Hydroxyl radical asbestos

Colquhoun and Schumacher [98] have shown that y-linolcnic acid and eicosapentaenoic acid, which inhibit Walker tumor growth in vivo, decreased proliferation and apoptotic index in these cells. Development of apoptosis was characterized by the enhancement of the formation of reactive oxygen species and products of lipid peroxidation and was accompanied by a decrease in the activities of mitochondrial complexes I, III, and IV, and the release of cytochrome c and caspase 3-like activation of DNA fragmentation. Earlier, a similar apoptotic mechanism of antitumor activity has been shown for the flavonoid quercetin [99], Kamp et al. [100] suggested that the asbestos-induced apoptosis in alveolar epithelial cells was mediated by iron-derived oxygen species, although authors did not hypothesize about the nature of these species (hydroxyl radicals, hydrogen peroxide, or iron complexes ). 

Jackson JH, Schraufstatter lU, Hyslop PA, et al. 1987. Role of oxidants in DNA damage Hydroxyl radical mediates the synergistic DNA damaging effects of asbestos and cigarette smoke. J Clin Invest 80 1090-1095. 

Schapira RM, Ohio AJ, Efifos RM, et al. 1994. Hydroxyl radicals are formed in the rat lung after asbestos instillation in vivo. Am J Resp Cell Mol Biol 10 573-579. 

In tracheal explants, the basal level of amosite asbestos uptake can be decreased by adding catalase, a scavenger of hydrogen peroxide, to the dust suspension, or by preincubating the dust with the iron chelator, deferoxamine (124), a chelator that prevents the reaction of iron with hydrogen peroxide to form a hydroxyl radical (6). The decreases in particle uptake are scavenger-chelator dose-dependent, but uptake cannot be reduced below about one-third to one-half the basal level (124). Conversely, uptake can be increased if amosite asbestos or titanium dioxide particles are preincubated with iron salt solutions to increase surface iron before they are applied to the explants (125). 

Fenton reaction. Therefore, iron complexed to the surface of silica and asbestos can catalyze a generation of the hydroxyl radical ... 

Emission source and ambient air pollution particles catalyze production of oxidants including the hydroxyl radical (3,4). This production of free radicals correlates with the concentrations of transition metals. As with silica and asbestos, it is likely that anthropogenic particles can present an oxidative stress to a living system with their exposure. 

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... 

Weitzman, S.A. and Graceffii, P. (1984). Asbestos catalyzes hydroxyl and superoxide radical generation from hydrogen peroxide. Arch. Biochem. Biophys. 228, 373-376. 

Recent reports show unexpected information on the role of free radicals in the health effects of nanotubes currently employed in many industries.31 Unlike asbestos and most toxic particles, nanotubes do not release but blunt free radicals, which are considered one of the features imparting toxicity to particulates. Multi-wall carbon nanotubes (MWCN) in aqueous suspension do not generate oxygen or carbon centered free radicals detectable with the spintrapping technique. Conversely, when in contact with an external source of hydroxyl (HO) or superoxide radicals (CL h MWCN exhibit a remarkable radical scavenging capacity (Figure 3). It is therefore possible that the inflammatory reaction reported in vivo should be ascribed to MWCN features other than particle derived free radical generation. 

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