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Updated: Apr 7, 2026
Analyzing Oxidative Stress in Murine Intestinal Organoids using Reactive Oxygen Species-Sensitive Fluorogenic Probe
Published on: September 17, 2021
[The relationship between acute gastric mucosal lesions (AGML) and oxidative stress from gastric acid]
Abstract:
Acute gastric mucosal lesions (AGML) are primary gastrointestinal affection and many people suffer from this disease. Although there are several causes in this disease, reactive oxygen species from mitochondria (mitROS) would like to be related deeply. Surprisingly, not only non-steroidal anti-inflammatory drugs (NSAIDs) but also gastric acid with moderate pH induces mitROS, and resulted in inducing cellular apoptosis. In addition, previous our study showed manganese superoxide dismutase (MnSOD) overexpressed gastric mucosal cells, which scavenge mitROS specifically, suppressed generating lipid peroxidation attributed from mitROS and cellular death. Therefore, mitROS from NSAIDs and gastric acid are likely to cause AGML, and control of mitROS suppresses AGML and other gastrointestinal disease.
Insights
Reactive oxygen species from mitochondria (mitROS) cause acute gastric mucosal lesions (AGML) via NSAIDs and gastric acid. Controlling mitROS effectively suppresses AGML and other gastrointestinal diseases.
Area of Science:
- Gastroenterology
- Mitochondrial Biology
- Cellular Physiology
Background:
- Acute gastric mucosal lesions (AGML) are common gastrointestinal issues.
- Mitochondrial reactive oxygen species (mitROS) are implicated in AGML pathogenesis.
- Both NSAIDs and gastric acid contribute to mitROS production.
Purpose of the Study:
- To investigate the role of mitROS in AGML development.
- To explore the potential of controlling mitROS for treating AGML.
Main Methods:
- Investigated the effects of NSAIDs and gastric acid on mitROS production.
- Examined cellular apoptosis induced by mitROS.
- Assessed the protective effects of manganese superoxide dismutase (MnSOD) overexpression.
Main Results:
- NSAIDs and gastric acid induce mitROS, leading to cellular apoptosis.
- Overexpression of MnSOD, which scavenges mitROS, suppressed lipid peroxidation and cell death.
- mitROS are a key factor in NSAID- and acid-induced AGML.
Conclusions:
- mitROS play a critical role in the pathogenesis of AGML.
- Targeting mitROS presents a promising therapeutic strategy for AGML and other gastrointestinal diseases.
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