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.

An ICT-Based Approach to Ratiometric Fluorescence Imaging of Hydrogen Peroxide Produced in Living Cells

Abstract: We present the synthesis, properties, and biological applications of Peroxy Lucifer 1 (PL1), a new fluorescent probe for imaging hydrogen peroxide produced in living cells by a ratiometric response PL1 utilizes a chemoselective boronate-based switch to detect hydrogen peroxide by modulation of internal charge transfer (ICT) within a 1,8-naphthalimide dye PL1 features high selectivity for hydrogen peroxide over similar reactive oxygen species, including superoxide, and nitric oxide, and a 65 nm shift in emission from blue-colored fluorescence to green-colored fluorescence upon reaction with peroxide Two-photon confocal microscopy experiments in live macrophages show that PL1 can ratiometrically visualize localized hydrogen peroxide bursts generated in living cells at immune response levels

Oxidative stress: the vulnerable β-cell

Abstract: Antioxidative defence mechanisms of pancreatic β-cells are particularly weak and can be overwhelmed by redox imbalance arising from overproduction of reactive oxygen and reactive nitrogen species. The consequences of this redox imbalance are lipid peroxidation, oxidation of proteins, DNA damage and interference of reactive species with signal transduction pathways, which contribute significantly to β-cell dysfunction and death in Type 1 and Type 2 diabetes mellitus. Reactive oxygen species, superoxide radicals (O 2 •− ), hydrogen peroxide (H 2 O 2 ) and, in a final iron-catalysed reaction step, the most reactive and toxic hydroxyl radicals (OH • ) are produced during both pro-inflammatory cytokine-mediated β-cell attack in Type 1 diabetes and glucolipotoxicity-mediated β-cell dysfunction in Type 2 diabetes. In combination with NO • , which is toxic in itself, as well as through its reaction with the O 2 •− and subsequent formation of peroxynitrite, reactive species play a central role in β-cell death during the deterioration of glucose tolerance in the development of diabetes.

Copper-ion-dependent damage to the bases in DNA in the presence of hydrogen peroxide.

Abstract: Mixtures of Cu2+ and H2O2 at pH 7.4 caused damage to the bases in DNA greater than that caused by mixtures of Fe3+ and H2O2. Addition of ascorbic acid to the Cu2+/H2O2 system caused a very large increase in base damage, much greater than that produced by the Fe3+/H2O2/ascorbic acid system. The products of base damage in the presence of Cu2+ were typical products that have been shown to result from attack of hydroxyl radicals upon the DNA bases. Cytosine glycol, thymine glycol, 8-hydroxyadenine and especially 8-hydroxyguanine were the major products in both the Cu2+/H2O2 and the Cu2+/H2O2/ascorbic acid systems. Base damage in DNA by these systems was inhibited by the chelating agents EDTA and nitrilotriacetic acid and by catalase, but not by superoxide dismutase, nor by the hydroxyl-radical scavenger mannitol. It is proposed that Cu2+ ions bound to the DNA react with H2O2 and ascorbic acid to generate hydroxyl radicals, which then immediately attack the DNA bases in a site-specific manner. A hypoxanthine/xanthine oxidase system also caused damage to the DNA bases in the presence of Cu2+ ions. This was inhibited by superoxide dismutase and catalase. The high activity of Cu2+ ions, when compared with Fe3- ions, in causing hydroxyl-radical-dependent damage to DNA and to other biomolecules, means that the availability of Cu2+ ions in vivo must be carefully controlled.