Oxygen-based free radicals

It therefore appears that for at least domains 4 and 6, hCP possesses metal binding sites in addition to the six integral copper atoms. Binding of ferrous iron at these sites could result in its oxidation and its removal from the plasma or in the reduction of oxygen-based free radicals. Binding of copper could result in its transport through the plasma (vide infra). 

ROS include oxygen-based free radicals such as superoxide, hydroxyl, alkoxyl, peroxyl, and hydroperoxyl (Table 1). Other ROS, such as hydrogen peroxide and lipid peroxides, can be converted into free radicals by transition... 

Iron toxicity is not a common problem in farm animals, but it can result from prolonged oral administration of the element. Ferrous ions are reported to generate oxygen-based free radicals, contributing to oxidative stress in the cell (see Chapter 5). Normally iron is protein-bound or in chemical form, which prevents it from causing oxidation. Chronic iron toxicity results in alimentary disturbances, reduced growth and phosphorus deficiency. 

In using the sulphur-containing compounds in this overview as antioxidants, it must be borne in mind that in the course of their inhibition of the oxidation process they are simultaneously attacked by oxygen-based free radicals and other products that form during the oxidation of hydrocarbons. As a result, the activity of the antioxidants in the decomposition of hydroperoxides change with time, an example of complex kinetics, one theme of this volume. 

Mediators of both the infiammatoiy and fibrotic responses have been associated with exposure to oxidants. Similarly, mediator release after incubation of cells with silica and asbestos can be the result of oxygen-based free radicals catalyzed by iron associated with the mineral oxide (Fig. 1). The increase in arachidonic acid metabolism after exposures of cells to particles and fibers can result from the eooxidation of arachidonate by metal-catalyzed oxidants. This is a lipid peroxidation that can be mediated by free radical production by the dust (83). In support of an association between metal-catalyzed oxidant generation and arachidonic acid products, the release of LTB4 by alveolar macrophages can increase with the eoneentrations of iron complexed to the surface of silica and asbestos (84). Similarly, the eellular release of eytokines postulated to participate in the infiammatory and fibrotic responses ean be associated with exposures to metal-dependent radicals (see Fig. 1). TNF-a produetion by alveolar macrophages after mineral oxide exposure can be inhibited by both the metal chelator deferoxamine and hydroxyl radical scavengers (74). The release of other cytokines pertinent to silica and asbestos exposure ean also be responsive to oxidative stress (85,86). The release of these pertinent mediators after dust exposures is likely to be controlled by oxidant-sensitive promoters such as nuclear factor (NF)-kB (87). After exposure to silica and asbestos, NF-kB can function as a promoter... 

A more detailed discussion of the role of IRPs in pathobiology, particularly the effects of oxygen and nitrogen-based free radicals on their activities is presented in Chapter 10. For a recent review see Cairo and Pietrangelo, (2000). 

Based on these new evidences and the results published from other laboratories, the reaction mechanism of 1 and ferrous ion was revised so that this reaction proceeded through short-lived oxygen-centered free radicals and then... 

Oxygen-derived free radicals are also a major source of DNA damage. Approximately 20 types of oxidatively altered DNA molecules have been identified. The nonspecific binding of Fe to DNA facilitates localized production of the hydroxyl radical, which can cause base alterations in the DNA (Fig. 24.9). It also can attack the deoxyribose backbone and cause strand breaks. This DNA damage can be repaired to some extent by the cell (see Chapter 12), or minimized by apoptosis of the cell. 

Another proposed consequence of the mechanism—based on the depletion of GSH following mustard exposure—is lipid peroxidation.52,53 According to this hypothesis, depletion of GSH allows the formation of oxygen-derived free radicals. The oxidizing compounds thus formed will react with membrane phospholipids to form lipid peroxides that could, in turn, lead to membrane alterations, changes in membrane fluidity, and eventual breakdown of cellular membranes. 

Hu and coworker developed the silica, titania, ceria, and y-alumina supported vanadium catalyst, which shown unique reactivity for the direct amination of toluene with hydroxylamine hydrochloride, over 50 % total yield of toluidines was obtained on the y-alumina supported vanadium catalyst operated at optimal conditions [87]. They also investigated a sodium metavanadate catalyzed one-step amination of benzene to aniline with hydroxylamine [88], The reaction became more efficient in the presence of oxygen. A free-radical mechanism was proposed based on the results of EPR, NMR, and UV-Vis characterization. Moreover, the catalytic activity of a series of vanadium complexes with N,0- or 0,0-ligands for the liquid-phase direct amination of benzene with hydroxylamine to aniline has been investigated [89]. [VO(OAc>2] was proved to be the most active catalyst for the amination because of its relatively greater electrophilicity and smaller steric hindrance of ligand. 

Both solvent-iaduced swelling and oxygen inhibition ate characteristic of all cross-linking negative resists based on free-radical chemistry. 

Some inorganic fillers are used as flame retardants in rubber base formulations. Flame retardants act in two ways (1) limiting or reducing access of oxygen to the combustion zone (2) reacting with free radicals (especially HO ), thus acting as terminator for combustion-propagation reaction. The additives most widely used as flame retardants for polymers are antimony oxides and alumina trihydrate. 

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