Cited by 179Neutrophil, Myeloperoxidase and Oxidative MechanismsRedox biology and oxidative stressInflammatory mediators and NSAID effects

Effects of omeprazole on neutrophil chemotaxis, super oxide production, degranulation, and translocation of cytochrome b-245.

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Wandall, J H·1992·Gut

Abstract

The effects of omeprazole on polymorphonuclear neutrophil (PMN) chemotaxis, superoxide generation, degranulation and translocation of cytochrome b-245 were investigated. Omeprazole (10(-6) - 5 x 10(-3) mol/l) reduced chemotaxis under agarose in a dose dependent manner, and the effect was irreversible. Superoxide anion generation was inhibited 50% at a concentration of 2.5 x 10(-5) mol/l and completely abolished at 5 x 10(-3) mol/l. Acid degraded omeprazole also inhibited O2- generation. Omeprazole did not scavenge O2- generated in a cell free xanthin-xanthine oxidase system. Degranulation by PMNs was inhibited only by omeprazole in concentrations above 10(-4) mol/l. Translocation of cytochrome b-245, essential for generation of O2-, was not affected by omeprazole. In conclusion, the anti-ulcer agent omeprazole in concentrations obtained during intravenous administration may inhibit the function of PMNs in vitro.

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  • PPIs have unfavorable effects on gastric functions and host defensive mechanisms, causing delayed gastric emptying, decreased gastric mucus viscosity, increased bacterial load and increased bacterial translocation.

    “PPIs have unfavorable effects on gastric functions and host defensive mechanisms, causing delayed gastric emptying, decreased gastric mucus viscosity, increased bacterial load and increased bacterial translocation[55-57].”

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Research works printed but not linked: 3

  1. Hersko A, Cicckanover A. Mechanism of intracellular protein breakdown. Ann Rev Biochem 1082; 51: 335-64.
  2. Bos A, Wever R, Roos D. Characteristics and quantification of the peroxidase in human neutrophils. Biochim Biophvs Acta 1978; 525: 37-44.
  3. Lindberg P, Nordberg P, Alminger T, Brandstrom A, Wallmark B. The mechanism of the gastric acid secretion inhibitor omeprazole. ] Med Chem 1986; 29: 1327-9.

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Authors
Wandall, J. H.
Affiliations
Massachusetts General Hospital (US)
Corresponding author
Wandall, J H
Venue
Gut
Publisher
BMJ
Published
1992-05-01
Volume
33
Issue
5
Pages
617-621
ISSN
0017-5749 (ISSN-L)
OpenAlex
W2148583557
Cited by
179
References
27
Citations by year
2024: 7 · 2023: 3 · 2022: 5 · 2021: 8 · 2020: 3 · 2019: 4 · 2018: 6 · 2017: 8 · 2016: 5 · 2015: 7 · 2014: 6 · 2013: 9 · 2012: 9
FWCI
1.45
Type
journal article
Language
en
Open access
Locations
  • Gut (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Health Sciences › Medicine › Pharmacology › Inflammatory mediators and NSAID effects
Keywords
omeprazole, neutrophil chemotaxis, superoxide production, neutrophil degranulation, H2 receptor antagonists, antiulcer drugs, drug immunotoxicity
MeSH terms
Chemotaxis, Leukocyte, Cytochrome b Group, Dose-Response Relationship, Drug, Humans, Neutrophils, Omeprazole, Superoxides, Cell Degranulation, In Vitro Techniques

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