Steric effects in Free Radical Chemistry


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Introduction

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Introduction

Learn more Check out. Abstract The relative importance of bond strength, steric effects, and polarity in determining the rate and orientation of free radical subsitution and free radical addition reaction is considered.

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Radicals and Radical Reactions Lecture notes. Substitution Reaction Free radical substitution mechanism. Understanding Chemistry, UK. Free Radicals Basic information on free radicals an their reactions. Steric effects in free radical chemistry Dissertation, By and large the best evidence for an increased susceptibility to oxidative injury comes from studies in zinc-deprived animals; these studies have demonstrated either increased free radical production or enhanced injury from exposure to an oxidative stress. Because this topic has recently been extensively reviewed, I opted to present this material in tabular form Table 1.

These studies clearly show that zinc deficiency can render an animal more sensitive to an oxidative stress. However, because the mechanism of the observed effect is not clear, it is difficult on the basis of these studies to conclude that zinc is an antioxidant.

The acute antioxidant effects of zinc are generally manifested in the presence of a demonstrable short-term increase in levels of this metal. One of the acute effects of zinc is an apparent stabilization of sulfhydryls, i. Detailed studies have shown that 8 mol of zinc is bound per 1 mol of octamer and that the amount of bound zinc closely correlates with enzyme activity. The protective effect of zinc was suggested to be due to maintenance of an essential sulfhydryl group group I secondary to decreased reactivity Gibbs et al.

Gibbs et al. There are numerous other examples of thiol-dependent enzymes and proteins containing thiol groups protected by zinc Table 2 last reviewed in Bray and Bettger Although in general, these mechanisms can be applied to any protein or peptide containing a sulfhydryl group, not all zinc-binding sulfhydryl groups can be protected from oxidation; an important example is zinc-metallothionein, in which sulfhydryl oxidation results in loss of the metal Fliss and Menard , Maret Several redox-active metals, including iron and copper Ambrosio et al.

Reaction 2 is commonly known as the Haber-Weiss reaction and is relatively slow. It has been suggested Haber and Weiss that trace amounts of soluble iron or copper in the presence of reducing agents AH 2 , such as ascorbate, can catalyze the formation of hydroxyl radical from superoxide via the metal-catalyzed Haber-Weiss reaction Fenton reaction reaction 6. Transition metals, like iron and copper, tend to undergo hydrolytic polymerization and precipitation in aqueous media at neutral pH Spiro et al.

It has been inferred that these metals can remain in solution in physiological media only by association with some high- or low-molecular-weight cellular components, such as nucleotides, peptides, polypeptides, proteins or DNA Chevion , Chvapil et al. Intracellular free iron is more likely to associate with low-molecular-weight ligands, such as nucleotides, citrate, glycine and glucose Halliwell and Gutteridge , whereas copper is more likely to associate with macromolecular structures, such as DNA, carbohydrates, enzymes, peptides and proteins Bhat and Hadi , Creeth et al.

Once complexed at one of these sites, movement of the metal is hindered, and the association site can now serve as a locus for repetitive free radical formation through repeated redox cycling of the metal. An excellent review on the subject of site specificity can be found in Chevion Numerous studies have demonstrated that both copper and iron play a critical role in the initiation and propagation of lipid peroxidation Fig.

This can initiate a propagative cascade of cyclical reactions, leading eventually to the repetitive formation of short-chain alkanes and lipid acid aldehydes, resulting in the destruction of lipid bilayers Kappus Another possible site of attack can include proteins. The hydroxy radical can then abstract a hydrogen from the amino-bearing carbon, leading to the formation of a carbon-centered protein radical that undergoes a series of reactions, resulting in hydrolysis of the amino group and the formation of an aldehyde or a protein carbonyl.

Once the amino group is hydrolyzed, the metal-binding site is disrupted, leading to dissociation of the metal.

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Because the oxidative modifications occur around the metal-binding site, the process of protein oxidation is clearly an example of site-specific reaction. An excellent review on the process of protein oxidation can be found in Stadtman The net result would be to displace the metal into the cytosolic compartment, where it can undergo hydrolytic polymerization and precipitation as unreactive polynuclear structures Eguchi and Saltman , Spiro et al. By virtue of similarities in coordination chemistry Cotton and Wilkinson , it has been proposed that zinc can compete with copper or iron for certain types of binding sites.

Since then, the antagonism has been characterized and shown to be competitive in nature. In a rather elegant study, Korbashi et al. There have been several other studies demonstrating similar phenomenon; these are summarized in Table 3. It was these earlier studies that provided the rationale for subsequent studies that examined the ability of zinc to attenuate cellular injury that might have a component of site-specific oxidative injury.

Antagonism of free radical formation in chemical, biochemical and cellular systems by zinc. The earliest reports to demonstrate possible antioxidant effects of zinc on oxidative tissue damage were related to catecholamine-induced myocardial injury, a process thought to involve the production of free radical intermediates Persoon-Rothert et al.

In vitro and in vivo studies demonstrated that zinc has an inhibitory effect on isoproteronol-induced cardiac oxidative injury Persoon-Rothert et al. Since then, we have published a series of studies describing the cardioprotective effects of zinc-bishistidinate in several in vitro and in vivo models of cardiac ischemic injury Table 4. There is substantial evidence documenting the presence of various reactive oxygen intermediates in tissue, blood or perfusates from postischemic organs Arroyo et al.

This topic has been the subject of many extensive reviews and is not discussed here Bulkley , Lucchesi and Mullane , Parks et al. Our studies were among the first to demonstrate the potential usefulness of zinc to attenuate ischemic and postischemic injury. Since then, there have been numerous studies demonstrating this property in a variety of ischemic tissues Table 5.

What should be apparent from this list is that investigators have tried different complexes of zinc, ranging from the simple chloride salt Matsushita et al. Although there have been claims that one complex is superior to another, unless one can demonstrate an additional effect chemical or therapeutic of the complexing agent, in all likelihood it plays little if any role in the overall protective effect other than acting as a delivery vehicle.

The fact remains that the one component that is common to all of these studies is the presence of the zinc.

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Whether any of these complexes eventually find their way into clinical usage remains to be seen but certainly should be the topic of additional studies. Virtually all of the evidence demonstrating that the attenuation of ischemic injury by zinc involves the inhibition of transition metal—mediated site-specific oxidative injury is derived from studies by our group. As part of this study, prolonged perfusion of isolated hearts with buffer containing zinc was shown to significantly decrease cardiac copper content.

More recent studies Powell et al. The involvement of site-directed phenomena in this process can be inferred by the observation that zinc also decreased protein oxidation in these ischemic hearts Powell et al. Although hesitant to imply that the complex that we use is different from all others that have been examined, the bishistidinate complex does have some unique chemical properties. With respect to copper, the formation constant of the histidinate complex of zinc is lower than that of the histidinate complex of copper The occurrence of this process is in fact suggested by the presence of increased excretion of copper from isolated hearts in the presence of zinc.

The production of oxidative species is a normal part of cellular respiration.


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Normally the cell has no difficulties with these species, is not harmed by them and may even use them to accomplish the myriad of reactions in normal metabolism. Problems only arise when the flux of oxidants becomes too great for the cellular antioxidant defense mechanisms to detoxify or when something happens to that system so it is insufficient to accomplish its normal functions. It is now apparent that oxidative injury is a component of many pathological states and that increasingly the involvement of site-directed modifications of proteins, lipids and DNA in oxidative injury is being implicated in these injurious processes.

Considering the role of redox-active transition metals in these processes, one must question whether a normal function of zinc is to modulate the reactivity of these metals. Studies from our group and others have clearly demonstrated the ability of zinc to antagonize transition metal—mediated oxidations and transfer of electrons under normal and pathologic conditions. Moreover, we and others have demonstrated that zinc is capable of inhibiting the process of protein oxidation. We now know that a protein that has been oxidatively modified is an aberrant protein and is subject to rapid destruction by a variety of intracellular proteolytic systems, including, but not limited to, the ubiquitinS proteasome for reviews, see Davies and Goldberg It has been proposed that one pathway to cellular injury and destruction is overactivation of these proteolytic systems.

Thus, the usefulness of any substance that can interfere with the initiating steps in this process becomes clear and is worthy of further study. In light of recent studies linking proteasome activation to apoptosis mediated by caspases for a review, see Thornberry and Lazebnik , research into the ability of zinc to inhibit these processes deserves more attention, particularly since zinc has been shown to be an antiapoptotic agent for a review, see Zalewski et al. Only by understanding the basic mechanisms by which zinc can exert its antioxidant properties will we be able to devise rational uses for this metal as an intervention not only in ischemic damage but also in other forms of oxidative injury.

I wish to thank Ellen Gurzenda for her assistance in the preparation of this manuscript as well as for the performance of some of the described studies. Oxford University Press is a department of the University of Oxford.

Organic Chemistry - Reagents, Field Effects, Stability, Bond Cleavage

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Article Navigation. Close mobile search navigation Article Navigation. Volume Article Contents. General Mechanisms. Attenuation of tissue and organ oxidative injury by acute administration of zinc.

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Future directions. Oxford Academic. Google Scholar. Cite Citation. Permissions Icon Permissions. TABLE 1. Effect of zinc deficiency on production of oxidative injury or species. Open in new tab. Open in new tab Download slide. TABLE 2. Potential mechanism for zinc as an inhibitor of site directed reactions. TABLE 3. TABLE 4. TABLE 5. Afanas et al Search ADS. Aiuto and Powell Characterization of the anti-arrhythmic effect of the trace element, zinc, and its potential relationship to inhibition of oxidative stress.

Ambrosio et al Improvement of postischemic myocardial function and metabolism induced by administration of deferoxamine at the time of reflow: the role of iron in the pathogenesis of reperfusion injury. Anderson and Desnick Purification and properties of delta-amino-levulinate dehydratase from human ernythrocytes. Angel et al a.

Angel et al b. Deferoxamine increases skin flap survival: additional evidence of free radical involvement in ischaemic flap surgery. Arroyo et al Ashmead et al Google Preview. Bagchi et al Comparative in vitro oxygen radical scavenging ability of zinc methionine and selected zinc salts and antioxidants. Bernhard et al Cadmium binding and metal cluster formation in metallothionein: a differential modification study. Bhat and Hadi DNA breakage by tannic acid and Cu II : sequence specificity of the reaction and involvement of active oxygen species. Bolli et al Direct evidence that oxygen-derived free radicals contribute to postischemic myocardial dysfunction in the intact dog.

Bray and Bettger Bray et al Effect of dietary zinc on endogenous free radical production in rat lung microsomes. Bulkley Burke and Fenton Effect of a zinc-deficient diet on lipid peroxidation in liver and tumor subcellular membranes. Chevion

Steric effects in Free Radical Chemistry Steric effects in Free Radical Chemistry
Steric effects in Free Radical Chemistry Steric effects in Free Radical Chemistry
Steric effects in Free Radical Chemistry Steric effects in Free Radical Chemistry
Steric effects in Free Radical Chemistry Steric effects in Free Radical Chemistry
Steric effects in Free Radical Chemistry Steric effects in Free Radical Chemistry
Steric effects in Free Radical Chemistry Steric effects in Free Radical Chemistry
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Steric effects in Free Radical Chemistry Steric effects in Free Radical Chemistry
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