What is gastric ulcer?
A gastric ulcer, also known as a stomach ulcer, is a type of peptic ulcer that occurs in the lining of the stomach. Peptic ulcers are open sores or lesions that develop in the mucous membrane of the digestive tract, typically in areas exposed to gastric acid and digestive enzymes. Gastric ulcers specifically occur in the stomach, while duodenal ulcers occur in the upper part of the small intestine (duodenum).
Gastric ulcers are commonly caused by an imbalance between the aggressive factors that damage the stomach lining and the protective mechanisms that normally prevent ulcer formation. Aggressive factors include:
- Helicobacter pylori Infection: Infection with the bacterium Helicobacter pylori (H. pylori) is a major cause of gastric ulcers. H. pylori can colonize the stomach lining and produce substances that weaken the protective mucous layer, allowing gastric acid and other digestive juices to damage the underlying stomach tissue.
- Nonsteroidal Anti-Inflammatory Drugs (NSAIDs): Chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin, ibuprofen, and naproxen can irritate and erode the gastric mucosa, leading to the development of gastric ulcers. NSAIDs inhibit the activity of cyclooxygenase (COX) enzymes, which are involved in the synthesis of prostaglandins that help protect the stomach lining.
- Excessive Alcohol Consumption: Chronic alcohol consumption can irritate and inflame the stomach lining, leading to the development of gastric ulcers. Alcohol can increase stomach acid production and impair the function of the mucous layer, making the stomach more susceptible to damage from gastric acid and other irritants.
- Smoking: Cigarette smoking is a risk factor for gastric ulcers as it can impair blood flow to the stomach lining, increase stomach acid production, and weaken the mucous barrier, making the stomach more vulnerable to injury.
- Stress: While acute stress is not a direct cause of gastric ulcers, it can exacerbate existing ulcer symptoms and delay healing by increasing stomach acid production and impairing blood flow to the stomach lining.
What is the relationship between gastric ulcer and oxidative stress?
The relationship between gastric ulcers and oxidative stress involves complex interactions between various factors that contribute to tissue damage, inflammation, and impaired healing in the stomach lining. Here’s how oxidative stress may be related to gastric ulcers:
- Reactive Oxygen Species (ROS) Production: Oxidative stress occurs when there is an imbalance between the production of reactive oxygen species (ROS) and the antioxidant defense mechanisms in the gastric mucosa. ROS, such as superoxide radicals, hydrogen peroxide, and hydroxyl radicals, can be generated during normal cellular metabolism or in response to external factors such as inflammation, infection, or exposure to toxins. Excessive production of ROS in the gastric mucosa can overwhelm antioxidant defenses and lead to oxidative damage to lipids, proteins, and DNA in gastric epithelial cells.
- Inflammation and Immune Response: Oxidative stress can activate inflammatory pathways and stimulate the release of pro-inflammatory cytokines, chemokines, and inflammatory mediators in the gastric mucosa. Chronic inflammation in the stomach lining is a hallmark of gastric ulcers and can exacerbate oxidative stress, disrupt the integrity of the gastric mucosal barrier, and impair tissue repair mechanisms. Inflammatory cells such as neutrophils and macrophages can also produce ROS as part of their antimicrobial defense mechanisms, further contributing to oxidative stress and tissue damage.
- Helicobacter pylori Infection: Infection with the bacterium Helicobacter pylori (H. pylori) is a major risk factor for gastric ulcers and is associated with oxidative stress in the gastric mucosa. H. pylori colonization of the stomach lining can induce oxidative stress through multiple mechanisms, including the production of ROS and reactive nitrogen species (RNS) by inflammatory cells, activation of inflammatory pathways, and disruption of mitochondrial function in gastric epithelial cells. Oxidative stress induced by H. pylori infection can lead to DNA damage, lipid peroxidation, and inflammation, contributing to mucosal injury and the development of gastric ulcers.
- Nonsteroidal Anti-Inflammatory Drugs (NSAIDs): Chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin, ibuprofen, and naproxen is another common cause of gastric ulcers and is associated with oxidative stress in the stomach lining. NSAIDs can impair the function of the gastric mucosal barrier, increase stomach acid production, and promote the generation of ROS, leading to oxidative damage to gastric epithelial cells and increased susceptibility to ulcer formation.
Overall, oxidative stress plays a critical role in the pathogenesis of gastric ulcers by promoting inflammation, disrupting mucosal integrity, impairing tissue repair mechanisms, and increasing susceptibility to injury from external insults such as H. pylori infection or NSAID use.