State of lipid peroxidation and antioxidant defense in chronic gastritis associated with Helicobacter pylori-infection in middle-aged males

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Helicobacter pylori is the most widespread human pathogen, with prevalence reaching up to 20—40% and 80— 90% of adult infection in developed and developing countries, respectively. Many authors consider this infection as a major factor in the development of gastric cancer. In case of H. pylori infection, free homogeneous oxidation is augmented, that elevates the blood amount of POL products. Hyperproduction of reactive oxygen species stimulates free radical POL, accompanied by membrane destruction, damage to proteins, lipids, and DNA. Thus, the destruction of the intracellular and cell outer membranes occurs resulting in cell death. In diseases associated with H. pylori infection, there is a dysregulation of the lipid peroxidation system — antioxidant defense contributing to inconsistency in the regeneration phases triggering disease progression. The aim of our work was to study indicators of POL (diene conjugates, malonic dialdehyde) and antioxidant protection (AOP) (superoxide dismutase enzymes, catalase) in chronic gastritis and chronic atrophic gastritis associated with H. pylori infection. In patients with CG associated with H. pylori as well as CAG and CAG associated with H. pylori they were featured with increased amount of primary (↑DC) and end TBA-active products of lipid peroxidation (↑MDA), whereas activity of superoxide dismutase was decreased, additionally highlighted with reduced catalase activity (↑CAT) in CAG and CAG associated with H. pylori. H. pylori just triggers the mechanisms of ROS generation in host cells. The energy of redox reactions is used by the microorganism to carry out its physiological functions and serves as a factor in its own pathogenicity, the ROS generated in such reactions can have a damaging effect on the structure of gastric mucosa. In addition, examining H. pylori genome has shown that it bears the genes encoding oxidative metabolism enzymes, such as SOD, catalase, nitroreductase, flavodoxin oxidoreductase. Long-term persistence of H. pylori in the gastric mucosa paralleled with its increased biomass accounts for it being the main source of ROS production able to augment lipid peroxidation and cause damage to the membrane structures and DNA of gastric epithelium cells.

About the authors

O. V. Smirnova

Research Institute of Medical Problems of the North, Federal Research Center KSC SB, RAS; Siberian Federal University

Author for correspondence.

Olga V. Smirnova - PhD, MD (Medicine), Associate Professor, Head of the Laboratory of Clinical Pathophysiology, Research Institute of Medical Problems of the North, FRC KSC SB RAS; Professor of the Department of Medical Biology, SibFU.

660022, Krasnoyarsk, Partizana Zheleznyaka str., 3G, Phone/fax: +7 (913) 567-97-19

Russian Federation

A. A. Sinyakov

Research Institute of Medical Problems of the North, Federal Research Center KSC SB, RAS


PhD (Biology), Researcher, Laboratory of Clinical Pathophysiology, Research Institute of Medical Problems of the North.


Russian Federation

N. M. Titova

Siberian Federal University


Titova N.M., PhD (Biology), Associate Professor, Associate Professor of the Department of Medical Biology.


Russian Federation


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Copyright (c) 2020 Smirnova O.V., Sinyakov A.A., Titova N.M.

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