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

Takeyama, Yuko; Oginö, Kazuhíde; Segawa, Hiroyuki; Kobayashi, Haruo; Uda, Takaaki; Houbara, Tatsuya

doi:10.1111/j.1600-0773.1995.tb00102.x

Cited by 18 publications

(10 citation statements)

References 34 publications

(17 reference statements)

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“…In fact, Zn(II) seemed to cause the most oxidative damage to proteins considering up-regulation of nearly three to four times as many protease/proteasome-encoding genes relative to that induced by other metals. This is not surprising knowing that excess Zn(II) can induce formation of ROS (Takeyama et al 1995) and Genes of key function categories (a-e; see inset key) that experienced mRNA level changes in a dose and/or time-dependent manner to Fe(II). Genes are indicated as circular nodes connected by three types of functional associations: operon (pink), chromosomal proximity (green), and phylogenetic pattern (blue).…”

Section: Reactive Oxygen Species Constitute a Major Component Of Tranmentioning

confidence: 92%

A systems view of haloarchaeal strategies to withstand stress from transition metals

Kaur¹,

Pan²,

Meislin³

et al. 2006

Genome Res.

104

157

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Given that transition metals are essential cofactors in central biological processes, misallocation of the wrong metal ion to a metalloprotein can have resounding and often detrimental effects on diverse aspects of cellular physiology. Therefore, in an attempt to characterize unique and shared responses to chemically similar metals, we have reconstructed physiological behaviors of Halobacterium NRC-1, an archaeal halophile, in sublethal levels of Mn(II), Fe(II), Co(II), Ni(II), Cu(II), and Zn(II). Over 20% of all genes responded transiently within minutes of exposure to Fe(II), perhaps reflecting immediate large-scale physiological adjustments to maintain homeostasis. At steady state, each transition metal induced growth arrest, attempts to minimize oxidative stress, toxic ion scavenging, increased protein turnover and DNA repair, and modulation of active ion transport. While several of these constitute generalized stress responses, up-regulation of active efflux of Co(II), Ni(II), Cu(II), and Zn(II), down-regulation of Mn(II) uptake and up-regulation of Fe(II) chelation, confer resistance to the respective metals. We have synthesized all of these discoveries into a unified systems-level model to provide an integrated perspective of responses to six transition metals with emphasis on experimentally verified regulatory mechanisms. Finally, through comparisons across global transcriptional responses to different metals, we provide insights into putative in vivo metal selectivity of metalloregulatory proteins and demonstrate that a systems approach can help rapidly unravel novel metabolic potential and regulatory programs of poorly studied organisms.[Supplemental material is available online at www.genome.org. The microarray data from this study have been submitted to GEO under accession nos. GSM109343-GSM109461 and GSM109514-GSM109522.]Transition metals such as manganese (Mn), iron (Fe), cobalt (Co), nickel (Ni) copper (Cu), and zinc (Zn) are essential cofactors in the physiology of all organisms. In fact, recent estimates suggest that over half of all proteins in every organism are metalloproteins (Degtyarenko 2000). Although essential in trace amounts, at higher levels these metals can be toxic to cells because they directly or indirectly compromise DNA, protein, and membrane integrity and function. For example, cycling in redox states of metals such as Fe and Cu and antioxidant scavenging by redoxinactive metals such as Zn can both cause oxidative damage to cell components through increased production of reactive oxygen species (ROS) (Nelson 1999). Organisms usually avoid metal toxicity through selective uptake, trafficking, and efflux of metal ions, enzymatic conversion of metals into non-or less-toxic redox states, or sequestering toxic metal ions with ferritins and metallothioneins (Silver 1992;Blindauer et al. 2002;Reindel et al. 2002;Zeth et al. 2004). These mechanisms are believed to be often regulated by free metal-ion concentration (Raab and Feldman 2003). In this regard, other factors such as salinity,...

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Section: Reactive Oxygen Species Constitute a Major Component Of Tranmentioning

confidence: 92%

A systems view of haloarchaeal strategies to withstand stress from transition metals

Kaur¹,

Pan²,

Meislin³

et al. 2006

Genome Res.

104

157

View full text Add to dashboard Cite

show abstract

“…Previous studies provided contradictory results about the effect of zinc on NADPH oxidase activation and consequently on production of reactive species, with some authors indicating that zinc induces neutrophils' oxidative burst (Benoni et al 1998;Lindahl et al 1998;Takeyama et al 1995) while in turn, others argued that zinc inhibits O 2…”

Section: Discussionmentioning

confidence: 96%

“…The authors observed that the MPO inhibitor prevented PMA-induced luminol amplified chemiluminescence response in a zinc concentrationdependent manner, suggesting that HOCl is involved in the process. Also, Takeyama et al (1995) reported that the addition of zinc, at 1,000 lM, increased the intracellular MPO activity.…”

Section: Discussionmentioning

confidence: 98%

“…Most reports in the literature referring to zinc indicate this metal as being relatively non-toxic and that animals, including humans, exhibit considerable tolerance to high zinc intake (Fosmire 1990). Nevertheless, in spite of its safety, some reports suggest that zinc may disturb the innate host defense response, by interfering in the activation of neutrophils and subsequent oxidative burst (Benoni et al 1998;Lindahl et al 1998;Takeyama et al 1995). Furthermore, is has also been argued that zinc inhibits superoxide radical (O 2 •-) production (DeCoursey et al 2003;Henderson et al 1988).…”

Section: Introductionmentioning

confidence: 92%

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Zinc activates neutrophils’ oxidative burst

et al. 2009

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Zinc has been shown to disturb the innate host defense response by interfering in the activation of neutrophils and subsequent oxidative burst, although the exact role of this metal, either as an activator or inhibitor, remains a matter of controversy among research groups. These apparent discrepancies may be due to experimental settings, through modification of zinc availability to neutrophils, or to inaccurate detections of reactive species. Thus, the main objective of the present study was to provide clarification on the role of zinc on the activation of human neutrophils and the subsequent oxidative burst. For that purpose, different detection methods and incubation media were used. The obtained results showed that phosphate buffers (PBS and HBSS) complex with zinc and interfere with the results obtained with this metal. By using Tris-G, it was clearly demonstrated that zinc, at low concentrations (5-12.5 microM), activates NADPH oxidase, mainly via protein kinase C, leading to the formation of superoxide radical (O(2*-). Higher concentrations of zinc results on a rapid dismutation of O2*- to oxygen and hydrogen peroxide, which in turn is used by myeloperoxidase to generate hypochlorous acid (HOCl).

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“…Whilst, decreased oxidative burst occurs in zinc deficiency (Keen and Gershwin 1990). High zinc ( ‡100 lM) suppresses oxidative burst (Yatsuyanagy et al 1987;Takeyama et al 1995). However, high zinc is toxic on neutrophil function (Hasegawa et al 2000).…”

Section: Parametersmentioning

confidence: 96%

Interrelationship Among Neutrophil Efficiency, Inflammation, Antioxidant Activity and Zinc Pool in Very Old Age

et al. 2005

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Neutrophils are the first barrier against infections. Aged neutrophils display impaired oxidative burst and phagocytosis with subsequent less capability to destroy bacteria. In successful ageing (nonagenarians), neutrophil efficiency (phagocytosis) increases. After ingested microbes, aged neutrophils are less prone to undergo apoptosis favouring chronic inflammation. Moreover, the superoxide dismutase (SOD) activity, which is necessary in avoiding ROS produced by oxidative burst, is limited in ageing. The mechanisms of age-related changes in neutrophil function are not fully understood, taking also into account that nonagenarians escape infections in comparison with elderly. Zinc pool may be involved because it is pivotal for neutrophil efficiency and SOD activity. Since zinc also controls the inflammation, via IL-6 and soluble factor of gp130 (sgp130), we have assessed the possible interrelationship among oxidative burst, apoptosis, inflammation, SOD, adhesion molecule Mac-1 and zinc pool in elderly and in nonagenarians. The oxidative burst and the capacity to increase Mac-1 after PMA stimulation decrease both in elderly and nonagenarians, but the latter display a slight increased neutrophil induced apoptosis, decreased sgp130, increased SOD, and more neutrophil zinc content, as it occurs in young-adults. Significant correlation exists between sgp130 and zinc pool in very old age. These findings suggest lower chronic inflammation in nonagenarians, via more zinc available, with subsequent long-life survival. Therefore, a more correct interrelationship among neutrophil efficiency, inflammation, antioxidant activity and zinc pool exists in successful ageing with subsequent more effectiveness to control the inflammatory response to pathogens.

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

Cited by 18 publications

References 34 publications

A systems view of haloarchaeal strategies to withstand stress from transition metals

A systems view of haloarchaeal strategies to withstand stress from transition metals

Zinc activates neutrophils’ oxidative burst

Interrelationship Among Neutrophil Efficiency, Inflammation, Antioxidant Activity and Zinc Pool in Very Old Age

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