Oxidative Stress In Helicobacter pylori-Assocaited Gastroduodenal Disease

Abstract

Summary Helicobacter pylori (H. pylori) is a spiral-shaped, Gram-negative rod, which induces the infiltration to the gastric mucosa by neutrophils, macrophages, and T and B lymphocytes; however, this immune and inflammatory response cannot completely clear the bacterial infection, and leaves the host prone to complications resulting from persistent inflammation. Resultantly, H. pylori infection causes chronic inflammation, accumulation of reactive oxygen species, and oxidative DNA damage in the gastric mucosa. Recent studies reveal that H. pylori injects bacterial proteins into the cytosol of the gastric host cell via the type IV injection system and regulates the intracellular signal transduction [1,2]. This mechanism provides a novel means of resolving how H. pylori survives in the acidic environment of the human stomach. During persistent gastric infections, chronic gastritis may remain asymptomatic or may evolve into more severe diseases, such as peptic ulcer disease or atrophic gastritis. In addition, infection with H. pylori increases the risk of developing gastric cancer and mucosa-associated lymphoid tissue lymphoma. Various gastric diseases, such as gastritis, ulcers, intestinal metaplasia, and gastric cancer, can be appropriately developed by inoculating this bacteria into Mongolian gerbils [3]. In addition, the successful eradication of H. pylori is useful as a preventive approach against gastric cancer [4]. This review focuses on the aspects of the oxidative mechanism in the H. pylori-associated gastric mucosal lesion formation.

Reactive oxygen species-quenching and anti-apoptotic effect of polaprezinc on indomethacin-induced small intestinal epithelial cell injury

“…8) and inhibited apoptosis (Fig. 6) in RIE-1 cells, it seems that the initial ROS production may have affected intracellular protein function, resulting in the indomethacin-induced This hypochlorous anion reacts with ammonia, derived from urea by H. pylori-associated urease, and yields a cytotoxic oxidant, monochloramine (NH 2 Cl), whose lipophilic properties allow it to freely penetrate biological membranes to oxidize intracellular components [29,30]. By contrast, the source of NSAID-induced ROS production is considered to be the mucosal epithelium.…”

NMR‐Based Metabonomics for Detection of Helicobacter pylori Infection in Gerbils: Which Is More Descriptive

“…The increment in the cis -aconitate level results from the activation of enzyme aconitase, which catalyzes the conversion of citrate to cis -aconitate, and of cis -aconitate to isocitrate. It is reported that H. pylori infection causes accumulation of reactive oxygen species (ROS) in the gastric mucosa [17], and intensification of ROS reduces in turn the activity of aconitase in rat liver [18]. These results imply a modulated energy metabolism in response to oxidative stress in infected mice, which partly explains the elevated glucose.…”

The Influence of Helicobacter pylori Eradication on Leptin, Soluble CD40 Ligand, Oxidative Stress and Body Composition in Patients with Peptic Ulcer Disease

“…, and oxidative DNA damage in gastric mucosa in animal and human models (8)(9)(10)(11)(12). ROS production of the blood samples from H. pylori infected subjects was significantly decreased 2 months after eradication (13).…”