title: Atrophic gastritis: deficient complex I of the respiratory chain in the mitochondria of corpus mucosal cells.
abstract: BACKGROUND
  Mitochondrial dysfunction is one of the most characteristic properties of the cancer cell. However, it is not known whether oxidative energy metabolism has already become altered in conditions of atrophic gastritis, a precancerous state of gastric disease. The purpose of our study was to comparatively characterize oxidative phosphorylation (OXPHOS) in the atrophic and nonatrophic gastric corpus mucosa.
  
  
  METHODS
  Mucosal biopsies were taken from 12 patients with corpus dominant atrophic gastritis and from 12 patients with nonatrophic mucosa (controls). One part of the tissue samples was permeabilized with saponin for analysis of the function of the respiratory chain using high-resolution respirometry, and another part was used for histopathological examination. The serum level of pepsinogen I (S-PGI) was determined with a specific enzyme immunoassay (EIA).
  
  
  RESULTS
  Compared to the control group, the maximal capacity of OXPHOS in the atrophy group was almost twofold lower, the respiratory chain complex I-dependent respiration, normalized to complex II-dependent respiration, was reduced, and respiratory control by ADP in the presence of succinate was increased in the atrophic corpus mucosa. In the whole cohort of the patients studied, serum S-PGI level correlated positively with complex I-dependent respiration or complex I-dependent to complex II-dependent respiration ratio.
  
  
  CONCLUSIONS
  Corpus dominant atrophic gastritis is characterized by decreased respiratory capacity and relative deficiency of the respiratory complex I of mitochondria in the mucosa, the latter defect probably limiting mitochondrial ATP production and energetic support of the secretory function of the zymogenic mucosal cells.
authors.affiliation: Department of Pathophysiology, Centre of Molecular and Clinical Medicine, Faculty of Medicine, University of Tartu, 19 Ravila Street, 50411 Tartu, Estonia.
authors.forename: Marju
authors.initials: M
authors.lastname: Gruno
authors.forename: Nadezhda
authors.initials: N
authors.lastname: Peet
authors.forename: Andres
authors.initials: A
authors.lastname: Tein
authors.forename: Riina
authors.initials: R
authors.lastname: Salupere
authors.forename: Meeli
authors.initials: M
authors.lastname: Sirotkina
authors.forename: Julio
authors.initials: J
authors.lastname: Valle
authors.forename: Ants
authors.initials: A
authors.lastname: Peetsalu
authors.forename: Enn K
authors.initials: EK
authors.lastname: Seppet
mesh_terms: D000368:Aged; D000752:Anemia, Pernicious / Q000150:complications / Q000378:metabolism / Q000473:pathology; D016022:Case-Control Studies; D019069:Cell Respiration / Q000502:physiology; D015331:Cohort Studies; D042967:Electron Transport Complex I / Q000378:metabolism*; D005260:Female; D005753:Gastric Mucosa / Q000378:metabolism* / Q000473:pathology; D005757:Gastritis, Atrophic / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D008928:Mitochondria / Q000378:metabolism*; D010085:Oxidative Phosphorylation; D010101:Oxygen Consumption / Q000502:physiology*; D020116:Pepsinogen A / Q000097:blood
chemical_list: D020116:Pepsinogen A; D042967:Electron Transport Complex I