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Gastric mucosal protection and superoxide dismutase
1Department of Internal Medicine, Yamaguchi University School of Medicine, Ube, Japan.
Journal of Clinical Gastroenterology
|January 1, 1988
Summary
Diethyldithiocarbamate and aminotriazole together reduced gastric mucosal SOD activity and blood flow, causing ulcers. Administering superoxide dismutase (SOD) protected against these ulcers, highlighting SOD's role in gastric defense.
Area of Science:
- Biochemistry
- Gastroenterology
- Physiology
Background:
- Gastric mucosal defense involves complex mechanisms.
- Reactive oxygen species (ROS) can damage the gastric lining.
- Superoxide dismutase (SOD) and catalase are key antioxidant enzymes.
Purpose of the Study:
- To investigate the role of SOD and catalase in gastric mucosal defense.
- To determine the involvement of SOD and GMBF in ulcer formation.
Main Methods:
- Administered diethyldithiocarbamate (DDC), a SOD inhibitor, and aminotriazole (AT), a catalase inhibitor, to rats.
- Assessed gastric mucosal SOD activity, gastric mucosal blood flow (GMBF), and ulcer incidence.
- Administered SOD to evaluate its protective effect against induced ulcers.
Main Results:
- DDC or AT alone slightly reduced SOD activity but did not cause ulcers or affect GMBF.
- Combined DDC and AT significantly decreased SOD activity and GMBF, leading to gastric ulcers.
- Exogenous SOD administration attenuated the DDC plus AT-induced gastric ulcers.
Conclusions:
- SOD plays a critical role in protecting the gastric mucosa against active oxygen species.
- Inhibition of both SOD and catalase compromises gastric mucosal defense, leading to ulceration.
- Gastric mucosal blood flow is important in the protective mechanisms against oxidative stress.