© 2017 Elsevier Inc. All rights reserved. Gastric and intestinal mucosa are continuously exposed to external and internal oxidants, such as cigarette smoking, alcohol, nonsteroidal antiinflammatory drugs, ischemia-reperfusion injury, chronic infections, and inflammatory disorders, making the gastrointestinal (GI) tract quite susceptible to ROS attack. In the normal cellular aerobic metabolism, the GI tract, can produce these reactive species as intermediates. Nonetheless, the cells from the gastric mucosa, having enzymatic or nonenzymatic antioxidant systems, protect them from the deleterious effects of ROS. Moreover, despite the protective barrier provided by the mucosa, microbial pathogens can induce oxidative injury and GI inflammatory responses, where the hypersecretion of gastric acid plays a relevant role. Nevertheless, it has also been shown that the timing and the magnitude of the lipoperoxidative events derived from ROS, could synchronize the cell proliferative and apoptotic events in the gastric mucosa. Probably, this is fundamental for the progression of the cell proliferation in the human gastric adenocarcinoma.