Iron hydroxyl radical, hydrogen peroxide

Colquhoun and Schumacher [98] have shown that y-linolcnic acid and eicosapentaenoic acid, which inhibit Walker tumor growth in vivo, decreased proliferation and apoptotic index in these cells. Development of apoptosis was characterized by the enhancement of the formation of reactive oxygen species and products of lipid peroxidation and was accompanied by a decrease in the activities of mitochondrial complexes I, III, and IV, and the release of cytochrome c and caspase 3-like activation of DNA fragmentation. Earlier, a similar apoptotic mechanism of antitumor activity has been shown for the flavonoid quercetin [99], Kamp et al. [100] suggested that the asbestos-induced apoptosis in alveolar epithelial cells was mediated by iron-derived oxygen species, although authors did not hypothesize about the nature of these species (hydroxyl radicals, hydrogen peroxide, or iron complexes ). 

The absence of substituents with free radical scavenging properties in most of the (3-blockers makes doubtful their efficacy as powerful antioxidants. Arouma et al. [293] tested the antioxidative properties of several 3-blockers in reactions with superoxide, hydroxyl radicals, hydrogen peroxide, and hypochlorous acid. It was demonstrated that most of the compounds tested were inactive in these experiments. Nonetheless, propranolol, verapamil, and flunarizine effectively inhibited iron ascorbate-stimulated microsomal lipid peroxidation and all drugs (excluding flunarizine) were effective scavengers of hydroxyl radicals. Contrary to Janero et al. [292], these authors did not find the inhibition of xanthine oxidase by propranolol. It was concluded that 3-blockers are not the effective in vivo antioxidants. 

Iron(II) hydroxyl radical, hydrogen peroxide determination, 641... 

Indeed, when present in concentrations sufficient to overwhelm normal antioxidant defences, ROS may be the principal mediators of lung injury (Said and Foda, 1989). These species, arising from the sequential one-electron reductions of oxygen, include the superoxide anion radical, hydrogen peroxide, hypochlorous ions and the hydroxyl radical. The latter species is thought to be formed either from superoxide in the ptesence of iron ions (Haber-Weiss reaction Junod, 1986) or from hydrogen peroxide, also catalysed by ferric ions (Fenton catalysis Kennedy et al., 1989). 

Zepp, R. G., B. C. Faust, and J. Hoigne, Hydroxyl Radical Formation in Aqueous Reactions (pH 3-8) of Iron(II) with Hydrogen Peroxide The Photo-Fenton Reaction, Environ. Sci. Technoi, 26, 313-319 (1992). 

Zepp RG, Faust BC, Hoigne J. Hydroxyl radical formation in aqueous reactions (pH 3-8) of iron(II) with hydrogen peroxide the photo-Fenton reaction. Environ Sci Technol 1992 26 313-319. 

Figure 27.10. Conversion of superoxide anion (02 ) to hydroxyl radical ( OH) in the presence of iron, or to hydrogen peroxide (H202) by superoxide dismutase (SOD), which is converted to hypochlorous acid by myeloperoxidase (MPO).

In the present study, carnosol, camosic acid and rosmarinic acid showed effective DPPH free radicals scavenging activity. Camosic acid, carnosol, rosmarinic acid and ursolic acid effectively inhibited pUC19 DNA strand break induced by Fenton reaction (28). The reaction of iron (II) with hydrogen peroxide is generally considered to yield the hydroxyl radicals (29). These compounds may react with and/or scavenge the hydroxyl radicals produced by Fenton reaction. 

In hemoglobin, iron is essentially in fee ferrous state. Upon degradation of fee globin and fee release of heme, feis iron(II)-protoporphyrin(IX) is able to transfer one electron to molecular oxygen to produce superoxide radicals, hydrogen peroxide and, finally, hydroxyl radicals, generating a lethal oxidative... 

One method of generating hydroxyl radicals is by a dding a soluble iron salt to an acid solution of hydrogen peroxide (Fenton s reagent) (176—180), ie ... 

The composition of I, and possibly its structure, may be deduced by identifying Q. Certain examples from peroxide chemistry will illustrate the scope of the method. The reactions of ferrous(nitriloacetate) and ferrous(ethylenediamine-N,N -diacetate) with hydrogen peroxide are complicated processes.1 A particular scavenger T did indeed divert the reaction at high concentrations of T. The required levels of T were, however, much higher than those that would have been needed to trap the hydroxyl radical, HO. It is thereby ruled out. With this and with spectroscopic evidence, a reactive hypervalent iron complex was suggested as the intermediate. 

In related work, the reactions of hydrogen peroxide with iron(II) complexes, including Feu(edta), were examined.3 Some experiments were carried out with added 5.5"-dimethyl-1-pyrroline-N-oxide (DMPO) as a trapping reagent fa so-called spin trap) for HO. These experiments were done to learn whether HO was truly as free as it is when generated photochemically. The hydroxyl radical adduct was indeed detected. but for some (not all) iron complexes evidence was obtained for an additional oxidizing intermediate, presumably an oxo-iron complex. 

McCormick ML, GR Buettner, BE Britigan (1998) Endogenous superoxide dismutase levels regulate iron-dependent hydroxyl radical formation in Escherichia coli exposed to hydrogen peroxide. J Bacterial 180 622-625. 

Puppo, A. and Halliwell, B. (1988). Formation of hydroxyl radicals from hydrogen peroxide in the presence of iron. Biochem. J. 249, 185-190. 

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. 

Starke, P.E., and Farber, J.L. (1985). Ferric iron and superoxide ions are required for the killing of cultured hepatocytes by hydrogen peroxide. Evidence for the participation of hydroxyl radicals formed by an iron catalyzed Haber-Weiss reaction. J. Biol. Chem. 260, 10099-10104. 

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