Abstract
H. pylori is a Gram (−) bacterium that infects the human stomach of approximately half of the world’s population. This bacterium is an important etiological agent for numerous gastric disorders such as chronic gastritis, peptic ulcers, mucosa-associated lymphoid tissue lymphoma, and gastric cancer. The infection is correlated with histological and pathological damage in mucosa, where both oxidative stress (elevated ROS and diminished antioxidant system) and apoptosis are enhanced. Bearing in mind that mitochondria are the major intracellular source of free radicals and, moreover, one of their possible targets and that their morphological and functional alterations are able to trigger apoptosis pathways, it could be reasonably assumed that mitochondria are key points in the pathology caused by the infection. Recently, the intrinsic apoptosis pathway has been exhaustively discussed in H. pylori infection, and all disturbances related to it have been described in epithelial cells (loss of membrane potential, increased cytosolic cytochrome c, higher levels of Bax and caspases, DNA fragmentation, etc.). It has been also observed that antioxidant supplements reduce these alterations and, ultimately, death by apoptosis. Additionally, antioxidants increase the effectiveness of antibiotics, by improving the eradication rate.
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This chapter was partly funded by a research grant PI-2008134 of Fundación para la Investigación Sanitaria en Castilla La-Mancha (FISCAM). The work of M. Calvino was funded by “La Fundación para la Investigación Biomédica del Hospital Universitario de la Princesa” and by “La Fundación Sociosanitaria de Castilla La-Mancha.” Spain.
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Parra-Cid, T., Calvino-Fernández, M., Benito-Martínez, S., Pérez-Gisbert, J. (2014). Role of Reactive Oxygen Species and Apoptosis in Helicobacter pylori Infection. In: Laher, I. (eds) Systems Biology of Free Radicals and Antioxidants. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-30018-9_143
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