Zinc hydroxide induced respiratory burst in rat neutrophils |
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Affiliation: | 1. Depeartment of Gynecologic Oncology and Minimally-invasive Surgery, Rotkreuzklinikum München, Frauenklinik Taxisstraße Munich, Germany;2. Munich Cancer Registry, Institute for Medical Information Processing, Biometry and Epidemiology, Ludwig-Maximilians-University (LMU), Munich, Germany;3. Department of Obstetrics and Gynecology, University Hospital, LMU Munich, Germany;4. Department of Obstetrics and Gynecology, University Hospital, Technical University Munich, Germany;5. Department of Obstetrics and Gynecology Städtisches Klinikum Harlaching Munich, Germany;6. Department of Obstetrics and Gynecology Klinikum Starnberg, Germany;7. Department of Obstetrics and Gynecology, Klinikum Dritter Orden, Munich, Germany;8. Department of Obstetrics and Gynecology, RoMed Kliniken, Rosenheim, Germany |
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Abstract: | The effects of zinc hydroxide on the respiratory burst and phagocytosis by rat neutrophils were examined. Zinc hydroxide induced an increase in oxygen consumption and O2− production. Electronmicroscopy showed that neutrophils engulfed zinc hydroxide particles by phagocytosis. Pertussis toxin (0.25, 0.5, 1.0 μ/ml) and EGTA (1, 2, 5 mM) inhibited zinc hydroxide-induced O2− production in a dose-dependent manner. The inhibitors of protein kinase C, 1-(5-isoquinolinesulfonyl)-2-methyl-piperazine and N-[2-(methylamino)ethyl]-5-isoquinolinesulfonamide inhibited zinc hydroxide-induced O2− production with IC50 values ranging between 10 μM and 25 μM. The inhibitory study using an inhibitor of myosin light chain kinase, 1-(5-iodonapthalene-1-sulfonyl)-1H- hexahydro-1,4-diazepine, showed IC50 values ranging from 5 μM to 10 μM. These findings indicate that zinc hydroxide induces respiratory burst and phagocytosis by rat neutrophils. |
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