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

2020 ◽  
Vol 10 (4) ◽  
pp. 741-746
Author(s):  
O. V. Smirnova ◽  
A. A. Sinyakov ◽  
N. M. Titova
Keyword(s):  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Chronic Gastritis ◽  
Antioxidant Defense ◽  
Host Cells ◽  
Gastric Epithelium ◽  
Metabolism Enzymes ◽  
H Pylori

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.

scholarly journals Helicobacter pylori Outer Membrane Vesicles and Extracellular Vesicles from Helicobacter pylori-Infected Cells in Gastric Disease Development

2021 ◽  
Vol 22 (9) ◽  
pp. 4823
Author(s):  
María Fernanda González ◽  
Paula Díaz ◽  
Alejandra Sandoval-Bórquez ◽  
Daniela Herrera ◽  
Andrew F. G. Quest
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Outer Membrane ◽  
Extracellular Vesicles ◽  
Membrane Vesicles ◽  
Outer Membrane Vesicles ◽  
Host Cells ◽  
Gastric Epithelium ◽  
Infected Cells ◽  
H Pylori

Extracellular vesicles (EVs) are cell-derived vesicles important in intercellular communication that play an essential role in host-pathogen interactions, spreading pathogen-derived as well as host-derived molecules during infection. Pathogens can induce changes in the composition of EVs derived from the infected cells and use them to manipulate their microenvironment and, for instance, modulate innate and adaptive inflammatory immune responses, both in a stimulatory or suppressive manner. Gastric cancer is one of the leading causes of cancer-related deaths worldwide and infection with Helicobacter pylori (H. pylori) is considered the main risk factor for developing this disease, which is characterized by a strong inflammatory component. EVs released by host cells infected with H. pylori contribute significantly to inflammation, and in doing so promote the development of disease. Additionally, H. pylori liberates vesicles, called outer membrane vesicles (H. pylori-OMVs), which contribute to atrophia and cell transformation in the gastric epithelium. In this review, the participation of both EVs from cells infected with H. pylori and H. pylori-OMVs associated with the development of gastric cancer will be discussed. By deciphering which functions of these external vesicles during H. pylori infection benefit the host or the pathogen, novel treatment strategies may become available to prevent disease.

scholarly journals Chronic gastritis and Helicobacter pylori in digestive form of Chagas' disease

1993 ◽  
Vol 35 (2) ◽  
pp. 117-121 ◽  
Author(s):  
A. J. A. Barbosa ◽  
D. M. M. Queiroz ◽  
A. M. M. F. Nogueira ◽  
M. J. A. Roquette Reis ◽  
E. N. Mendes ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Atrophic Gastritis ◽  
Chagas Disease ◽  
Chronic Gastritis ◽  
Antral Mucosa ◽  
Common Cause ◽  
Superficial Gastritis ◽  
H Pylori ◽  
Inflammatory Changes

Patients with the digestive form of Chagas'disease frequently present chronic gastritis. As the microorganism Helicobacter pylori is now accepted as the most common cause of human chronic gastritis, the present work was undertaken to verify a possible relationship between the presence of this bacterium and inflammatory changes of antral mucosa in chagasic patients. Seventeen chagasics, with megaesophagus and or megacolon were studied. Fragments from two different regions of antral mucosa were obtained by endoscopy, fixed in 4% neutral formaldehyde and embedded in paraffin. The sections were stained by haematoxylin and eosin for histology analysis, and by carbolfuchsin for H. pylori identification. H. pylori was found in 16 (94.1%) chagasic patients, all of them presenting chronic gastritis. Superficial gastritis was seen in 9 (52.9%) while atrophic gastritis was present in 8 (47.1%) patients. H. pylori was present on gastric mucosa of 8 (100%) patients with atrophic gastritis and of 8 (88.8%) patients with superficial gastritis. We concluded that the microorganism H. pylori should be considered a possible factor connected with the etiopathogenesis of chronic superficial and atrophic gastritis frequently observed in patients with the digestive form of Chagas' disease.

Expression of Cytokeratins 7 and 20 in Helicobacter pylori-associated Chronic Gastritis in Children

2004 ◽  
Vol 7 (2) ◽  
pp. 180-186 ◽  
Author(s):  
M. Cohen ◽  
E. Cueto Rúa ◽  
N. Balcarce ◽  
R. Drut
Keyword(s):  
Helicobacter Pylori ◽  
Chronic Gastritis ◽  
Structural Changes ◽  
Periodic Acid ◽  
Gastric Epithelium ◽  
Surface Epithelium ◽  
Ki 67 ◽  
Periodic Acid Schiff ◽  
Group A ◽  
H Pylori

Helicobacter pylori gastric infection induces structural changes in the gastric epithelium. Among them, variations in the expression of cytokeratins have been reported in adult patients. In the present study, we describe the expression of CK7 and CK20 in gastric samples taken from the antrum in three groups of pediatric patients: (A) Helicobacter pylori-associated chronic gastritis (mean age: 11.4 years); (B) previous H. pylori chronic gastritis patients (mean age: 9.4 years); and (C) controls (mean age: 8.8 years). In all, the presence of sulfomucins was assessed with Alcian blue-periodic acid-Schiff pH 1.0. Immunoreactivity was graded as absent (0), weak (1 +), moderate (2+), or intense (3+), in accordance with the intensity of the staining, and its distribution as focal or diffuse. CK7 reactivity was 2 + either focal or diffuse in all group A biopsies. The reactivity was more evident in the cells at the neck of the glands, in the areas with more inflammatory infiltrates, decorating long vertical segments of epithelium. In groups B and C, CK7 reactivity was also focal and 1 + at the cells of the necks of the glands. However, group B presented longer vertical segments of positive cells as compared to group C, and shorter than those of group A. The deeper glandular structures were focally 1 + in both groups. CK20 expression was comparable in all three groups, depicting a 2+ diffuse reactivity at the surface epithelium and interposed pits with absence or focal reactivity at the neck and coiled gland areas. Ki-67 immunostaining paralleled that of the CK7. Staining for sulfated mucosubstances was positive in two of five cases of groups A and B, and in none of the cases of group C. We conclude that: (1) the long segments of CK7-positive glandular necks in H. pylori cases most probably indicate intense regenerative activity during active inflammation; (2) eradication of H. pylori does not warrant ad integrum restitution since long segments of Ki-67+, CK7+ cells at the germinative compartment of the glands (as well as cells with sulfomucins) were still recognizable in ex- H. pylori patients; (3) finally, differing from what happens in adults, children somehow manage to maintain fully differentiated CK20+ superficial epithelium while the H. pylori is in action.

scholarly journals Mechanisms of interacting Helicobacter pylori with gastric mucosal epithelium. II. A reaction of gastric epithelium on Helicobacter pylori colonization and persistence

2019 ◽  
Vol 9 (2) ◽  
pp. 253-261
Author(s):  
O. K. Pozdeev ◽  
A. O. Pozdeeva ◽  
Yu. V. Valeeva ◽  
P. E. Gulyaev ◽  
A. N. Savinova
Keyword(s):  
Helicobacter Pylori ◽  
T Cell ◽  
Epithelial Cell ◽  
Gastric Mucosa ◽  
Mapk Pathway ◽  
Bacterial Colonization ◽  
Gastric Epithelium ◽  
T Cell Subsets ◽  
H Pylori ◽  
Apoptotic Factors

Gastric and duodenal recurrent inflammatory diseases have a high prevalence, but the role played by microbes in its development remained unclear. However, the data published in 1983 by Marshall and Warren about isolatingHelicobacter pylorifrom the stomach mucosa of the patient with gastritis and proposing relevant cultivation methods was the turning point in investigating etiology of the upper digestive tract inflammatory disorders. Moreover, it was shown that the majority ofH. pylorispp. are found within the gastric lumen upon colonization, whereas around 20% of them are attached to the epithelial cells in the stomach. In addition, effects of interacting H. pylori with gastric epithelium and activation of some defense mechanisms due to bacterial colonization and spreading were analyzed. It was found that along with triggering pro-inflammatory response induced by proteins VacA as well as phosphorylated/unphosphorylated CagA, wherein the latter is able to induce a set of protective reactionsH. pyloridisrupts intercellular contacts, affects epithelial cell polarity and proliferation, and activates SHP-2 phosphatase resulting in emerging diverse types of cellular responses. The activation mechanisms for the mitogen-activated protein kinase (MAPK) pathway were discussed. The ability ofH. pylorito regulate apoptosis, particularly via its suppression, by expressing ERK kinase and protein MCL1 facilitating bacterial survival in the gastric mucosa as well as beneficial effects related to bacterial circulation on gastric epithelial cell survival elicited by anti-apoptotic factors were also examined. Of note, persistence of H. pylori are mainly determined by activating transcriptional factors including NF-κB, NFAT, SRF, T-cell lymphoid enhancing factor (TCF/LEF), regulating activity of MCL1 protein, in turn, being one of the main anti-apoptotic factors, as well as induced production of the migration inhibitory factor (MIF). The role of VacA cytotoxin in triggering epithelial cell apoptosis via caspase-mediated pathways was also considered. Infection withH. pyloriis accompanied by release of proinflammatory cytokine cocktail detected bothin vitroandin vivo. In particular, bacterial urease activating transcriptional factor NF-κB was shown to play a crucial role in inducing cytokine production. Moreover, such signaling pathways may be activated afterH. pyloriis attached to the cognate receptor in the gastric epithelial surface by interacting with CD74 and MHC class II molecules. Finally, a role for various CD4+T cell subsets, particularly type 17 T helper cells (Th17) in inducing immune response against H. pylori antigens in gastric mucosa was revealed were also discussed. 

Intrafamilial Infection of Helicobacter Pylori: Abnormal Gastric Epithelial Cells, Pedestal-Rich H. Pylori Adherence, and a Gene Mutation in a Child with Protein-Losing Gastroenteropathy

2019 ◽  
Vol 2 (3) ◽  
pp. 83-99
Author(s):  
T.W. Wan ◽  
O. Khokhlova ◽  
W. Higuchi ◽  
I. Protasova ◽  
Olga V. Peryanova ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Epithelial Cells ◽  
Gene Mutation ◽  
Virulence Factor ◽  
East Asian ◽  
Gastric Epithelium ◽  
Gastric Epithelial Cells ◽  
H Pylori

Abstract Helicobacter pylori, one of the most prevalent human pathogens, colonizes the gastric mucosa and is associated with gastric diseases, such as gastritis and peptic ulcers, and is also a bacterial risk factor for gastric cancer. Cytotoxin-associated gene A (CagA) protein, a major virulence factor of H. pylori, is phosphorylated in cells at its Glu-Pro-IIe-Tyr-Ala (EPIYA) motif and is considered to trigger gastric cancer. CagA is classified into two forms, Western CagA with EPIYA-ABC and East Asian CagA with EPIYA-ABD, with the latter associated with a high risk of developing gastric cancer. CagA causes morphological transformation of cells, yielding the “hummingbird” phenotype in AGS cells and possibly membranous pedestals in the gastric epithelium, albeit rarely. H. pylori adherence to the gastric mucosa is not yet fully understood. Here, we describe an intrafamilial infection case of H. pylori, focusing on the gastric epithelium, H. pylori adherence, and a gene mutation in a child with protein-losing gastroenteropathy (characterized by excessive loss of plasma proteins into the gastrointestinal tract). H. pylori, which also infected family members (mother and father), was genetically a single clone with the virulence genes of an East Asian type. The patient’ gastric mucosa exhibited some unique features. Endoscopy revealed the presence of protein plugs on the mucosal surface, which were immunoelectrophoretically similar to serum proteins. Electron microscopy revealed abnormal gastric epithelial cells, totally covered with the secretions or possessing small swollen structures and irregular microvilli. The patient’s H. pylori infection was characterized by frequently occurring thick pedestals, formed along adherent H. pylori. The serum protein level returned to normal and the protein plugs disappeared after the successful eradication of H. pylori, albeit with lag periods for healing. He had a mutation in the OCRL1 gene, associated with Dent disease (asymptomatic proteinuria). Thus, in the patient’s gastric mucosa, we found the abnormal gastric epithelial cells, which may be caused by an OCRL1 mutation or H. pylori, and pedestal-rich H. pylori infection, possibly caused by a higher level of action of CagA in the abnormal epithelial cells. The data suggests a novel H. pylori virulence factor associated with “excessive plasma protein release”.

scholarly journals Influence of duodenogastric reflux in the gastric mucosa histological changes of rats infected with Helicobacter pylori

2016 ◽  
Vol 43 (4) ◽  
pp. 235-242 ◽  
Author(s):  
JOSÉ CARLOS RIBEIRO DE ARAUJO ◽  
JORGE JOSÉ DE CARVALHO ◽  
HUMBERTO OLIVEIRA SERRA
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Chronic Gastritis ◽  
Partial Gastrectomy ◽  
Duodenogastric Reflux ◽  
Histological Changes ◽  
Positive Correlation ◽  
Male Wistar Rats ◽  
H Pylori ◽  
The One

ABSTRACT Objective: to evaluate the influence of Duodenal reflux in histological changes of the gastric mucosa of rats infected with Helicobacter pylori submitted to pyloroplasty. Methods: after two weeks of acclimation, we infected 30 male Wistar rats with Helicobacter pylori. We randomly divided them into three groups: one submitted to pyloroplasty, another to partial gastrectomy and the third, only infected, was not operated. After six months of surgery, euthanasia was carried out. Gastric fragments were studied by light microscopy to count the number of H. pylori, and to observe the histological changes (gastritis, metaplasia, dysplasia and neoplasia). We confirmed these changes by immunohistochemistry using the molecular markers PCNA and TGF-beta. Results: the animals submitted to pyloroplasty had higher percentage of colonization by H. pylori (median=58.5; gastrectomy=16.5; control=14.5). There was a positive correlation between the amount of H. pylori and the occurrence of chronic gastritis present in the antral fragments. Neoplasia occurred in 40% of rats from the group submitted to pyloroplasty. The staining with PCNA and TGF-ß confirmed the histopathological changes visualized by optical microscopy. Conclusions: the antral region was the one with the highest concentration of H. pylori, regardless of the group. There was a positive correlation between the appearance of benign disorders (chronic gastritis, metaplasia, dysplasia) and cancer in mice infected with H. pylori submitted to pyloroplasty.

scholarly journals Eradication of Helicobacter pylori Infection Restores ki67, p53, and Cyclin D1 Immunoreactivity in the Human Gastric Epithelium

2016 ◽  
Vol 9 ◽  
pp. CGast.S38330 ◽  
Author(s):  
Konstantinos Triantafyllou ◽  
Vasilios Papadopoulos ◽  
Theodoras Emanouil ◽  
Paraskevas Gkolfakis ◽  
Vasileia Damaskou ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Cyclin D1 ◽  
Chronic Gastritis ◽  
Helicobacter Pylori Infection ◽  
Gastric Epithelium ◽  
Ki67 Expression ◽  
P53 Immunoreactivity ◽  
Infection Eradication

Introduction We evaluated the effect of Helicobacter pylori (HP) eradication on p53, cyclin D1 expression, and cell proliferation in gastric mucosa. Materials and Methods We assessed p53, cyclin D1, and ki67 immunoexpression in gastric mucosa from 31 HP chronic gastritis patients and 12 controls. Reassessment was performed 6 months after successful HP eradication. Results Successful eradication resulted in significant decrease of p53 (1.53 ± 0.16 vs 0.83 ± 0.19, P = 0.01) and ki67 (9.84 ± 0.96 vs 4.77 ± 0.27, P < 0.001) staining in the antrum. Similarly, p53 immunoreactivity significantly decreased in the corpus (1.27 ± 0.20 vs 0.46 ± 0.15, P = 0.02), while there was a trend for decreased corpus cyclin D1 and ki67 expression (0.17 ± 0.07 vs 0.0, P = 0.08 and 8.71 ± 1.24 vs 5.85 ± 0.54, P = 0.09, respectively). Importantly, after successful HP eradication, the immunoreactivity of the studied parameters was similar to that of controls. Conclusion Successful HP infection eradication restores p53, cyclin D1, and ki67 immunoreactivity in the gastric mucosa to the level of controls.

scholarly journals Changes in Serum Levels of Growth Factors in Chronic Gastritis

2019 ◽  
Vol 23 (3) ◽  
pp. 250-256
Author(s):  
L. V. Matveeva ◽  
L. M. Mosina ◽  
M. A. Stenina
Keyword(s):  
Helicobacter Pylori ◽  
Growth Factors ◽  
Gastric Mucosa ◽  
Chronic Gastritis ◽  
Venous Blood ◽  
Serum Levels ◽  
Diagnostic Value ◽  
Gastric Epithelium ◽  
Macrophage Colony ◽  
Endothelial Growth Factor

Chronic inflammation, contributing to atrophy of the gastric epithelium, can develop in the induction of Helicobacter pylori and other microorganisms secretion of cytokines by cells of the gastric mucosa, including growth factors. Violation of the processes of repair of the gastric mucosa in terms of immune and microbiotic imbalance is the basis of ulcer and carcinogenesis. The aim of the study was to determine the serum level and diagnostic value of growth factors in exacerbation of chronic gastritis. Materials and methods . With informed consent in 122 patients with exacerbation of chronic gastritis and 40 healthy volunteers, sampling of gastrobioptates with esophagogastroduodenoscopy (for histological and microbiological examination), 5 ml of venous blood with serum separation (for enzyme immunoassay of serum levels of growth factors) was performed. Results . The amount of granulocyte-macrophage colony stimulating factor, erythropoietin, vascular endothelial growth factor (VEGF) in the serum of patients with atrophic gastritis exceeded the values of healthy individuals, were directly related to the degree and stage of gastritis, Helicobacter pylori infection, and among themselves. The greatest diagnostic value in atrophy gastric epithelial was determined in VEGF (sensitivity - 95,9%, specificity - 48,98%, criterion more 225 pg/ml, AUC 0,654, p = 0,0072). Conclusion. Determination of serum growth factors, especially VEGF, with exacerbation of chronic gastritis is diagnostically valuable, should be used for early diagnosis of atrophy of the gastric epithelium.

scholarly journals Evaluation of the lipid peroxidation reactions activity in middle-aged men with chronic gastritis on the background of H. pylori infection

2019 ◽  
Vol 74 (3) ◽  
pp. 149-156
Author(s):  
Marina A. Darenskaya ◽  
Olga V. Smirnova ◽  
Edward V. Kasparov ◽  
Lyudmila A. Grebenkina ◽  
Aleksandr A. Sinyakov ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Atrophic Gastritis ◽  
Chronic Gastritis ◽  
Antioxidant Defense ◽  
Chronic Atrophic Gastritis ◽  
Stress Reactions ◽  
Middle Aged ◽  
Glutathione S Transferase ◽  
Group 2 ◽  
H Pylori

Background: There is not enough information about the course of the processes of lipid peroxidation-antioxidant defense in middle-aged men who are at risk of developing gastric cancer on the Correa cascade. Aims: To analyze of the processes of lipid peroxidation activity and antioxidant defense in men with chronic gastritis and chronic atrophic gastritis in combination with and without the presence of Helicobacter pylori. Materials and methods: 173 middle-aged men with an established diagnosis of chronic gastritis were examined, which were divided into 4 groups: group 1 ― patients with chronic gastritis without H. pylori (n=58), group 2 ― patients with chronic gastritis in combination with H. pylori (n=61), group 3 ― patients with chronic atrophic gastritis without H. pylori (n=28), group 4 ― patients with chronic atrophic gastritis in combination with H. pylori (n=26). Evaluation of the content of parameters of the lipid peroxidation system and the antioxidant components activity using spectrophotometric research methods was carried out. For statistical analysis, the software package Statistica 7.0 (Stat Soft, USA) was used. The study was conducted during 20132015. Results: Infection H. pylori with chronic and chronic atrophic gastritis accompanied by significant changes in the system of lipid peroxidation, and antioxidant defense components in the form of primary and accumulation of end products, insufficient activity of antioxidant enzymes ― superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase and reducing content of reduced glutathione. The use of an integrating factor to assess the severity of prooxidant activity confirms the development of antioxidant deficiency in patients of these groups. Conclusions: In patients with chronic and chronic atrophic gastritis, combined with H. Pylori infection, a more pronounced progression of oxidative stress reactions and a significant lack of antioxidant factors were found in comparison with patients with these forms of gastritis without H. pylori.

scholarly journals A COMPLEX DIAGNOSTICS OF EARLY GASTRIC CANCER ASSOCIATED WITH HELICOBACTER PYLORI INFECTION IN THE ADULT POPULATION OF THE KRASNOYARSK TERRITORY

2021 ◽  
Author(s):  
O. V. Smirnova ◽  
V. V. Tsukanov ◽  
A. A. Sinyakov ◽  
O. L. Moskalenko ◽  
N. G. Elmanova ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Helicobacter Pylori ◽  
Early Gastric Cancer ◽  
Glutathione Peroxidase ◽  
Atrophic Gastritis ◽  
Antioxidant Defense ◽  
Adult Population ◽  
Chronic Atrophic Gastritis

The aim of our study was to evaluate the clinical-anamnestic, serological, immunological and biochemical tests used for early diagnostics of gastric cancer associated with Helicobacter pylori infection in the adult population of the Krasnoyarsk Territory.Materials and methods: The control group consisted of 104 apparently healthy blood donors, the comparison group – 97 patients with chronic atrophic gastritis as well as a group of patients with early gastric cancer comprising 98 subjects. Assessment of monocyte and neutrophil spontaneous and induced chemiluminescence (CL) was carried out on a 36-channel biochemiluminometer "BLM - 3607". Phagocytosis was measured by using a Beckman Coulter FC 500 flow cytometer. A Varyan Cary Eclipse spectrofluorometer was used to study lipid peroxidation and factors of the antioxidant defense system.Results and discussion: While studying the phagocytic arm of immunity, it was found that all patients with early gastric cancer were reported to have parameters of the maximum intensity for neutrophil spontaneous CL from 17831 c.u. and lower, whereas induced CL reached at least 30,000 c.u.. Phagocytic activity of neutrophilic granulocytes in patients with early gastric cancer was 36% or less. While studying the indicators of monocytes, it was found that spontaneous and induced CL decreased from 454 c.u. and 1186 c.u., respectively, in the patients with early gastric cancer. Monocytic activity in early gastric cancer was 34% or less. In the study of lipid peroxidation, an antioxidant defense in patients with chronic atrophic gastritis and gastric cancer had increased malondialdehyde (MDA) level. Patients with gastric cancer had decreased activity of the enzyme catalase (CAT), whereas subjects with chronic atrophic gastritis had reduced glutathione peroxidase (GPO) level. In contrast, patients with early gastric cancer were featured with increased GPO activity. We have proposed coefficients for assessing the factors of the AOD system in patients: the ratio for superoxide dismutase to catalase activity (SOD / CAT) as well as the ratio for superoxide dismutase to glutathione peroxidase activity (SOD / GPO).Conclusion: During the study, threshold values of parameters were obtained for assigning groups at high risk of developing early gastric cancer, which can be used for screening in adult population.

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