Related Experiment Video
Updated: Aug 11, 2026

Mouse- and Human-derived Primary Gastric Epithelial Monolayer Culture for the Study of Regeneration
Published on: May 7, 2018
O6-alkyltransferase activity in normal and abnormal gastric mucosa
1Jack Birch Unit for Environmental Carcinogenesis, Department of Biology, University of York, UK.
The DNA repair enzyme O6-alkyltransferase activity is significantly higher in stomachs with chronic atrophic gastritis or intestinal metaplasia. This suggests these conditions may induce the enzyme, impacting DNA repair in gastric mucosa.
Area of Science:
- Gastroenterology
- Molecular Biology
- Oncology
Background:
- Gastric mucosa integrity is crucial for digestive health.
- DNA repair mechanisms, like O6-alkyltransferase, protect against cellular damage.
- Abnormalities in gastric mucosa are linked to various gastrointestinal diseases.
Purpose of the Study:
- To investigate the activity of the DNA repair enzyme O6-alkyltransferase in stomachs with abnormal gastric mucosa.
- To compare O6-alkyltransferase activity in normal versus abnormal gastric tissues.
- To explore potential correlations between histological changes and enzyme levels.
Main Methods:
- Studied O6-alkyltransferase activity in human stomach tissue samples.
- Compared enzyme activity between normal stomachs and those with macroscopic abnormalities (ulcer, cancer).
- Assessed enzyme activity in stomachs with histological evidence of chronic atrophic gastritis and intestinal metaplasia.
Main Results:
- O6-alkyltransferase activity was not significantly different in stomachs with gastric ulcer, duodenal ulcer, or gastric cancer compared to normal.
- Significantly higher O6-alkyltransferase activity (mean 398 fmole/mg) was observed in stomachs with chronic atrophic gastritis or intestinal metaplasia.
- Normal stomach tissue showed a mean activity of 228 fmole/mg (P < 0.001).
Conclusions:
- Histological changes like chronic atrophic gastritis and intestinal metaplasia are associated with increased O6-alkyltransferase activity.
- The study speculates that the conditions causing these histological changes may also induce O6-alkyltransferase.
- Elevated O6-alkyltransferase in precancerous lesions suggests a potential role in DNA repair during gastric mucosal transformation.
More Related Videos
03:05Establishment and Evaluation of a Risk Prediction Model for Pathological Escalation of Gastric Low-Grade Intraepithelial Neoplasia
Published on: February 16, 2024
06:21Multi-Gene Single Nucleotide Polymorphism Detection in Gastric Cancer Based on Ion Semiconductor Sequencing Platform
Published on: May 10, 2024
Related Concept Videos
Pathophysiology of Peptic Ulcer Disease: Injurious Factors
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds to M3...
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors
Drugs for Peptic Ulcer Disease: Sucralfate as Mucosal Protective Agents
In this scenario, mucosal protective agents like sucralfate play an essential role. Sucralfate, a complex of sulfated sucrose and aluminum hydroxide, demonstrates its usefulness in acidic conditions,...
Mucosal Barrier of the Stomach
Within parietal cells, carbonic acid is first formed through the reaction of water and carbon dioxide. The dissociation of carbonic acid releases bicarbonate and hydrogen ions. The bicarbonate...
Gastritis-II: Pathophysiology
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
Gastritis II: Pathophysiology