Redox cycle

The final step of the reaction involves the transfer of two electrons from iron-sulfur clusters to coenzyme Q. Coenzyme Q is a mobile electron carrier. Its isoprenoid tail makes it highly hydrophobic, and it diffuses freely in the hydrophobic core of the inner mitochondrial membrane. As a result, it shuttles electrons from Complexes I and II to Complex III. The redox cycle of UQ is shown in Figure 21.5, and the overall scheme is shown schematically in Figure 21.6. 

Ni has a coordination sphere of 5 or 6 mixed S-, N-, 0-donors and is believed to undergo redox cycling between III, II and I oxidation states. 

Scheme 10.16 Redox cycle of flavins. The cycle is depicted with a two-electron reduction of flavin by NAD(P)H and two one-electron oxidations.

A redox cycle involving the ferric-ferrous couple may be the key mechanism in combustion catalysis by iron compounds. 

The annual cycle depicted in Figure 3 could, therefore, be due to a redox cycle whose kinetics are controlled by pH, decay processes in the sediment, and temperature. 

The shallow nature of Pond 3513 makes chemical processes occurring In the sediment extremely Important. More work will be needed, however, to elucidate the redox cycle. 

Similar disproportionation is likely to occur during catalytic hydrocarbon oxidation since the Bl2Mo20g catalyst is subjected to continuous redox cycling under such conditions. Therefore, any kinetic or catalytic information about Bi2Mo20n is suspect unless the absence of surface restructuring can be confirmed. 

The difference in catalytic activity between the La- and the Ba-based hexa-aluminates results from the following reasons the first difference is the valence of cation in the mirror pleuie between tri-valent lanthanum ion and di-valent barium ion. The second is the crystal structure between magnetoplumbite and P-alumina, which are different in the coordination of ions and concentration of Frenkel-type defect in mirror plane. The redox cycle of transition metal in hexa-aluminate lattice, which closely related with catalytic activity, is affected sensitively with these two factors. 

Transition metal oxides represent a prominent class of partial oxidation catalysts [1-3]. Nevertheless, materials belonging to this class are also active in catalytic combustion. Total oxidation processes for environmental protection are mostly carried out industriaUy on the much more expensive noble metal-based catalysts [4]. Total oxidation is directly related to partial oxidation, athough opposes to it. Thus, investigations on the mechanism of catalytic combustion by transition metal oxides can be useful both to avoid it in partial oxidation and to develop new cheaper materials for catalytic combustion processes. However, although some aspects of the selective oxidation mechanisms appear to be rather established, like the involvement of lattice catalyst oxygen (nucleophilic oxygen) in Mars-van Krevelen type redox cycles [5], others are still uncompletely clarified. Even less is known on the mechanism of total oxidation over transition metal oxides [1-4,6]. 

The effect of prolonged antioxidant therapy in relation to normal physiological processes (for example, redox cycling, cell-cell signalling, transcription factor activation) must be assessed. It is conceivable that the overload of one antioxidant by dietary supplementation (for example, a-tocopherol) may shift the levels of other antioxidants (for example, by decreasing ascorbate and /3-carotene concentrations), with unknown consequences. To assess the potential for lipid-soluble antioxidant treatment in inflammatory diseases such as RA, further investigations into these questions will be needed. 

Hard, S. and Kanner, J. (1989). Haemoglobin and myoglobin as inhibitors of hydroxyl radical generation in a model system of iron redox cycle. Free Rad. Res. Commun, 6, 1-10. 

Hiraishi, H., Razandi, M., Terano, A. and Ivey, K.J. (1990). Antioxidant defenses of culture gastric mucosal cells against toxic oxygen metabolites. Role of glutathione redox cycle and endogenous catalase. Gastroenterology 98, A544. 

Elevated O2 concentrations Exposure to activated phagocytic cells Exposure to redox cycling drugs (e.g. alloxan, paraquat, menadione)... 

Kass, G.E., Duddy, S.K. and Orrenius, S. (1989). Activation of hepatocyte protein kinase C by redox-cycling quinones. Biochem. J. 260, 499-507. 

Roy, D, Floyd, R.A. and Liehr, J.G. (1991). Elevated 8-hydroxy-deoxy anosine levels in DNA of diethylstilbcstrol-treated Syrian hamsters covalent DNA damage by free radicals generated by redox cycling of diethyl-stilbestrol. Cancer Res. 51, 3882-3885. 

Nitric Oxide Synthase 266 4.5 Iron Redox Cycle Modifiers 272... 

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