Gastric Antioxidant, Nitrites, and Mucosal Lipoperoxidation in Chronic Gastritis and Helicobacter pylori Infection

Abstract

We have evaluated gastric juice pH, nitrites and vitamin C levels, mucosal glutathione, and malondialdehyde, a marker of lipid peroxidation, in patients with chronic gastritis undergoing endoscopy. Patients had chronic gastritis with (n = 28) or without (n = 60) atrophy and/or concomitant Helicobacter pylori infection. Nineteen healthy subjects, without major macroscopic or histologic changes, were included as controls. Ten subjects were studied before and after H. pylori eradication. Vitamin C levels were low in atrophic gastritis (p < 0.006) and H. pylori infection (p < 0.02). Nitrite concentrations and pH were significantly higher in atrophy (p < 0.005 and 0.0001). Glutathione turnover was higher than normal in gastritis, with higher levels of oxidized glutathione (p < 0.02). Gastric malondialdehyde levels were significantly increased by gastritis (p < 0.05) and H. pylori infection (p < 0.05). Overall, more active gastritis coincided with lower vitamin C levels and higher malondialdehyde levels. After H. pylori eradication a drop in mucosal MDA levels was observed (p = 0.04). In summary, chronic gastritis and H. pylori infection correlate with increased free-radical production, reduced gastric vitamin C levels, and increased glutathione turnover. The possible implications of these changes in the pathogenesis of gastric damage and in carcinogenesis are intriguing.

Water-Soluble Vitamin Deficiencies in Complicated Peptic Ulcer Patients Soon after Ulcer Onset in Japan

“…Although vitamin C is locally secreted into gastric juices under physiological conditions, hypochlorhydria, a pH exceeding 4, is associated with lower vitamin C levels in gastric juices (22,23). H. pylori infection is known to decrease vitamin C levels in gastric juices (24,25). Thus, a decrease in vitamin C levels in gastric juices may be one of causes of peptic ulcer development.…”

Manganese Superoxide Dismutase Polymorphism and Risk of Gastric Lesions, and Its Effects on Chemoprevention in a Chinese Population

“…pylori infection is the major contributor to the development of gastric cancer and precancerous gastric lesions in Linqu (15,20,38). H. pylori infection-induced chronic inflammation could cause oxidative stress by producing ROS, including O 2 − (22)(23)(24)(25). It has been shown that H. pylorirelated gastritis is accompanied by an increased oxygen free radical formation and peroxidative damage (22,39).…”

“…Because exposure to H. pylori and other risk factors results in an inflammatory reaction and DNA damage of gastric epithelial cells with the generation of ROS (21)(22)(23)(24)(25)(26), and MnSOD is the primary antioxidant enzyme in the mitochondria against ROS, we selected MnSOD as a candidate gene for this study. We investigated the relationship between MnSOD Val 16 Ala polymorphism and the risk of advanced gastric lesions, and the possible interaction between this polymorphism and environmental risk factors.…”

Implications of antioxidant enzymes in human gastric neoplasms

“…All of these may cause point mutations in DNA by base substitution and can accumulate, but 8OHdG is considered to be the main DNA modification produced by ROS (18) and consequently is used as an index of damage to the base sequence of DNA (19). HP-related gastritis is characterized by increased free radical production and peroxidative damage (20).…”