Bactericidal properties of hydrogen peroxide and copper or iron-containing complex ions in relation to leukocyte function

Elżanowska, H.; Wolcott, Robert G.; Hannum, Diane M.; Hurst, James K.

doi:10.1016/0891-5849(94)00150-i

Cited by 36 publications

(41 citation statements)

References 47 publications

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“…The mechanisms by which copper ions inhibit or kill overloaded cells are not known (18), but a redox cycling system of cupric ions, dihydrogen peroxide, and ascorbate severely impaired the respiration of E. coli cells (8). The general biocidal properties of copper can be described.…”

Section: Discussionmentioning

confidence: 99%

“…In the case of iron, the actual toxic oxidants might be the hydroxyl radical, formed by a one-electron reduction of dihydrogen peroxide, the instable higher valent ferryl ion (cupryl in case of copper), or peroxy complexes as well as secondary radicals generated by reactions with medium components (8).…”

Section: Discussionmentioning

confidence: 99%

“…Probably, overall metallic copper oxidation was diminished even so, while at the same time, the Cu(II)/Cu(I) ratio was shifted in favor of the more toxic cuprous ion. Nevertheless, both cuprous-ion-and cupric-ion-mediated bactericidal mechanisms involve the inhibition of cellular energy-transducing capabilities and accumulated damage at multiple, yet unknown cellular sites (8).…”

Section: Discussionmentioning

confidence: 99%

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Contribution of Copper Ion Resistance to Survival of Escherichia coli on Metallic Copper Surfaces

Santo

Taudte

Nies

et al. 2008

Appl Environ Microbiol

281

220

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Bacterial contamination of touch surfaces poses a serious threat for public health. The use of bactericidal surface materials, such as copper and its alloys, might constitute a way to aid the use of antibiotics and disinfectants, thus minimizing the risk of emergence and spread of multiresistant germs. The survival of Escherichia coli on metallic copper surfaces has been studied previously; however, the mechanisms underlying bacterial inactivation on copper surfaces have not been elucidated. Data presented in this study suggest that bacteria are killed rapidly on dry copper surfaces. Several factors, such as copper ion toxicity, copper chelators, cold, osmotic stress, and reactive oxygen species, but not anaerobiosis, influenced killing rates. Strains deleted in copper detoxification systems were slightly more sensitive than was the wild type. Preadaptation to copper enhanced survival rates upon copper surface exposure. This study constitutes a first step toward understanding the reasons for metallic copper surface-mediated killing of bacteria.Copper, both in its metallic and ionic forms, has been exploited empirically since ancient times for medical uses in countless cultures around the globe. Later, the therapeutic powers of this metal were accredited to its antimicrobial properties for the curing of various wound and skin diseases.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Contribution of Copper Ion Resistance to Survival of Escherichia coli on Metallic Copper Surfaces

Santo

Taudte

Nies

et al. 2008

Appl Environ Microbiol

281

220

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“…In the absence of significant MPO activity and limited capacity to form peroxynitrite, the only recognized microbicidal mechanisms available to these cells involve metal-mediated Fenton reactions (43,69). However, Ullrich and coworkers have presented data indicating that inhibition of COX-2 activity within LPS-stimulated RAW cells correlates with nitration of some of its own tyrosyl groups; the inhibitory reaction was arachidonate and NO 2 -dependent and could not be catalyzed by MPO or catalase in ex vivo assays, the inference being that it is autocatalytic (17).…”

Section: Physiological Implicationsmentioning

confidence: 99%

“…Similarly, inclusion of catalase in the xanthine/XO assay promoted dye oxidation. The fluorescent oxidation product formed immediately upon exposure to ≤ 10 μM HOCl or < 50 μM radiolyticallygenerated NO 2 · , and to oxidants generated in a standard Fenton system comprising 20 μM H 2 O 2 , 1.0 μM Cu 2+ , and 1.0 mM ascorbate (43). Complete oxidation of DCHF on ∼1×10 8 beads was attained upon bolus addition of 50 μM aliquots of peroxynitrite in either CO 2 -free PBS or in 100 mM bicarbonate, pH 7.4, when the total added oxidant reached ∼1 mM.…”

Section: Selectivities Of Probes For Various Oxidantsmentioning

confidence: 99%

Pathways for Intracellular Generation of Oxidants and Tyrosine Nitration by a Macrophage Cell Line

2007

Self Cite

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Two transformed murine macrophage cell lines (RAW 264.7 ATCC TIB-71 and CRL-2278) were examined for oxidant production at various times following activation by using a set of fluorescence and ESR-active probes. Stimulation with a soluble agonist or activation with bacterial lipopolysaccharide plus γ-interferon caused only very small initial increases in O 2 consumption above basal rates; however, at 2-4 h post-activation, respiration increased to 2-3 fold and remained at these elevated levels over the subsequent lifetime of the cell (20-30 h). Oxidation reactions were confined primarily within the cell, as was demonstrated by using phagocytosable dichlorodihydrofluorescein-conjugated latex beads and cyclic hydroxylamines with differing membrane permeabilities. From the intrinsic reactivities of these probes and the time course of their oxidations, one infers induction of apparent peroxidase activity beginning at ∼2 h post-activation, coinciding with the increase in overall respiratory rate; this acquired capability was accompanied by accumulation of a stable horseradish peroxidase-reactive oxidant, presumably H 2 O 2 , in the extracellular medium,. Nitrite ion rapidly accumulated in the extracellular medium over a period of 5-8 h post-activation in both cell lines, indicating the presence of active nitric oxide synthase (iNOS) during that period. Prostaglandin endoperoxide H synthase (COX-2) activity was detected at 15-20 h post-activation by use of sensitive peroxide assay in conjunction with a COX-2 specific inhibitor (DuP-697). Superoxide formation was detected by reaction with hydroethidine within the first hour following activation, but not thereafter. Consistent with the absence of significant respiratory stimulation, the amount of O 2 ·-formed was very small; comparative reactions of cyclic hydroxylamine probes indicated that virtually none of the O 2 ·-was discharged into the external medium. Myeloperoxidase (MPO) activity was probed at various times post-activation by using fluorescein-conjugated polyacrylamide beads, which efficiently trap MPO-generated HOCl in neutrophils to give stable chlorofluorescein products. However, chlorination of the dye was not detected under any conditions in RAW cells, virtually precluding MPO involvement in their intracellular reactions. This same probe was used to determine changes in intraphagosomal pH, which increased slowly from ∼6.5 to ∼8.2 over a 20 h post-phagocytosis period. The cumulative data suggest activation is followed by sequential induction of an endogenous peroxidase, iNOS, and COX-2, with NADPH oxidase-derived O 2 ·-playing a minimal role in direct generation of intracellular oxidants. To account for reported observations of intracellular tyrosine nitration late in the life cycles of macrophages, we propose a novel mechanism wherein iNOS-generated NO 2 -is used by COX-2 to produce NO 2 · as a terminal microbicidal oxidant and nitrating agent.The existence of motile phagocytic cells involved with host defense in higher organisms has been known sin...

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Hydroxyl radical production by ascorbate and hydrogen peroxide

Nappi

Vass

2000

neurotox res

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Ascorbate (AH') and certain other biological reductants have long been known to produce the cytotoxic hydroxyl radical ('OH) when oxidized by hydrogen peroxide (H202) in the presence of copper or iron catalysts. The present study documents the in vitro production of the "OH solely from the oxidation of AH-by H202, independent of mediation by transition metals. Hydroxyl radical generation resulting from the AH'/H202 system was quantitatively documented by the specific radical-mediated hydroxylation of salicylic acid, a reaction that was readily assayed with HPLC coupled with electrochemical detection. Two ascorbate-copper complexes (e.g., AH-/Cu2+-EDTA/H202 and AH'/Cu2+-EDTA) and a copper/H202 system also generated 'OH, but less effectively than the AH'/H202 system. The ability of AH-and H202 to generate cytotoxic "OH documents a reaction mechanism that may account for cytotoxic activity in some cellular environments where metal catalysts are lacking.

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Bactericidal properties of hydrogen peroxide and copper or iron-containing complex ions in relation to leukocyte function

Cited by 36 publications

References 47 publications

Contribution of Copper Ion Resistance to Survival of Escherichia coli on Metallic Copper Surfaces

Contribution of Copper Ion Resistance to Survival of Escherichia coli on Metallic Copper Surfaces

Pathways for Intracellular Generation of Oxidants and Tyrosine Nitration by a Macrophage Cell Line

Hydroxyl radical production by ascorbate and hydrogen peroxide

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