Peroxides and hydroxylation

Bachowski GJ, Girotti AW (1988) Light-stimulated formation of hydrogen peroxide and hydroxyl radical in the presence of uroporphyrin and ascorbate. Free Radic Biol Med 5 3-6... 

Herz, H., Blake, D.R and Grootveld, M. (1994). Multicomponent investigations of the hydrogen peroxide- and hydroxyl radical-scavenging antioxidant capacities of biofluids the roles of endogenous pyruvate and lactate. Free Rad. Res. Commun. (in press). 

Smith, C., Mitchinson, M.J., Amoma, O. and Halliwell, B. (1992). Stimulation of lipid peroxidation and hydroxyl radical generation by the contents of human atherosclerotic lessions. Biochem. J. 286, 901-905. 

Nitrosoarenes are readily formed by the oxidation of primary N-hydroxy arylamines and several mechanisms appear to be involved. These include 1) the metal-catalyzed oxidation/reduction to nitrosoarenes, azoxyarenes and arylamines (144) 2) the 02-dependent, metal-catalyzed oxidation to nitrosoarenes (145) 3) the 02-dependent, hemoglobin-mediated co-oxidation to nitrosoarenes and methe-moglobin (146) and 4) the 0 2-dependent conversion of N-hydroxy arylamines to nitrosoarenes, nitrosophenols and nitroarenes (147,148). Each of these processes can involve intermediate nitroxide radicals, superoxide anion radicals, hydrogen peroxide and hydroxyl radicals, all of which have been observed in model systems (149,151). Although these radicals are electrophilic and have been suggested to result in DNA damage (151,152), a causal relationship has not yet been established. Nitrosoarenes, on the other hand, are readily formed in in vitro metabolic incubations (2,153) and have been shown to react covalently with lipids (154), proteins (28,155) and GSH (17,156-159). Nitrosoarenes are also readily reduced to N-hydroxy arylamines by ascorbic acid (17,160) and by reduced pyridine nucleotides (9,161). 

In 1977, Kellogg and Fridovich [28] showed that superoxide produced by the XO-acetaldehyde system initiated the oxidation of liposomes and hemolysis of erythrocytes. Lipid peroxidation was inhibited by SOD and catalase but not the hydroxyl radical scavenger mannitol. Gutteridge et al. [29] showed that the superoxide-generating system (aldehyde-XO) oxidized lipid micelles and decomposed deoxyribose. Superoxide and iron ions are apparently involved in the NADPH-dependent lipid peroxidation in human placental mitochondria [30], Ohyashiki and Nunomura [31] have found that the ferric ion-dependent lipid peroxidation of phospholipid liposomes was enhanced under acidic conditions (from pH 7.4 to 5.5). This reaction was inhibited by SOD, catalase, and hydroxyl radical scavengers. Ohyashiki and Nunomura suggested that superoxide, hydrogen peroxide, and hydroxyl radicals participate in the initiation of liposome oxidation. It has also been shown [32] that SOD inhibited the chain oxidation of methyl linoleate (but not methyl oleate) in phosphate buffer. 

In addition, superoxide, hydrogen peroxide and hydroxyl radicals can be interconverted via the so-called Haber-Weiss reaction ... 

Buettner, G. R., and Need, M. J., 1985, Hydrogen peroxide and hydroxyl free radical... 

Procarbazine (Matulane) may autooxidize spontaneously, and during this reaction hydrogen peroxide and hydroxyl free radicals are generated. These highly reactive products may degrade DNA and serve as one mechanism of procarbazine-induced cytotoxicity. Cell toxicity also may be the result of a transmethylation reaction that can occur between the A-methyl group of procarbazine and the N7 position of guanine. 

Kinins, neuropeptides, and histamine are also released at the site of tissue injury, as are complement components, cytokines, and other products of leukocytes and platelets. Stimulation of the neutrophil membranes produces oxygen-derived free radicals. Superoxide anion is formed by the reduction of molecular oxygen, which may stimulate the production of other reactive molecules such as hydrogen peroxide and hydroxyl radicals. The interaction of these substances with arachidonic acid results in the generation of chemotactic substances, thus perpetuating the inflammatory process. 

Oxygen Structural atom of water and most organic molecules in biological systems required for respiration by most organisms. Induces convulsions at high Pojl very toxic as ozone, superoxide, peroxide, and hydroxyl radicals/ ... 

Ozgova S, Hermanek J, Gut I. 2003. Different antioxidant effects of polyphenols on lipid peroxidation and hydroxyl radicals in the NADPH-, Fe-ascorbate- and Fe-microsomal systems. Biochem Pharmacol 66 1127-1237. 

In the parameter G, all factors are incorporated from the right-hand part of Equation4.55, except for the bulk concentrations of hydrogen peroxide and hydroxyl ions. With E = 0.45 V vs. SCE, the parameter is defined as G. ... 

This book does not follow a chronological sequence but rather builds up in a hierarchy of complexity. Some basic principles of 51V NMR spectroscopy are discussed this is followed by a description of the self-condensation reactions of vanadate itself. The reactions with simple monodentate ligands are then described, and this proceeds to more complicated systems such as diols, -hydroxy acids, amino acids, peptides, and so on. Aspects of this sequence are later revisited but with interest now directed toward the influence of ligand electronic properties on coordination and reactivity. The influences of ligands, particularly those of hydrogen peroxide and hydroxyl amine, on heteroligand reactivity are compared and contrasted. There is a brief discussion of the vanadium-dependent haloperoxidases and model systems. There is also some discussion of vanadium in the environment and of some technological applications. Because vanadium pollution is inextricably linked to vanadium(V) chemistry, some discussion of vanadium as a pollutant is provided. This book provides only a very brief discussion of vanadium oxidation states other than V(V) and also does not discuss vanadium redox activity, except in a peripheral manner where required. It does, however, briefly cover the catalytic reactions of peroxovanadates and haloperoxidases model compounds. 

Fig. 8-3. Reduction of oxygen by a one-electron transfer mechanism. Each of the four reaction steps involves addition of one electron and one proton, giving rise to peroxy radicals, hydrogen peroxide, and hydroxyl radicals as intermediate products (a). The crifresponding organic species are formed when oxygen reacts with organic radicals R- (b).

Fig. 2.7. The sequential reduction of oxygen via superoxide radical, peroxide and hydroxyl radical to water.

It should be noted that when the 0-0 bond is broken, the O2 molecule bound at Fe + receives four electron equivalents and yields a water molecule and an oxide on Fe +, at least, formally. The stable oxygenated form and the unstable peroxide intermediate provide the four-electron reduction of O2 at once. As is well known, if an O2 molecule receives four electrons one at a time, three active oxygen species, superoxide, peroxide, and hydroxyl radical, will be produced during the O2 reduction. Cytochrome c oxidase must reduce O2 totally without releasing these species, which are extremely toxic to the cell. The four-electron reduction of this enzyme may be the strategy of this enzyme for safe O2 reduction (without damaging cells). 

Several groups have obtained data Indicating that changes In calcium flux from ellcitor-treated plant cells may serve as a second messenger in phytoalexin Initiation (77-80). The altered calcium flux may In turn be caused by rapid depolarizatlon/polarizatlon and redox perturbation of the plant cell membrane (56 81-85). For Instance, production of superoxide anion, hydrogen peroxide and hydroxyl radicals have been observed In plant tissues undergoing hypersensitive reactions (86-89). 

Formation of hydrogen peroxide and hydroxyl radical from excess of SAR being not neutralized by SOD... 

The uptake of aminoglycosides into proximal renal tubular epithelial cells is limited to the luminal cell border and is saturable. Less frequent administration of doses larger than needed for saturation of this uptake may therefore reduce drug accumulation in the renal cortex (98). In vitro and in vivo data have provided evidence that partially reduced oxygen metabolites (superoxide anion, hydrogen peroxide, and hydroxyl radical), which are generated by renal cortical mitochondria, are important mediators of aminoglycoside-induced acute renal insufficiency (99). 

Doroshow JH Role of Hydrogen Peroxide and Hydroxyl Radical Formation in the Killing of Ehrlich Tumor Cells by Anticancer Quinones. Proc. Natl. Acad. Sci. USA 986 83(12) 4514-8. 

Eilin PJ, Strulowitz JA, Wolin MS, et al Absence of a Role for Superoxide Anion, Hydrogen Peroxide and Hydroxyl Radical in Endothelium-mediated Relaxation of Rabbit Aorta. Blood Vessels 1985 22 (2) 65-73. 

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