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Oxidative Medicine and Cellular Longevity
Volume 2017, Article ID 1320241, 14 pages
Research Article

Oxidative Phosphorylation System in Gastric Carcinomas and Gastritis

1Laura-Bassi Centre of Expertise, Research Program for Receptor Biochemistry and Tumor Metabolism, Department of Pediatrics, Paracelsus Medical University, 5020 Salzburg, Austria
2Institute of Pathology, Paracelsus Medical University, 5020 Salzburg, Austria
3Division of Molecular Biology, Department of Microbiology, Paris-Lodron University, 5020 Salzburg, Austria
4Department of Medicine and Department of Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine and Veterans Affairs Tennessee Valley Healthcare System, Nashville, TN 37232, USA
5Department of Pediatrics, Paracelsus Medical University, 5020 Salzburg, Austria

Correspondence should be addressed to René G. Feichtinger; ta.klas@regnithcief.r

Received 31 January 2017; Revised 10 April 2017; Accepted 10 May 2017; Published 28 June 2017

Academic Editor: Maik Hüttemann

Copyright © 2017 René G. Feichtinger et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Switching of cellular energy production from oxidative phosphorylation (OXPHOS) by mitochondria to aerobic glycolysis occurs in many types of tumors. However, the significance of this switching for the development of gastric carcinoma and what connection it may have to Helicobacter pylori infection of the gut, a primary cause of gastric cancer, are poorly understood. Therefore, we investigated the expression of OXPHOS complexes in two types of human gastric carcinomas (“intestinal” and “diffuse”), bacterial gastritis with and without metaplasia, and chemically induced gastritis by using immunohistochemistry. Furthermore, we analyzed the effect of HP infection on several key mitochondrial proteins. Complex I expression was significantly reduced in intestinal type (but not diffuse) gastric carcinomas compared to adjacent control tissue, and the reduction was independent of HP infection. Significantly, higher complex I and complex II expression was present in large tumors. Furthermore, higher complex II and complex III protein levels were also obvious in grade 3 versus grade 2. No differences of OXPHOS complexes and markers of mitochondrial biogenesis were found between bacterially caused and chemically induced gastritis. Thus, intestinal gastric carcinomas, but not precancerous stages, are frequently characterized by loss of complex I, and this pathophysiology occurs independently of HP infection.