Topic
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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TL;DR: The mechanism for enhanced desorption of chloroaliphatic compounds from a silty loam soil by modified Fenton's reagent was investigated using a series of probe compounds of varying hydrophobicities as discussed by the authors.
Abstract: The mechanism for enhanced desorption of chloroaliphatic compounds from a silty loam soil by modified Fenton's reagent was investigated using a series of probe compounds of varying hydrophobicities. Hexachloroethane, which has negligible reactivity with hydroxyl radicals, was transformed more rapidly in modified Fenton's reactions (≥0.3 M hydrogen peroxide) than it was lost by gas-purge desorption, suggesting the existence of a non-hydroxyl radical mechanism. The addition of excess 2-propanol to scavenge hydroxyl radicals slowed, but did not stop, the desorption and degradation of hexachloroethane. In the presence of the reductant scavenger chloroform, hexachloroethane did not desorb and was not degraded, indicating that a reductive pathway in vigorous Fenton-like reactions is responsible for enhanced contaminant desorption. Fenton-like degradation of hexachloroethane yielded the reduced product pentachloroethane, confirming the presence of a reductive mechanism. In the presence of excess 2-propanol, tolu...
187 citations
TL;DR: In this article, the authors present a systematic study of O2 reduction on the (111) facets of eight transition metals (Rh, Ir, Ni, Pd, Pt, Cu, Ag, and Au) based on periodic density functional theory.
187 citations
TL;DR: It is concluded that brain mitochondria exposed to oxygen radicals in vitro show an inhibition of respiratory activity similar to that reported by other investigators as occurring in mitochondria in vivo following transient cerebral ischemia, suggesting oxygen radicals may contribute to this type of cell damage.
Abstract: Respiratory activity of isolated rat brain mitochondria was measured following in vitro exposure to oxygen radicals. The radicals were generated by hypoxanthine and xanthine oxidase in the presence of a suitable iron chelate and caused a severe inhibition of respiration stimulated by phosphate plus ADP (with malate + glutamate as substrate). The damage could be prevented by catalase or high concentrations of mannitol, but not by superoxide dismutase. A similar effect was observed when hypoxanthine and xanthine oxidase were replaced by glucose and glucose oxidase or by hydrogen peroxide. Most of the findings indicate that the hydroxyl radical is the damaging agent. It is concluded that brain mitochondria exposed to oxygen radicals in vitro show an inhibition of respiratory activity similar to that reported by other investigators as occurring in mitochondria in vivo following transient cerebral ischemia. Therefore, oxygen radicals may contribute to this type of cell damage.
186 citations
TL;DR: In this article, a six-coordinatc vanadium complex, LVO(OEt)(EtOH), where H 2 L=N-(2-hydroxyphenyl)salicylideneamine, is shown to be a catalyst precursor in the oxidation of bromide by hydrogen peroxide in DMF solution.
Abstract: A six-coordinatc vanadium(V) complex, LVO(OEt)(EtOH), where H 2 L=N-(2-hydroxyphenyl)salicylideneamine, is shown to be a catalyst precursor in the oxidation of bromide by hydrogen peroxide in DMF solution. The oxidized bromine specie is trapped by organic substrate and, by product analysis, is shown to be a two-electron-oxidized species, rather than a bromine radical. The bromination reaction is quantitative with respect to hydrogen peroxide. The acid dependence of the stoichiometry of the bromination reaction is etablished. Using UV/vis spectrophotometry, 51 V NMR spectroscopy, and kinetic data
186 citations
TL;DR: The reaction of kynurenine pathway catabolites with copper and iron, as well as interactions with the major lenticular structural proteins, the alpha-crystallins, support the possibility that 3HK and 3HAA may be cofactors in the oxidative damage of proteins through interactions with redox-active metals and especially copper.
Abstract: The kynurenine pathway catabolite 3-hydroxykynurenine (3HK) and redox-active metals such as copper and iron are implicated in cataractogenesis. Here we investigate the reaction of kynurenine pathway catabolites with copper and iron, as well as interactions with the major lenticular structural proteins, the alpha-crystallins. The o-aminophenol kynurenine catabolites 3HK and 3-hydroxyanthranilic acid (3HAA) reduced Cu(II)>Fe(III) to Cu(I) and Fe(II), respectively, whereas quinolinic acid and the nonphenolic kynurenine catabolites kynurenine and anthranilic acid did not reduce either metal. Both 3HK and 3HAA generated superoxide and hydrogen peroxide in a copper-dependent manner. In addition, 3HK and 3HAA fostered copper-dependent alpha-crystallin cross-linking. 3HK- or 3HAA-modifed alpha-crystallin showed enhanced redox activity in comparison to unmodified alpha-crystallin or ascorbate-modified alpha-crystallin. These data support the possibility that 3HK and 3HAA may be cofactors in the oxidative damage of proteins, such as alpha-crystallin, through interactions with redox-active metals and especially copper. These findings may have relevance for understanding cataractogenesis and other degenerative conditions in which the kynurenine pathway is activated.
186 citations