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Hydrogen peroxide

About: Hydrogen peroxide is a research topic. Over the lifetime, 42583 publications have been published within this topic receiving 1043732 citations. The topic is also known as: H2O2 & dioxidane.


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Journal ArticleDOI
TL;DR: Significant antibacterial activity can be maintained easily when using honey as a wound dressing, even on a heavily exuding wound, because Concentrations of hydrogen peroxide generated are very low in comparison to those typically applied to a wound, thus, cytotoxic damage by hydrogenperoxide is very low.
Abstract: Objective: Honey is an effective antiseptic wound dressing, mainly the result of the antibacterial activity of hydrogen peroxide that is produced in honey by the enzyme glucose oxidase. Because the rate of production of hydrogen peroxide is known to vary disproportionately when honey is diluted, and dilution of honey dressings will vary according to the amount of wound exudate, it is important to know more about the production of hydrogen peroxide at different concentrations of honey. Design: The rates of hydrogen peroxide production by honey with respect to honey dilution were measured in eight different samples of honey from six different floral sources. Settings: Honey Research Unit, Waikato University, Hamilton, New Zealand. Main Results: The maximum levels of accumulated hydrogen peroxide occurred in honey solutions diluted to concentrations between 30% and 50% (v/v) with at least 50% of the maximum levels occurring at 15-67% (v/v). This is equivalent to a 10 cm × 10 cm dressing containing 20 mL of h...

240 citations

Book ChapterDOI
TL;DR: This chapter describes three assays for the quantitation of the cyanide resistant oxidative metabolism of macrophages, measuring O 2 – and H 2 O 2 production and nitroblue tetrazolium (NBT) reduction by cells cultured in 96-well microplates with the aid of an enzyme immunoassay microplate reader fitted with appropriate filters for the photometric determination of the respective reaction products.
Abstract: Publisher Summary This chapter describes three assays for the quantitation of the cyanide resistant oxidative metabolism of macrophages. Macrophages of various tissue origins produce copious amounts of superoxide (O 2 – ) and hydrogen peroxide (H 2 O 2 ) when adequately stimulated. This process is accompanied by a marked increment in oxygen uptake and an increased utilization of glucose via the hexose monophosphate shunt (HMPS). The coordinated sequence of reactions is known as the “oxidative” or “respiratory” burst. The three methods have in common the measurement of O 2 – and H 2 O 2 production and nitroblue tetrazolium (NBT) reduction by cells cultured in 96-well microplates with the aid of an enzyme immunoassay microplate reader fitted with appropriate filters for the photometric determination of the respective reaction products. The microassay of O 2 – production is based on the reduction of ferricytochrome c by O 2 – , the specificity of reduction being controlled by its inhibition by superoxide dismutase. The length of time for which O 2 – production occurs at a linear rate depends on the type of macrophage, on the cell density, and on the nature of the stimulus.

240 citations

Journal ArticleDOI
TL;DR: Treatment of Saccharomyces cerevisiae cells with low concentrations of either hydrogen peroxide or menadione induces adaptive responses which protect cells from the lethal effects of subsequent challenge with higher concentrations of these oxidants.
Abstract: Treatment of Saccharomyces cerevisiae cells with low concentrations of either hydrogen peroxide or menadione (a superoxide-generating agent) induces adaptive responses which protect cells from the lethal effects of subsequent challenge with higher concentrations of these oxidants. Pretreatment with menadione is protective against cell killing by hydrogen peroxide; however, pretreatment with hydrogen peroxide is unable to protect cells from subsequent challenge with menadione. This suggests that the adaptive responses to these two different oxidants may be distinct.

240 citations

01 Jan 1996
TL;DR: The fur mutants, which have an intracellular iron overload, were more sensitive to HOCl, supporting the generation of hydroxyl radicals upon HOCl exposure via a Fenton-type reaction.
Abstract: We have investigated the mechanisms of killing of Escherichia coli by HOCl by identifying protective functions. HOCl challenges were performed on cultures arrested in stationary phase and in exponential phase. Resistance to HOCl in both cases was largely mediated by genes involved in resistance to hydrogen peroxide (H2O2). In stationary phase, a mutation in rpoS, which controls the expression of starvation genes including those which protect against oxidative stress, renders the cells hypersensitive to killing by HOCl. RpoS-regulated genes responsible for this sensitivity were dps, which encodes a DNA-binding protein, and, to a lesser extent, katE and katG, encoding catalases; all three are involved in resistance to H2O2. In exponential phase, induction of the oxyR regulon, an adaptive response to H2O2, protected against HOCl exposure, and the oxyR2 constitutive mutant is more resistant than the wild-type strain. The genes involved in this oxyR-dependent resistance have not yet been identified, but they differ from those primarily involved in resistance to H2O2, including katG, ahp, and dps. Pretreatment with HOCl conferred resistance to H2O2 in an OxyR-independent manner, suggesting a specific adaptive response to HOCl. fur mutants, which have an intracellular iron overload, were more sensitive to HOCl, supporting the generation of hydroxyl radicals upon HOCl exposure via a Fenton-type reaction. Mutations in recombinational repair genes (recA or recB) increased sensitivity to HOCl, indicative of DNA strand breaks. Sensitivity was visible in the wild type only at concentrations above 0.6 mg/liter, but it was observed at much lower concentrations in dps recA mutants.

239 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20242
20231,644
20223,392
2021897
20201,112
20191,301