Zinc hydroxide induced respiratory burst in rat neutrophils

Oginö, Kazuhíde; Izumi, Yukie; Segawa, Hiroyuki; Takeyama, Yuko; Ishiyama, H.; Houbara, Tatsuya; Uda, Takaaki; Yamashita, Shuji

doi:10.1016/0926-6917(94)90082-5

Cited by 12 publications

(8 citation statements)

References 24 publications

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“…The effect of zinc on the oxidative metabolism, crucial for the production of the oxygen metabolites which are essential to the microbicidal function of the PMN cells (Morel et al 1991), has not been uniformly-reported in the literature. Experimental conditions and stimulus applied varied, and the generation of oxygen metabolites in human PMN was decreased or enhanced in a number of studies depending on the experimental conditions (Beswick et al 1986;Yatsuyanagi et al 1990;Ogino et al 1994). It seemed therefore plausible that the killing function of the zinc-treated PMN cells in our experiments would be affected.…”

Section: Discussionmentioning

confidence: 86%

The effect of zinc on bacterial phagocytosis, killing and cytoprotection in human polymorphonuclear leucocytes

Sunzel

Holm

Reuterving

et al. 1995

APMIS

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Sunzel, B., Holm, S., Reuterving C.-O., Soderberg, T., Hallmans, G . & Hanstrom, L. The effect of zinc on bacterial phagocytosis, killing and cytoprotection in human polymorphonuclear leucocytes.An in vitro study examining the effects of zinc treatment on human PMN cell phagocytosis and killing of Staphylococcus aureus and Staphylococcus epidermidis and the cytoprotection of zinc against staphylococcal toxins. Phagocytosis was studied by transmission electron microscopy using different microbiological techniques, one of which was designed to follow the kinetics of bacterial killing. No effect was found on phagocytosis and bacterial killing. The cytotoxic effects of a crude toxin and an a-toxin extracted from Staphylococcus aureus preparations were studied on human PMN cells using the standard 5'Cr release assay. Both toxins induced a dose-dependent leakage of 51Cr, indicating cell membrane damage. These results were confirmed by electron microscopy during the phagocytosis of S. uureus, where severe PMN cellular degeneration was observed. The addition of zinc to PMN cells strongly inhibited the release of S'Cr. In conclusion, our results show that zinc in higher than physiological concentrations does not inhibit PMN cell functions such as phagocytosis and intracellular killing of S. aureus and S. epidermidis. The addition of zinc may be beneficial in certain clinical situations, such as wound healing, zinc deficiency and infections involving toxin-producing bacteria, e.g. S. aureus.

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Section: Discussionmentioning

confidence: 86%

The effect of zinc on bacterial phagocytosis, killing and cytoprotection in human polymorphonuclear leucocytes

Sunzel

Holm

Reuterving

et al. 1995

APMIS

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“…Neutrophil preparation. Rat polymorphonuclear leukocytes (neutrophils) were prepared according to the method described previously (Ogino et al 1994) from peritoneal exudates of male Wistar rats (200-250 g). Briefly, the rats were injected intraperitoneally with 20 ml of sterile 12% (w/v) sodium caseinate in iso-osmotic (0.9"h) NaCI, and peritoneal exudates were collected after 12 hr.…”

Section: Methodsmentioning

confidence: 99%

Effects of Zinc on Production of Active Oxygen Species by Rat Neutrophils

Takeyama

Oginö

Segawa

et al. 1995

Pharmacology & Toxicology

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The effects of zinc on the production of active oxygen species were investigated in rat neutrophils by chemiluminescence and spectrophotometric assays. The luminol-dependent chemiluminescence in unstimulated neutrophils showed a single peak. Zinc at concentrations lower than 0.1 mM augmented the intensity of chemiluminescence and showed a bimodal pattern, the first peak of which was inhibited by superoxide dismutase and catalase, while the second peak disappeared in the presence of catalase, but was unaffected by superoxide dismutase. At the same concentrations of zinc, O2- and H2O2 production increased, but secretion and activity of myeloperoxidase were not affected. Zinc at 0.1 mM enhanced the second peak of luminol-dependent chemiluminescence, and concomitantly O2- and H2O2 production of neutrophils stimulated with formyl-methionyl-leucyl-phenylalanine. Homogenized neutrophils showed a bimodal pattern on induction by zinc, the second peak of which was inhibited slightly by catalase and completely by sodium azide, but was not inhibited by superoxide dismutase. Zinc-induced O2- production was inhibited by pertussis toxin, but was not significantly inhibited by a protein kinase C inhibitor, 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride (H-7), or a calmodulin antagonist, N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7). These results suggest that zinc can augment luminol-dependent chemiluminescence by increasing O2- production through the classical signal transduction pathway, and by increasing H2O2 not via O2-.

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“…The proton current inhibitor Zn 2+ reduces NADPH oxidase activity substantially in numerous studies (34, 81, 91, 120, 122, 145, 154, 208, 210, 251, 307, 353, 356, 388, 414, 417, 435, 458, 468, 491, 525, 534). This effect is not on the oxidase itself, because electron currents are unaffected by millimolar Zn 2+ (120, 403, 442).…”

Section: Roles In Innate Immunitymentioning

confidence: 99%

Voltage-Gated Proton Channels: Molecular Biology, Physiology, and Pathophysiology of the H_VFamily

DeCoursey

2013

Physiological Reviews

204

268

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Voltage-gated proton channels (HV) are unique, in part because the ion they conduct is unique. HV channels are perfectly selective for protons and have a very small unitary conductance, both arguably manifestations of the extremely low H+ concentration in physiological solutions. They open with membrane depolarization, but their voltage dependence is strongly regulated by the pH gradient across the membrane (ΔpH), with the result that in most species they normally conduct only outward current. The HV channel protein is strikingly similar to the voltage-sensing domain (VSD, the first four membrane-spanning segments) of voltage-gated K+ and Na+ channels. In higher species, HV channels exist as dimers in which each protomer has its own conduction pathway, yet gating is cooperative. HV channels are phylogenetically diverse, distributed from humans to unicellular marine life, and perhaps even plants. Correspondingly, HV functions vary widely as well, from promoting calcification in coccolithophores and triggering bioluminescent flashes in dinoflagellates to facilitating killing bacteria, airway pH regulation, basophil histamine release, sperm maturation, and B lymphocyte responses in humans. Recent evidence that hHV1 may exacerbate breast cancer metastasis and cerebral damage from ischemic stroke highlights the rapidly expanding recognition of the clinical importance of hHV1.

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Zinc hydroxide induced respiratory burst in rat neutrophils

Cited by 12 publications

References 24 publications

The effect of zinc on bacterial phagocytosis, killing and cytoprotection in human polymorphonuclear leucocytes

The effect of zinc on bacterial phagocytosis, killing and cytoprotection in human polymorphonuclear leucocytes

Effects of Zinc on Production of Active Oxygen Species by Rat Neutrophils

Voltage-Gated Proton Channels: Molecular Biology, Physiology, and Pathophysiology of the H_VFamily

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Zinc hydroxide induced respiratory burst in rat neutrophils

Cited by 12 publications

References 24 publications

The effect of zinc on bacterial phagocytosis, killing and cytoprotection in human polymorphonuclear leucocytes

The effect of zinc on bacterial phagocytosis, killing and cytoprotection in human polymorphonuclear leucocytes

Effects of Zinc on Production of Active Oxygen Species by Rat Neutrophils

Voltage-Gated Proton Channels: Molecular Biology, Physiology, and Pathophysiology of the HVFamily

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Voltage-Gated Proton Channels: Molecular Biology, Physiology, and Pathophysiology of the H_VFamily