What is gastritis?
Gastritis is a medical term used to describe inflammation of the lining of the stomach. This inflammation can be acute, meaning it occurs suddenly and is usually short-lived, or chronic, indicating a persistent or recurrent condition.
What is the relationship between gastritis and oxidative stress?
The relationship between gastritis and oxidative stress involves a complex interplay of inflammatory processes, cellular damage, and antioxidant defense mechanisms within the stomach lining. Oxidative stress refers to an imbalance between the production of reactive oxygen species (ROS) and the body’s antioxidant defenses, leading to cellular damage and dysfunction. Several factors contribute to oxidative stress in gastritis:
- Inflammation: Gastritis is characterized by inflammation of the gastric mucosa, which can be triggered by various factors such as Helicobacter pylori infection, NSAID use, alcohol consumption, or autoimmune disorders. Inflammatory cells, including neutrophils, macrophages, and lymphocytes, produce ROS as part of the immune response to eliminate pathogens and damaged cells. Chronic inflammation in gastritis leads to sustained ROS production, contributing to oxidative stress and tissue damage in the stomach lining.
- Helicobacter pylori infection: H. pylori is a common bacterial pathogen associated with gastritis and peptic ulcers. The bacterium colonizes the gastric mucosa and induces inflammation through various mechanisms, including the release of pro-inflammatory cytokines, activation of immune cells, and disruption of gastric epithelial barrier function. H. pylori infection leads to increased ROS production and oxidative stress in the gastric mucosa, contributing to tissue damage and progression of gastritis.
- NSAID-induced injury: Nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin, ibuprofen, and naproxen are known to cause gastritis and peptic ulcers by inhibiting cyclooxygenase enzymes and reducing prostaglandin synthesis. NSAIDs also promote oxidative stress by disrupting mitochondrial function, inhibiting antioxidant enzymes, and increasing ROS production in gastric epithelial cells. Chronic NSAID use leads to sustained oxidative stress and mucosal damage, exacerbating gastritis and increasing the risk of complications such as gastrointestinal bleeding.
- Alcohol consumption: Excessive alcohol consumption can irritate the gastric mucosa and promote inflammation, leading to gastritis and mucosal injury. Alcohol metabolism generates ROS and reactive aldehydes, which induce oxidative stress and lipid peroxidation in gastric epithelial cells. Chronic alcohol consumption also impairs antioxidant defense mechanisms, further exacerbating oxidative stress and tissue damage in the stomach lining.
- Antioxidant defense mechanisms: The gastric mucosa is equipped with antioxidant defense mechanisms to counteract oxidative stress and protect against cellular damage. Antioxidant enzymes such as superoxide dismutase (SOD), catalase, and glutathione peroxidase neutralize ROS and prevent oxidative damage to gastric epithelial cells. However, under conditions of chronic inflammation or excessive ROS production, antioxidant defenses may become overwhelmed, leading to sustained oxidative stress and tissue injury in gastritis.
Overall, oxidative stress plays a significant role in the pathogenesis and progression of gastritis by promoting inflammation, mucosal damage, and impairment of antioxidant defense mechanisms within the stomach lining.