxidative Stress-Related Gastrointestinal Diseases

Oxidative stress (OS) occurs due to an imbalance between the production of reactive oxygen species (ROS) and reactive nitrogen species (RNS) and the endogenous antioxidant defense system. This imbalance leads to cellular injury and subsequent dysfunctions that can result in a wide range of disorders [1,2]. Reactive species represent byproducts of normal cellular metabolism and are normally neutralized by a variety of cellular antioxidants: enzymatic, such as catalase (CAT) and superoxide dismutase (SOD), or non-enzymatic, such as glutathione [3]. Reactive species are generated in response to factors like UV radiation, smoking, alcohol consumption, the use of non-steroidal anti-inflammatory drugs (NSAIDs), infections, ischemia-reperfusion injury, and inflammation (Figure 1) [4,5]. While low to moderate levels of ROS and RNS have positive effects on several physiological functions, such as fighting pathogens, promoting wound healing, and aiding in tissue repair, they also serve as important signaling biomolecules [6,7]. However, excessive production can disrupt the body’s balance and lead to oxidative damage in tissues. For this reason, OS has been implicated in various disease processes, including aging, ischemia-reperfusion injury, hypertension, atherosclerosis, diabetic neuropathies, renal diseases, neurological disorders, inflammatory bowel disease and cancer [8,9].