Hydrogen redox cycles

A combination of cat. Ybt and A1 is effective for the photo-induced catalytic hydrogenative debromination of alkyl bromide (Scheme 28) [69]. The ytterbium catalyst forms a reversible redox cycle in the presence of Al. In both vanadium- and ytterbium-catalyzed reactions, the multi-component redox systems are achieved by an appropriate combination of a catalyst and a co-reductant as described in the pinacol coupling, which is mostly dependent on their redox potentials. 

Iron chelators can also be used to selectively bind iron in areas where oxidative stress is observed, thereby preventing the iron from taking part in Fenton reactions without interfering with normal iron homeostasis. Charkoudian et al. have developed boronic acid and boronic ester masked prochelators, which do not bind metals unless exposed to hydrogen peroxide (237,238). The binding of these chelators to iron(III) prevents redox cycling. Similar studies of these systems have been performed by a separate group (239,240). 

In accord with this mechanism, free peroxyl radical of the reaction product hydroperoxide activates the inactive ferrous form of enzyme (Reaction (1)). Then, active ferric enzyme oxidizes substrate to form a bound substrate radical, which reacts with dioxygen (Reaction (4)). The bound peroxyl radical may again oxidize ferrous enzyme, completing redox cycling, or dissociate and abstract a hydrogen atom from substrate (Reaction (6)). 

The bound peroxyl radical may again oxidize ferrous enzyme, completing redox cycling, or dissociate and abstract a hydrogen atom from substrate (Reaction (6)). 

The production of active oxygen species may lead to a cycle of oxidation and reduction (redox cycle) with electrons being donated to oxygen to yield superoxide. This is the case with paraquat and also a number of cytotoxic quinones. Thus, there is a cyclic process, which produces superoxide by adding electrons from paraquat (see chap. 7) or a semiquinone, for example, to oxygen (Fig. 6.10). The superoxide produced may then be metabolized to hydrogen peroxide by superoxide dismutase, which is further metabolized to water by catalase (Fig. 6.10). 

Depletion of other cofactors such as UTP, NADH, and NADPH may also be involved in cell injury either directly or indirectly. Thus, the role of NADPH in maintaining reduced GSH levels means that excessive GSH oxidation such as caused by certain quinines, which undergo redox cycling, may in turn cause NADPH depletion (see below). Alternatively, NADPH may be oxidized if it donates electrons to the foreign compound directly. However, NADPH may be regenerated by inter conversion of NAD+ to NADP+. Some quinones such as menadione, l,2-dibromo-3-chloropropane (DBCP), and hydrogen peroxide also cause depletion of NAD, but probably by different mechanisms. Thus, with menadione, the depletion may be the result of... 

Several mechanistic proposals have been advanced, ranging from metal catalysis to redox cycles with Pd clusters or isolated Pd/PdO species (325-327). It is fair to assume that activation of ethylene occurs by hydrogen abstraction by palladium clusters, whereas H abstraction from acetic acid occurs on PdO (oxidized clusters) ... 

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