H. pylori and mitochondrial changes in epithelial cells. The role of oxidative stress

ABSTRACT

Infection with H. pylori plays a role in the pathogenesis of gastritis,peptic ulcer, gastric carcinoma, and gastric lymphoma, butmechanisms leading to the various clinical manifestations remainobscure and are the primary focus of research in this field.Proliferation and apoptosis are essential in the maintenance ofgastric tissue homeostasis, and changes seen in their balance maycondition gastric mucosal changes during infection. Thus, excessiveapoptosis or proliferation inhibition will result in cell massloss, which is observed in gastric ulcers. On the other hand, acceleratedepithelial cell turnover is characteristic of carcinogenic mucosas.There is also scientific evidence that demonstrates an associationbetween H. pylori infection and exacerbated synthesis offree radicals, the latter being well known as a primary cause of celldeath.A thorough review of the literature and the results of our experimentalresearch lead to conclude that H. pylori-induced oxidativestress activates the intrinsic pathway of apoptosis. Structuraland functional changes caused by this process on mitochondrialorganelles lie at the origin of gastric mucosal toxicity, and lead tothe development of the various manifestations associated with thisinfection. Based on these data we suggest that therapy with antioxidantsshould prove beneficial for the clinical management ofpatients with H. pylori infection(AU)