Association of Adenosine Deaminase, Superoxide Dismutase, and Catalase Activities with Helicobacter pylori | Semantic Scholar (2024)

This study is the first to exhibit the characteristics of high‐SOD activity strains representing multiple bands in zymograms and the correlation between H. pylori SOD activity and gastric cancer.

Serum level of SOD was significantly higher in patients with chronic gastritis infected with H.pylori compared to controls, and significantly higher than in controls with the same underlying cause of infection, Helicobacter pylori.

Serum level of SOD was significantly higher in patients with chronic gastritis infected with H.pylori compared to controls, and significantly higher than in control groups, indicating that other factors involved in the response to oxidative stress are likely to be required for virulence.

Gastric human neoplasms showed significant changes in antioxidant enzymes, that represent the first line in antioxidant protection against radical attack, important in enhancing the understanding of the role that these enzymes play in the promotion/suppression of the carcinogenesis cascade in human gastric mucosa.

The result of this study indicated that gastric cancer patients were characterized by increased protein oxidation, whereas there was no significant difference in oxidative stress parameters and antioxidant enzyme activity between the Anti-HP IgG positive and negative gastric cancers patients.

SOD1-7958A and SOD2-16Ala/-genotypes increase the risk of gastric cancer in Chinese Han population, and there were additive interactions between the two genotypes and the other three risk factors.

This result supports a previous study indicating that adenosine deaminase is involved in the regulatory system of chronic atrophic gastritis and gastric cancer risk and supports the idea that gastric atrophy caused by Helicobacter pylori infection is a risk factor for Gastric cancer.

There is paucity of studies regarding this issue in the paediatric population, and reactive species (oxygen or nitrogen) are considered factors that influence gastro duodenal mucosal changes in H.pylori-infected patients.

Serum ADA activity was significantly higher in patients with cutaneous anthrax than in the controls and a positive correlation was observed between ADA activity and lymphocyte counts.

Investigation of prolidase, adenosine deaminase, glutathione s-transferase and glutathion reductase activities in patients with abortus imminens finds no evidence of blockages in these enzymes.

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In chronic antral gastritis there was a positive relationship between the SOD activity and both the severity and activity of inflammation and it is presumed that HP-associated gastritis is predominant in the antrum.

There were noticeable intra and inter-correlations, which indicated possible relations between DNA and free radical metabolizing enzymes in gastric juices of patients with gastric cancer, ulcer, gastritis and from healthy subjects.

It is demonstrated that H. pylori induces enhanced production of ROS in GC, and enhances membrane damage, and the dose-dependent protective abilities of selected ROS scavengers on LDH leakage were determined.

This study demonstrates that H. pylori induces enhanced production of ROS and DNA damage in association with human gastric mucosal cells and that the 87-kDa cytotoxin protein plays a prime role in the induction of oxidative stress andDNA damage.

It was found that in the subjects with normal or increased gastric acid secretion, ADA activities were higher in specimens taken from the gastric fundus than in slices coming from the antral region, and a positive correlation between ADA activity and basal or maximal acid output values was found.

In five of the nine cases reported with low ADA activity values, a second determination a few days later evidenced a rise in the ADA activity over 43 U·/'1 to values well within the range of tuberculous effusion, however, among the largest series of ADA and tuberculosis no cases with a value of ADA activity <43 U-/·1 were described.

The critical mutations in the iceA1 gene in some isolates from patients with peptic ulcers suggested that IceA does not participate in the pathogenesis ofpeptic ulcer in Japan, and showed that iceA 1 sequence variations may be useful tools for analysis of the population genetics of H. pylori.

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