Ozone induced

Ozonolysis (Section 6 19) Ozone induced cleavage of a car bon-carbon double or triple bond... 

When the films were treated in either an oxygen plasma environment or under UV/ozone irradiation, the rates of oxidation were faster for the plasma process. Irradiation of chitosan solution showed that UV/ozone induces depolymerization. In both plasma and UV/ozone reactions, the main active component for surface modification was UV irradiation at a wavelength below 360 nm [231]. 

Deborde M, S Rabouan, J-P Duguet, B Legube (2005) Kinetics of aqueous ozone induced oxidation of some endocrine disrupters. Environ Sci Technol 39 6086-6092. 

Meadows, J., Smith, R.C. and Reeves, J. (1986). Uric acid protects membranes and linolenic acid from ozone-induced oxidation. Biochem. Biophys. Res. Commun. 137, 536-541. 

Allegra, L., Moavero, N.E. and Rampoldi, C. (1991). Ozone-induced impairment of mucociliary transport and its prevention with M-acetylcysteine. Am. J. Med. 91, 67S-71S. 

Hatch, G.E., Slade, R., Crissman, K., Norwood, J. and Koren, H. (1990). Ozone-induced alterations in vitamin C concentrations in bronchoalveolat lavage fluid of humans, rats and guinea-pi. Am. Rev. Resp. Dis. 141, A253. 

Hotchkiss, J.A., Harkema, J.R. and Henderson, R.F. (1991). Effect of cumulative ozone exposure on ozone-induced nasal epithelial hyperplasia and secretory cell metaplasia in rats. Exp. Lung Res. 15, 589-600. 

Katsumata, U., Inoue, H., Miura, M., Kimura, K. and Takishima, T. (1989). Involvement of superoxide anion in ozone-induced airway hyperresponsiveness. Am. Rev. Resp. Dis. 139, A500. 

H. A. (1986). Ozone-induced change in bronchial reactivity to methacholine and airway inflammation in humans. J. Appl. Physiol. 60, 1321-1325. 

Yeadon, M. and Payne, A.N. (1989). Ozone-induced bronchial hyperreactivity to histamine and ovalbumin in sensitised guinea-p differences between intravenous and aerosol challenge. Eur. Resp. J. 2, 2995. 

Yeadon, M., Wilkinson, D. and Payne, A.N. (1990). Ozone induces bronchial hyperresponsiveness to inhaled substance P through functional inhibition of enkephalinase. Br. J. Pharmacol. 99, 191P. 

SCD Sulfur chemiluminescence detector (flame and flameless) Ozone-induced CL... 

Ozone induces CL in the oxidized hydrocarbons (RH) by disproportionation of the formed peroxyl radicals [113,120,121]. This reaction produces a carbonyl compound in the triplet state, which is the source of luminescence. 

Pendino, K J. et al., Inhibition of macrophages with gadolinium chloride abrogates ozone-induced pulmonary injury and inflammatory mediator production, Am. J. Respir. Cell Molec. Biol., 13, 125, 1995. 

Kleeberger, S.R., et al., Toll-like receptor 4 mediates ozone-induced murine lung hyperpermeability via inducible nitric oxide synthase, Am. J. Physiol. Lung. Cell. Mol. Physiol. 280, 2,L326, 2001. 

ROS are the key signaling molecules during plant response to ozone, whereas ethylene, SA, and JA function as second messengers and regulate the induction and the spread of oxidative stress symptoms. An increased ethylene and S A production promotes ozone-induced cell death, whereas JA acts as a cell-protective component and limits ozone-induced damage. " ... 

It appears that the development of tolerance is a useful tool to determine the mechanism of ozone-induced pulmonary edema. However, in the light of the findings that repeated intermittent exposures of mice to nitrogen dioxide produced less protection from the effects of a lethal dose... 

All these rapidly reacting intermediates are potentially harmful to the cell and might play a role in ozone toxicity. Furthermore, the potential for ozone-induced free-radical chain reactions exists. It appears likely that more than one radical is formed, either directly from ozone or as a result of the interaction of ozone with normal cellular constituents. 

Less is known about the interaction of ozone with other macromolecules. Alterations of nucleic acids in solution have been reported by Qiristensen and Giese, and in Escherichia coli by Prat et in studies with relatively high concentrations of ozone. Both purines and pyrimidines are attacked by ozone. However, the detailed chemistry of the reaction, including the intermediates and end products, has not been fiilly elucidated. This may be important, in view of the chromosomal effects of ozone, although such effects are most likely due to the interaction of an ozone-induced intermediate with DNA, rather than to ozone itself. 

As discussed above, ufa, which are present primarily in cellular membranes, appear to be particularly susceptible to oxidative degradation by ozone. Various studies of membrane lipid peroxidation have implicated this process in damage to organelles, including mitochondria, micro-somes, and lysosomes, as well as to the cell membrane itself. By analogy, it is conceivable that many of the findings in cells and subcellular components described in other sections of this chapter are secondary to ozone-induced lipid peroxidation. However, this remains conjectural. 

Mitochondrial swelling occurs in vitro in association with lipid peroxidation of the mitochondrial membrane. However, the biochemical concomitants of ozone-induced damage to lung mitochondria have not been extensively studied. 

As discussed in detail by Dillard et al. and by Mittman et al. the possible relationship of lysosomal proteases to chronic lung disease has been inferred from the finding of an increased incidence of emphysema in subjects deficient in serum ai>antitrypsin factor, an -globulin that can inhibit lysosomal proteases. (No effect of ozone on serum aj-antitrypsin inhibitor was noted in rabbits chronically exposed to ozone. ) Thus, an ozone-induced increase in concentrations of such enzymes in the lung might produce excess proteolysis and result in eventual chronic lung disease. However, the available evidence is inadequate to support the belief that such a process occurs in humans intermittently exposed to ozone. Further studies of this potential hazard would be of value. 

In a recent abstract, Hussain et al presented evidence that exposure of rats to ozone at 0.8 ppm for up to a week resulted in an increased rate of collagen thesis. Such a finding might be relevant to ozone-induced fibrosis. Obviously, further study of the biochemical effects of ozone on lung collagen and elastin are in order, particularly in conjunction with chronic-exposure experiments. 

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