Sublethal doses of exogenous hydrogen peroxide prime human neutrophils to formyl peptide
| Autor: | Enno K. Ruuge, A. V. Ledenev, Vladimir R. Muzykantov, E. A. Puchnina-Artushenko |
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| Rok vydání: | 1993 |
| Předmět: |
inorganic chemicals
Agonist Neutrophils medicine.drug_class Neutrophile Immunology Inflammation Oxidative phosphorylation Pharmacology Toxicology chemistry.chemical_compound Superoxides Centrifugation Density Gradient medicine Humans Cytotoxic T cell Pharmacology (medical) Hydrogen peroxide Superoxide hemic and immune systems Chemotaxis Hydrogen Peroxide N-Formylmethionine Leucyl-Phenylalanine chemistry Biochemistry Tetradecanoylphorbol Acetate medicine.symptom Oxidation-Reduction |
| Zdroj: | Agents and Actions. 39:C192-C194 |
| ISSN: | 1420-908X 0065-4299 |
| DOI: | 10.1007/bf01972763 |
| Popis: | Hydrogen peroxide (H2O2) is an oxidative agent important in inflammation and ischemia. Neutrophils (PMNs) are a main source of H2O2 in the inflammatory focus. However, after recruitment into the inflammatory or ischemic zone of the heart, the PMN itself might serve as a target for exogenous H2O2. In the present work we found that PMNs are very resistant to the cytotoxic action of H2O2 (LD50 for PMNs is about 30–50 mM, whereas for endothelial cells it is about 200–300 μM). Unexpectedly, treatment of PMNs by H2O2 at a sublethal dose of 10 mM leads to a subsequent increase in the generation of superoxide anion in response to the chemoattractant peptide FMLP (twofold increase in O 2 − generation 30 min after treatment by H2O2 as compared with nontreated control cells). H2O2 itself does not induce O 2 − generation by PMNs. Therefore, any H2O2 that accumulated in the inflammatory or ischemic zone might alter the functional activity of PMNs and prime them to subsequent agonist activation. |
| Databáze: | OpenAIRE |
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