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Primary research
Javad Sharifi-Rad
Shahid Beheshti University of Medical Sciences School of Medicine
Corresponding Author
ORCiD: https://orcid.org/0000-0002-7301-8151
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: Gastritis is a superficial and prevalent inflammatory lesion that is considered a public health concernoncecause gastric ulcers and gastric cancer, especially due to Helicobacter pylori infection. Proton pump inhibitors, such as omeprazole, are the most widely used drugs in order to treat this illness. The aim of the study was evaluating the cytogenetic effects of omeprazole in stomach epithelial cells of patients with gastritis in presence and absence of H. pylori, using to this the application of cytogenetic biomarkers and measurements of catalse and superoxide dismutase.
Methods: The study included 152 patients from the Gastroenterology Outpatient Clinic of Hospital Getúlio Vargas, Teresina - PI, that reported the continuous and prolonged use of omeprazole in doses of 20, 30 and 40 mg/kg. The participants were divided into groups: (1) patients without gastritis (n = 32); (2) patients without gastritis but with use of OME (n = 24); (3) patients with gastritis (n = 26); (4) patients with gastritis undergoing OME therapy (n = 26); (5) patients with gastritis and H. pylori (n = 22) and (6) patients with gastritis and H. pylori on OME therapy (n = 22).
Results: OME induces cytogenetic risks in the epithelium of the stomach due to the formation of micronuclei (group 6> 1,2,3,4,5; group 5> 1,2,3; group 4> 1,2,3); bridges (groups 4 and 6> 1,2,3,5 and group 2> 3,5); buds (groups 2,4,6>, 1,3,5); binucleated cells (group 6> 1,2,3,4,5; group 4> 1,2,3); groups 2 and 3> 1); picnoses (group 6> 1,2,3,4,5), groups 2 and 5> 1,3; group 4> 1,2,3,5); cariorrexis (groups 6 and 4> 1,2,3,5; groups 2,3,5> 1) and karyolysis (groups 2,4, and 6> 1,3,5; groups 3 and 5> 1). These data show that omeprazole induces cytogenetic risks, especially due to infection with H. pylori, thus indicating the clastogenic and/or aneugenic effects, chromosomes changing, gene expression, cytotoxicity and apoptosis.
Conclusions: These risks can be attributed to several mechanisms that are still unclear, including oxidative damage, as observed by increases in catalase and superoxide dismutase. Positive correlations between these antioxidant enzymes were obtained with the formation of micronuclei, and negative for picnoses. Thus, the continuous and prolonged use of omeprazole induces genetic instability, which can be monitored, in cytogenetic analyzes, as anticipation for cancer, especially gastric.
Keywords
Citogenetic biomarkers, oxidative stress, apoptosis, genetic instability
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CURRENT STATUS: Under Review
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Posted 02 Nov, 2021
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Review #1 received
Received 16 Nov, 2021
Reviewer #3 agreed
On 11 Nov, 2021
Reviewer #4 agreed
On 11 Nov, 2021
Reviewer #2 agreed
On 11 Nov, 2021
Reviews received
Received 11 Nov, 2021
Reviewer #1 agreed
On 10 Nov, 2021
Reviewers invited
Invitations sent on 09 Nov, 2021
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On 29 Oct, 2021
Submission checks complete
On 28 Oct, 2021
Editor invited
On 28 Oct, 2021
First submitted
On 23 Oct, 2021
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Subject Areas
Cancer Biology
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This preprint is under consideration at Cancer Cell International. A preprint is a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Primary research
Javad Sharifi-Rad
Shahid Beheshti University of Medical Sciences School of Medicine
Corresponding Author
ORCiD: https://orcid.org/0000-0002-7301-8151
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Under Review
Version 1
Posted 02 Nov, 2021
No community comments so far
Review #1 received
Received 16 Nov, 2021
Reviewer #3 agreed
On 11 Nov, 2021
Reviewer #4 agreed
On 11 Nov, 2021
Reviewer #2 agreed
On 11 Nov, 2021
Reviews received
Received 11 Nov, 2021
Reviewer #1 agreed
On 10 Nov, 2021
Reviewers invited
Invitations sent on 09 Nov, 2021
Editor assigned
On 29 Oct, 2021
Submission checks complete
On 28 Oct, 2021
Editor invited
On 28 Oct, 2021
First submitted
On 23 Oct, 2021
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Cancer Biology
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: Gastritis is a superficial and prevalent inflammatory lesion that is considered a public health concernoncecause gastric ulcers and gastric cancer, especially due to Helicobacter pylori infection. Proton pump inhibitors, such as omeprazole, are the most widely used drugs in order to treat this illness. The aim of the study was evaluating the cytogenetic effects of omeprazole in stomach epithelial cells of patients with gastritis in presence and absence of H. pylori, using to this the application of cytogenetic biomarkers and measurements of catalse and superoxide dismutase.
Methods: The study included 152 patients from the Gastroenterology Outpatient Clinic of Hospital Getúlio Vargas, Teresina - PI, that reported the continuous and prolonged use of omeprazole in doses of 20, 30 and 40 mg/kg. The participants were divided into groups: (1) patients without gastritis (n = 32); (2) patients without gastritis but with use of OME (n = 24); (3) patients with gastritis (n = 26); (4) patients with gastritis undergoing OME therapy (n = 26); (5) patients with gastritis and H. pylori (n = 22) and (6) patients with gastritis and H. pylori on OME therapy (n = 22).
Results: OME induces cytogenetic risks in the epithelium of the stomach due to the formation of micronuclei (group 6> 1,2,3,4,5; group 5> 1,2,3; group 4> 1,2,3); bridges (groups 4 and 6> 1,2,3,5 and group 2> 3,5); buds (groups 2,4,6>, 1,3,5); binucleated cells (group 6> 1,2,3,4,5; group 4> 1,2,3); groups 2 and 3> 1); picnoses (group 6> 1,2,3,4,5), groups 2 and 5> 1,3; group 4> 1,2,3,5); cariorrexis (groups 6 and 4> 1,2,3,5; groups 2,3,5> 1) and karyolysis (groups 2,4, and 6> 1,3,5; groups 3 and 5> 1). These data show that omeprazole induces cytogenetic risks, especially due to infection with H. pylori, thus indicating the clastogenic and/or aneugenic effects, chromosomes changing, gene expression, cytotoxicity and apoptosis.
Conclusions: These risks can be attributed to several mechanisms that are still unclear, including oxidative damage, as observed by increases in catalase and superoxide dismutase. Positive correlations between these antioxidant enzymes were obtained with the formation of micronuclei, and negative for picnoses. Thus, the continuous and prolonged use of omeprazole induces genetic instability, which can be monitored, in cytogenetic analyzes, as anticipation for cancer, especially gastric.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Figure 7
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