Atrophic gastritis: deficient complex I of the respiratory chain in the mitochondria of corpus mucosal cells

Gruno, Marju; Peet, Nadezhda; Tein, Andres; Salupere, Riina; Sirotkina, Meeli; Valle, Julio; Peetsalu, Ants; Seppet, Enn

doi:10.1007/s00535-008-2231-4

Cited by 36 publications

(26 citation statements)

References 63 publications

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“…However, there is substantial evidence that oxygenderived free radicals play an important role in the pathogenesis of the injury of various tissues including the digestive system [30]. Excess ROS, in turn, causes defects in the mitochondrial genome, thus leading to impaired oxidative phosphorylation, which not only limits ATP generation but also further promotes ROS production [31]. The involvement of oxygen-derived free radicals, such as the superoxide anion, hydrogen peroxide and hydroxyl radical, has been well established in the pathogenesis of ischaemic injury of the gastrointestinal mucosa and in other models of mucosal damage induced by NSAIDs, ethanol, haemorrhagic shock, feeding restriction stress, platelet-activating factor and Helicobacter pylori [30].…”

Section: Discussionmentioning

confidence: 99%

Gastrin-Releasing Peptide Receptor Antagonist or N-acetylcysteine combined with Omeprazol Protect against Mitochondrial Complex II Inhibition in a Rat Model of Gastritis

Rezin¹,

Petronilho²,

Araújo³

et al. 2010

Basic &Amp; Clinical Pharmacology &Amp; Toxicology

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The pathophysiology of gastritis involves an imbalance between gastric acid attack and mucosal defence. In addition, the gastric mucosal injury results in adenosine triphosphate (ATP) depletion leading to mitochondrial dysfunction. Several studies have shown the association of mitochondrial disorders with gastrointestinal dysfunction. In the present study, we investigated the activity of mitochondrial respiratory chain complexes activity in the stomach of rats with gastritis induced by indomethacin (IDM) and treated with omeprazole (OM), N-acetylcysteine (NAC) and the gastrin-releasing peptide receptor (GRPR) antagonist RC-3095. Adult male Wistar rats were pre-treated for 7 days with OM, NAC, RC-3095, combination of OM plus RC-3095, OM plus NAC and water (control). The animals were then submitted to fasting for 24 hr; IDM was administered. The rats were killed 6 hr later, and the stomachs were used for evaluation of macroscopic damage and respiratory chain activity. Our results showed that complex I and IV activities were not affected by administration of IDM. On the other hand, complex II and III activities were inhibited. In addition, OM plus RC-3095 and OM plus NAC did not reverse complex II activity inhibition. However, the complex III activity inhibition was reversed only with the combined use of OM plus RC-3095 and OM plus NAC. Our results are in agreement with previous studies indicating mitochondrial dysfunction in the pathophysiology of gastrointestinal tract disease and we suggest that GRPR antagonism might be a novel therapeutic strategy in gastritis.

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Section: Discussionmentioning

confidence: 99%

Gastrin-Releasing Peptide Receptor Antagonist or N-acetylcysteine combined with Omeprazol Protect against Mitochondrial Complex II Inhibition in a Rat Model of Gastritis

Rezin¹,

Petronilho²,

Araújo³

et al. 2010

Basic &Amp; Clinical Pharmacology &Amp; Toxicology

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“…Bioenergetic studies on the gastric epithelium are relatively limited, especially with respect to investigating human stomach diseases and the use of compound biomarkers [8,10,11,[20][21][22][23][24][25][26][27][28][29][30] . The main purpose of this study was to examine the suitability of using biochemical parameters (cellular respiration, ATP, GSH, and caspase activity) as biomarkers for the gastric mucosa.…”

Section: Discussionmentioning

confidence: 99%

“…Oxidative phosphorylation was measured in permeabilized corpus mucosal biopsies [22] . Cellular respiration was about 2-fold lower in patients with atrophic gastritis compared to non-atrophic gastritis.…”

Section: Discussionmentioning

confidence: 99%

“…Cellular respiration was about 2-fold lower in patients with atrophic gastritis compared to non-atrophic gastritis. This effect was attributed to a deficiency of complex Ⅰ of the respiratory chain [22] . Furthermore, limiting cellular bioenergetics was proposed to cause dysfunction of the zymogenic mucosal cells [23] .…”

Section: Discussionmentioning

confidence: 99%

“…The mitochondria are also the target of self-generated reactive oxygen species. Premalignant atrophic gastritis and gastric carcinoma are both associated with decreased respiratory capacity and mitochondrial complex Ⅰ defici ency [22,30] . Therefore, investigating metabolic biomarkers in the gastric mucosa is much needed and future studies should determine whether they can be used to explore the mechanisms of diseases involving the gastric mucosa.…”

Section: Discussionmentioning

confidence: 99%

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Profiling cellular bioenergetics, glutathione levels, and caspase activities in stomach biopsies of patients with upper gastrointestinal symptoms

Alfazari

Al-Dabbagh

Al-Dhaheri

et al. 2015

WJG

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AIM:To measure biochemical parameters in stomach biopsies and test their suitability as diagnostic biomarkers for gastritis and precancerous lesions. METHODS:Biopsies were obtained from the stomachs of two groups of patients (n = 40) undergoing fiberoptic endoscopy due to upper gastrointestinal symptoms. In the first group (n = 17), only the corpus region was examined. Biopsies were processed for microscopic examination and measurement of mitochondrial O2 consumption (cellular respiration), cellular adenosine triphosphate (ATP), glutathione (GSH), and caspase activity. In the second group of patients (n = 23), both corpus and antral regions were studied. Some biopsies were processed for microscopic examination, while the others were used for measurements of cellular respiration and GSH level. RESULTS:Microscopic examinations of gastric corpus biopsies from 17 patients revealed normal mucosae in 8 patients, superficial gastritis in 7 patients, and chronic atrophic gastritis in 1 patient. In patients with normal histology, the rate (mean ± SD) of cellular respiration was 0.17 ± 0.02 μmol/L O2 min -1 mg -1, ATP content was 487 ± 493 pmol/mg, and GSH was 469 ± 98 pmol/mg. Caspase activity was detected in 3 out of 8 specimens. The values of ATP and caspase activity were highly variable. The presence of superficial gastritis had insignificant effects on the measured biomarkers. In the patient with atrophic gastritis, cellular respiration was high and Prospective Study ORIGINAL ARTICLEAlfazari AS et al . Bioenergetics of normal and abnormal gastric mucosae ATP was relatively low, suggesting uncoupling oxidative phosphorylation. In the second cohort of patients, the examined biopsies showed either normal or superficial gastritis. The rate of cellular respiration (O2. μmol/L min -1 mg -1 ) was slightly higher in the corpus than the antrum (0.18 ± 0.05 vs 0.15 ± 0.04, P = 0.019). The value of GSH was about the same in both tissues (310 ± 135 vs 322 ± 155, P = 0.692). CONCLUSION:The corpus mucosa was metabolically more active than the antrum tissue. The data in this study will help in understanding the pathophysiology of gastric mucosa.

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Mitochondria metabonomics of Huangqi Jianzhong Tang against chronic atrophic gastritis

Zhang

Liang

Qin

2020

Biomedical Chromatography

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Huangqi Jianzhong Tang (HQJZ) is a representative prescription used for clinical treatment of chronic atrophic gastritis (CAG) in Chinese medicine. Our previous study had revealed that energy regulation was one of the important mechanisms of HQJZ action against CAG. In this study, ultra‐high‐performance liquid chromatography coupled with quadrupole‐Exactive mass spectrometry (UHPLC‐Q‐Exactive MS) based metabonomics was used to find the potential mitochondrial biomarkers and metabolic pathways of HQJZ in CAG rats, which focused on a specific organelle (mitochondria) isolated from gastric tissue samples. A total of 16 biomarkers from CAG tissues were identified with 11 of these significantly regulated by HQJZ treatment. These biomarkers was mainly involved in glycine, serine, and threonine metabolism; aminoacyl‐tRNA biosynthesis metabolism; and taurine and hypotaurine metabolism. Our results show that HQJZ could protect from CAG by altering the mitochondrial function. These findings deepen our understanding of the mitochondrial metabolic changes that occur with CAG and shine a light on the mechanism of HQJZ.

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Atrophic gastritis: deficient complex I of the respiratory chain in the mitochondria of corpus mucosal cells

Cited by 36 publications

References 63 publications

Gastrin-Releasing Peptide Receptor Antagonist or N-acetylcysteine combined with Omeprazol Protect against Mitochondrial Complex II Inhibition in a Rat Model of Gastritis

Gastrin-Releasing Peptide Receptor Antagonist or N-acetylcysteine combined with Omeprazol Protect against Mitochondrial Complex II Inhibition in a Rat Model of Gastritis

Profiling cellular bioenergetics, glutathione levels, and caspase activities in stomach biopsies of patients with upper gastrointestinal symptoms

Mitochondria metabonomics of Huangqi Jianzhong Tang against chronic atrophic gastritis

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