Hydroxyl from Fenton reaction

Lopes GKB, Schulman FIM, Flermes-Lima M. Polyphenol tannic acid inhibits hydroxyl radical formation from Fenton reaction by complexing ferrous ions. Biochim Biophys Acta 1999 1472 142-152. 

Halliwell et al. (55) have described a model that uses hydroxyl radicals generated from Fenton reaction to degrade 2-deoxy-D-ribose. The decomposed products of deoxyribose are 2-thiobarbituric acid-reactive substances (TEARS). If the antioxidant present in the system scavenges hydroxyl radicals generated, deoxyribose is protected and the amount of TEARS produced is less. 

Hydroxyl radical was generated from Fenton reaction with the mixing of FeSO (2.27 iM) and H2O2 (227 iM). Superoxide radical was generated from a hypoxanthine-xanthine oxidase (HPX-XOD) reaction system. Both hydroxyl radical and superoxide were trapped by 5,5-dimethyl-1-pyrroline-l-oxide (DMPO). 

Humans Hydrogen peroxide has been used as an enema or as a cleaning agent for endoscopes and may cause mucosal damage when applied to the surface of the gut wall. Hydrogen peroxide enteritis can mimic an acute ulcerative, ischaemic or pseudomembranous colitis, and ranges from a reversible, clinically inapparent process to an acute, toxic fulminant colitis associated with perforation and death (Bilotta and Waye, 1989). It is conceivable that anecdotal reports of exacerbation of IBD by iron supplementation (Kawai et al. 1992) are mediated by hydroxyl radical production by the Fenton reaction. 

In the presence of trace amounts of iron, superoxide can then reduce Fe3+ to molecular oxygen and Fe2+. The sum of this reaction (equation 2) plus the Fenton reaction (equation 1) produces molecular oxygen plus hydroxyl radical, plus hydroxyl anion from superoxide and hydrogen peroxide, in the presence of catalytic amounts of iron - the so-called Haber-Weiss reaction (equation 3) (Haber and Weiss, 1934). 

For a long time one question remained unanswered the efficiency of the Fenton reaction as the in vivo producer of hydroxyl radicals due to the low rate of Reaction (2) (the rate constant is equal to 42.11 mol 1 s 1 [18]). It is known that under in vitro conditions the rate of Fenton reaction can be sharply enhanced by chelators such as EDTA, but for a long time no effective in vivo chelators have been found. From this point of view new findings obtained by Chen and Schopfer [19] who found that peroxidases catalyze hydroxyl radical formation in plants deserve consideration. These authors showed that horseradish peroxidase (HRP) compound III is a catalyst of the Fenton reaction and that this compound is one to two orders of magnitude more active than Fe EDTA. 

Of course, superoxide may reduce ferric to ferrous ions and by this again catalyze hydroxyl radical formation. Thus, the oxidation of ferrous ions could be just a futile cycle, leading to the same Fenton reaction. However, the competition between the reduction of ferric ions by superoxide and the oxidation of ferrous ions by dioxygen depends on the one-electron reduction potential of the [Fe3+/Fe2+] pair, which varied from +0.6 to —0.4 V in biological systems [173] and which is difficult to predict.)... 

MF effects on FA relatives and healthy donors. (Fanconi anemia is an autosomal recessive disease associated with the overproduction of free radicals, Chapter 31.) It has been shown earlier [215] that FA leukocytes produce the enhanced amount of hydroxyl or hydroxyl-like free radicals, which are probably formed by the Fenton reaction. It was suggested that MF would be able to accelerate hydroxyl radical production by FA leukocytes. Indeed, we found that MF significantly enhanced luminol-amplified CL produced by non-stimulated and PMA-stimulated FA leukocytes but did not affect at all oxygen radical production by leukocytes from FA relatives and healthy donors (Table 21.3). It is interesting that MF did not also affect the calcium ionophore A23187-stimulated CL by FA leukocytes, indicating the absence of the calcium-mediated mechanism of MF activity, at least for FA leukocytes. 

Chelators of transition metals, mainly iron and copper, are usually considered as antioxidants because of their ability to inhibit free radical-mediated damaging processes. Actually, the so-called chelating therapy has been in the use probably even earlier than antioxidant therapy because it is an obvious pathway to treat the development of pathologies depending on metal overload (such as calcium overload in atherosclerosis or iron overload in thalassemia) with compounds capable of removing metals from an organism. Understanding of chelators as antioxidants came later when much attention was drawn to the possibility of in vivo hydroxyl radical formation via the Fenton reaction ... 

Another function of ascorbic add is to generate Fe(II) from Fe (III), which is part of the Haber-Weiss-Fenton Reaction (77). In that reaction, peroxide is reduced to the hydroxyl radical, HO, an extremely powerful oxidizing agent. It should also be noted that ascorbic acid can chelate metals 18 and will promote the carbohydrate-amine browning reaction (79-20). 

However, under certain circumstances, such as in the presence of transition metal ions, hydroxyl radicals may result from either the Haber-Weiss reaction or the Fenton reaction, which cause lipid peroxidation and cell injury (Fig. 6.10). 

Hydroxyl radical was generated through the photo-Fenton reaction. The first step in the reaction was photoreduction of ferric hydroxy complex by radiation from a black light ... 

Kuo (1992) suggested that dye decolorization can result from both oxidation and coagulation processes. During the oxidation process, hydroxyl radicals may attack an organic substrate such as an unsaturated dye molecule. Thus, the chromophore of the dye molecule would be destroyed and decolorized. Ferric ions generated from Fenton s reaction might form fer-ric-hydroxo complexes with hydroxide ions, as shown in Equation (6.145) and Equation (6.146) ... 

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