Damage oxides

The titanium oxide film consists of mtile or anatase (31) and is typically 250-A thick. It is insoluble, repairable, and nonporous in many chemical media and provides excellent corrosion resistance. The oxide is fully stable in aqueous environments over a range of pH, from highly oxidizing to mildly reducing. However, when this oxide film is broken, the corrosion rate is very rapid. Usually the presence of a small amount of water is sufficient to repair the damaged oxide film. In a seawater solution, this film is maintained in the passive region from ca 0.2 to 10 V versus the saturated calomel electrode (32,33). 

Field Observations Canadian workers using ambient oxidant dose have correlated meteorologic variables with plant injury.A correlation was discovered when an empirical relationship involving evapotrans-piration (the coefficient of evaporation) was developed and used to modify the dose information. This empirical relationship has been used on a limited basis to predict damaging oxidant concentrations from monitored meteorologic conditions. 

H. Bernstein, C. M. Payne, C. Bernstein, J. Schneider, S. E. Beard and C. L. Crowley, Activation of the promoters of genes associated with DNA damage, oxidative stress, ER stress and protein malfolding by the bile salt, deoxycholate, Toxicol. Lett., 1999, 108(1), 37. 

One difference between the peroxisomal and mitochondrial pathways is in the chemistry of the first step. In peroxisomes, the flavoprotein acyl-CoA oxidase that introduces the double bond passes electrons directly to 02, producing H202 (Fig. 17-13). This strong and potentially damaging oxidant is immediately cleaved to H20 and 02 by catalase. Recall that in mitochondria, the electrons removed in the first oxidation step pass through the respiratory chain to 02 to produce H20, and this process is accompanied by ATP synthesis. In peroxisomes, the energy released in the first oxidative step of fatty acid breakdown is not conserved as ATP, but is dissipated as heat. 

Antioxidant nutrients are believed to slow the progression of arteriosclerosis because of their ability to inhibit the damaging oxidative processes... 

Culmsee C, Bondada S, Mattson MP. 2001. Hippocampal neurons of mice deficient in DNA-dependent protein kinase exhibit increased vulnerability to DNA damage, oxidative stress and excitotoxicity. Mol Brain Res 87 ... 

Tirapazamine (21, Scheme 9) is a benzotriazine di-iV-oxide bioreductive anticancer prodrug. Tirapazamine is activated to a DNA-damaging oxidizing radical by cytochrome P450 reductase and other one-electron reductases in the absence of oxygen.38,39 Tirapazamine has been demonstrated to be effective in killing... 

The mitochondria have emerged as a central component of the intrinsic apoptotic signaling pathways and are now known to control apoptosis via the release of apopto-genic proteins (Fig.15.8). The apoptotic signals that are channeled through the mitochondrial pathway of apoptosis include various stresses like DNA damage, oxidative stress, UV radiation, protein kinase inhibition, and growth factor deprivation. 

There are also other avenues by which -NO may serve a protective role in ischemia-reperfusion phenomena. Under these circumstances, known to include a high rate of production of oxygen free radicals, -NO can react with Oi to divert Oi through ONOO -dependent (and potentially less damaging) oxidative and decomposition pathways. Nitric oxide may also confer protection by reacting with iron to form iron-nitrosyl compounds. By binding free coordination sites of iron, -NO can limit Fenton chemistry and iron-dependent electron transfer reactions (Kanner etal., 1991 Ignarro,... 

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