Predicting Fenton-Driven Degradation Using Contaminant Analog

The reaction of hydrogen peroxide (H2O2) and Fe(II) (Fenton's reaction) generates hydroxyl radicals (?OH) that can be used to oxidize contaminants in soils and aquifers. In such environments, several factors can limit the effectiveness of chemical oxidation, including reactions involving H2O2 that do not yield ?OH, ?OH reactions with nontargeted chemicals, and insufficient iron in the soil or aquifer. Consequently, site-specific studies may be necessary to evaluate the feasibility of chemical oxidation using H2O2. Here, the degradation of a contaminant analog, α-(4-pyridyl-1-oxide) N-tert-butylnitrone (4POBN), was used to estimate ?OH concentration and simplify testing procedures. A kinetic model was developed, calibrated using 4POBN degradation kinetics, and used to predict the disappearance of 2-chlorophenol (2CP), a representative target. Good agreement between predicted (Y) and measured (X) values for 2CP (Y = 0.95X) suggests that the kinetics of analog degradation can be used to predict the degradation rate of compounds for which the rate constant for reaction with ?OH is known.     

Modeling the Transformation of Chromophoric Natural Organic Matter during UV/H2O2 Advanced Oxidation

This research developed a differential kinetic model to predict the partial degradation of natural organic matter (NOM) during ultraviolet plus hydrogen peroxide (UV/H2O2) advanced oxidation treatment. The absorbance of 254?nm UV, representing chromophoric NOM (CNOM) was used as a surrogate to track the degradation of NOM. To obtain reaction rate constants not available in the literature, i.e., reactions between the hydroxyl radical (?OH) and NOM, experiments were conducted with “synthetic” water, using isolated Suwannee River NOM, and parameter estimation was applied to obtain the unknown model parameters. The reaction rate constant for the reaction between ?OH and total organic carbon (TOC), k?OH,TOC, was estimated at 1.14(±0.10)×104??L?mg-1?s-1, and the reaction rate constant between ?OH and CNOM, k?OH,CNOM, was estimated at 3.04(±0.33)×104??L?mol-1?s-1. The model was evaluated on two natural waters to predict the degradation of CNOM and H2O2 during UV/H2O2 treatment. Model predictions of CNOM degradation agreed well with the experimental results for UV/H2O2 treatment of the natural waters, with errors up to 6%. For the natural water with additional alkalinity, the model also predicted well the slower degradation of CNOM during UV/H2O2 treatment, owing to scavenging of ?OH by carbonate species. The model, however, underpredicted the degradation of H2O2, suggesting that, when NOM is present, mechanisms besides the photolysis of H2O2 contribute appreciably to H2O2 degradation.     

Destruction of a Carbon Tetrachloride Dense Nonaqueous Phase Liquid by Modified Fenton’s Reagent

Destruction of a dense nonaqueous phase liquid (DNAPL) by soluble iron (III)-catalyzed and pyrolusite (β-MnO2)-catalyzed Fenton’s reactions (hydrogen peroxide and transition metal catalysts) was investigated using carbon tetrachloride (CT) as a model contaminant. In the system amended with 5 mM soluble iron (III), 24% of the CT DNAPL was destroyed after 3 h while CT dissolution in parallel fill-and-draw systems was minimal, indicating that CT was degraded more rapidly than it dissolved into the aqueous phase. Fenton’s reactions catalyzed by the naturally occurring manganese oxide pyrolusite were even more effective in destroying CT DNAPLs, with 53% degradation after 3 h. Although Fenton’s reactions are characterized by hydroxyl radical generation, carbon tetrachloride is unreactive with hydroxyl radicals; therefore, a transient oxygen species other than hydroxyl radicals formed through Fenton’s propagation reactions was likely responsible for CT destruction. These results demonstrate that Fenton-like reactions in which nonhydroxyl radical species are generated may provide an effective method for the in situ treatment of DNAPLs.     

Ozone Degradation of Iodinated Pharmaceutical Compounds

This study investigates the aqueous degradation of four iodinated x-ray contrast media (ICM) compounds (diatrizoate, iomeprol, iopromide, and iopamidol) by ozone and combined ozone and hydrogen peroxide. In laboratory scale experiments, second-order kinetic rate constants for the reactions of the ICM compounds with molecular ozone and hydroxyl radicals, and overall at pH 7.5, were determined. For the four ICM compounds the degradation rate constants with molecular ozone were low and in the range of 1–20?M?1?s?1, whereas the rate constants with hydroxyl radicals were in the range of 1×109–3×109?M?1?s?1. Diatrizoate had the lowest rate constant of the four compounds with respect to molecular ozone reactions. At pH 7.5, the extent of compound degradation was proportional to the applied ozone dose and inversely related to the initial compound concentration at a given ozone dose. At this pH approximately 90% of the degradation could be attributed to hydroxyl radical reactions. Enhancement of the radical mechanism by the addition of hydrogen peroxide during ozonation led to complete removal of the nonionic compounds, and >80% removal of diatrizoate, at relatively low oxidant mass ratios (H2O2/O3<0.25). A similar enhancement in compound degradation was evident with the presence of small concentrations of humic substances ( ～ 4–5?mg?L?1). Ozone oxidation led to major cleavage of the ICM compounds and the release of inorganic iodine; the proportion of iodine release was similar among the nonionic ICM compounds but much greater for diatrizoate.     

Adverse health effects of PM10 particles: involvement of iron in generation of hydroxyl radical

OBJECTIVES: Environmental particles < 10 microns average aerodynamic diameter (PM10) are associated with mortality, exacerbation of airways diseases, and decrement in lung function. It is hypothesised that PM10 particles, along with other pathogenic particles, generate free radicals at their surface in reactions involving iron, and that this is a factor in the pathogenicity of PM10 particles. Identification of free radical activity in PM10 and examination of the content and role of iron in this process was undertaken. METHODS: Free radical activity was detected with a supercoiled plasmid, phi X174 RF1 DNA, and measured as scission of the supercoiled DNA (mediated by free radicals) by scanning laser densitometry. The role of the hydroxyl radical was confirmed by the use of the specific scavenger mannitol, and the role of iron investigated with the iron chelator desferrioxamine-B (DSF-B). Iron released from PM10 particles at pH 7.2 and pH 4.6 (to mimic conditions on the lung surface and in macrophage phagolysosomes, respectively) was assessed spectrophotometrically with the Fe++ chelator ferrozine and the Fe+ + + chelator DSF-B. RESULTS: PM10 particles showed significant free radical activity by their ability to degrade supercoiled DNA. A substantial part of this activity was due to the generation of hydroxyl radicals, as shown by partial protection with mannitol. Similarly, DSF-B also conferred protection against the damage caused to plasmid DNA indicating the role of iron in generation of hydroxyl radicals. Negligible Fe++ was released at either pH 7.2 or pH 4.6 by contrast with Fe+ + +, which was released in substantial quantities at both pHs, although twice as much was released at pH 4.6. CONCLUSIONS: PM10 particles generate the hydroxyl radical, a highly deleterious free radical, in aqueous solution. This occurs by an iron dependent process and hydroxyl radicals could play a part in the pathogenicity of PM10 particles. Iron release was greatest at the pH of the lysosome (pH 4.6) indicating that iron may be mobilised inside macrophages after phagocytosis, leading to oxidative stress in the macrophages.     

Free radical generation at the solid/liquid interface in iron containing minerals

The potential for free radical release has been measured by means of the spin trapping technique on three kinds of iron containing particulate: two asbestos fibers (chrysotile and crocidolite); an iron-exchanged zeolite and two iron oxides (magnetite and haematite). DMPO (5,5'-dimethyl-1-pirroline-N-oxide), used as spin trap in aqueous suspensions of the solids, reveals the presence of the hydroxyl and carboxylate radicals giving rise respectively to the two adducts [DMPO-OH] and [DMPO-CO2], each characterized by a well-defined EPR spectrum. Two target molecules have been considered: the formate ion to evidence potential for hydrogen abstraction in any biological compartment and hydrogen peroxide, always present in the phagosome during phagocytosis. The kinetics of decomposition of hydrogen peroxide has also been measured on all solids. Ferrozine and desferrioxamine, specific chelators of Fe(II) and Fe(III) respectively, have been used to remove selectively iron ions. Iron is implicated in free radical release but the amount of iron at the surface is unrelated to the amount of radicals formed. Only few surface ions in a particular redox and coordination state are active. Three different kinds of sites have been evidenced: one acting as H abstracter, the other as a heterogeneous catalyst for hydroxyl radical release, the third one related to catalysis of hydrogen peroxide disproportionation. In both mechanisms of free radical release, the Fe-exchanged zeolite mimics the behaviour of asbestos whereas the two oxides are mostly inert. Conversely magnetite turns out to be an excellent catalyst for hydrogen peroxide disproportionation while haematite is inactive also in this reaction. The results agree with the implication of a radicalic mechanism in the in vitro DNA damage and in the in vivo toxicity of asbestos.     

铁粉-H_2O_2对PdCl_3SC(NH_2)_2~-的还原

以含PdCl_3SC(NH_2)_2~-溶液为原料,采用Fe-H_2O_2还原法回收溶液中的钯,研究了还原过程的机理,考察了pH、还原时间、H_2O_2用量和铁粉用量对还原率的影响。结果表明,铁粉被氧化后的Fe~(2+)可催化H_2O_2而产生氧化能力极强的·OH自由基,该自由基对复杂的PdCl_3SC(NH_2)_2~-结构具有很强的破坏力,使稳定的PdCl_3SC(NH_2)_2~-以PdCl _4~(2-)形态分离出来,提高了铁对钯的还原性能。在溶液体积20mL,25℃,pH=2,H_2O_2用量0.10mL/mL,反应时间60min和铁粉用量0.50mg/mL的条件下,钯的平均还原率可达99.25%。     

Effects of Reagent Concentrations on Advanced Oxidation of Amoxicillin by Photo-Fenton Treatment

The degradation and mineralization of amoxicillin in an aqueous solution was accomplished by using a photo-Fenton treatment. An ultraviolet light source with a 254-nm wavelength was used with hydrogen peroxide (H2O2) and iron(II). The effects of reagent concentrations on amoxicillin degradation and mineralization were investigated systematically by using the Box-Behnken statistical experiment design. Amoxicillin (10–200??mgL-1), H2O2 (10–500??mgL-1), and iron(II) (0–50??mgL-1) concentrations were considered independent variables; the percent amoxicillin degradation and the total organic carbon (TOC) removal (mineralization) were the objective functions to be maximized. Both H2O2 and iron(II) concentrations affected the extent of the amoxicillin degradation and mineralization. The amoxicillin degradation was completed within 2.5?min, and 53% mineralization took place within 60?min. The optimum H2O2∶Fe∶amoxicillin ratio that resulted in complete amoxicillin degradation and 53% mineralization was 100∶40∶105??mgL-1.     

Reduction of 2,4,6-Trinitrotoluene and Hexahydro-1,3,5-trinitro-1,3,5-triazine by Hydroxyl-Complexed Fe(II)

The reduction kinetics of two explosives, 2,4,6-trinitrotoluene (TNT) and hexahydro-1,3,5-trinitro-1,3,5-triazine (RDX), by Fe(II) was investigated in aqueous systems. A dilute ferrous iron solution effectively reduces these nitroaromatic (NAC) and nitramine (NAM) compounds between pH 6.75 and 9.2. Observed reaction rates are first order in monohydroxl and dihydroxyl ferrous iron [FeOH+ or Fe(OH)20], and NAC/NAM concentrations. The reaction does not require the presence of a mediating surface. Intrinsic rate constants for TNT and RDX reduction by monohydroxyl ferrous iron are 2.00(±0.17)E+09 and 2.04(±0.24)E+06?M?2?s?1, respectively. The reduction half-lives at neutral pH were on the order of minutes for TNT and hours for RDX, yielding rates faster than any known natural process or current bioremediation technique. The use of a mobile reductant, such as hydroxyl-complexed Fe(II) or other aqueous Fe(II) complexes, for NAC/NAMs could be an effective remediation technique at contaminated sites.     

Reactions of OH and eaq- adducts of cytosine and its nucleosides or nucleotides with Cu(II) ions in dilute aqueous solutions: a steady-state and pulse radiolysis study

The reactions of OH and eaq- adducts of cytosine, cytidine and deoxycytidine in the presence of Cu(II) ions have been studied by product analysis and pulse radiolysis. The product analysis studies show that the degradation of the base is enhanced in N2O-saturated conditions in the presence of Cu(II) ions and the major radiolytic products are Cu(I), cytosine glycols and 5(6)-hydroxycytosine. It is also interesting to note that the yields of Cu(I) are equivalent to cytosine degradation yields, which suggests that the interaction of the OH adducts with Cu(II) ions restricts the radical recombination reactions (known to be the major physicochemical repair process) which partly regenerate the parent cytosine. The rate constants of the reactions of cytosine OH adducts with Cu(II) ions determined by pulse radiolysis lie between 10(7) and 10(8) dm3 mol-1 s-1. The growth in the transient absorption spectra of cytosine OH adducts in the range 330-400 nm, observed in the presence of copper(II) ions in free and complexed state, suggests formation of copper radical adduct which decays by water insertion at the copper-carbon bond to give glycol as the major product. Such copper radical adduct formation was also observed in the case of cytidine and deoxycytidine. The protonated electron adducts (at the hetero atoms) of cytosine, cytidine and deoxycytidine transfer electrons to the Cu(II) ions with rate constants of 10(8) and 10(9) dm3 mol-1 s-1. Here no adduct formation is observed. The steady-state results show that such electron transfer reactions regenerate the parent molecules themselves. Hence such electron transfer reactions do not contribute to enhanced base degradation in the presence of copper ions.     

In vivo monitoring of norepinephrine and hydroxyl free radical generation by ferrous iron in the myocardium with a microdialysis technique

1. We examined in vivo monitoring of norepinephrine and hydroxyl radical generation in rat myocardium with a microdialysis technique. For this purpose, we designed the microdialysis probe holding system which includes loose fixation of the tube and synchronization of the movement of the heart and the probe. 2. The hydroxyl free radical (.OH) reacts with salicylate and generates 2,3- and 2,5-dihydroxybenzoic acid (DHBA) which can be measured electrochemically in picomole quantity by high performance liquid chromatography (HPLC). 3. After probe implantation, norepinephrine concentration of dialysate decreased over the first 150 min and then reached an almost steady level. A positive linear correlation between the ferrous iron and .OH formation trapped as 2,3-DHBA (R2 = 0.960) and 2,5-DHBA (R2 = 0.982) was observed using the microdialysis technique. 4. The present results indicate that non-enzymatic oxidation in the extracellular fluid may play a key role in hydroxyl radical generation by ferrous iron.     

Contaminant Adsorption and Oxidation via Fenton Reaction

A ground-water treatment process is described in which contaminants are adsorbed onto granulated activated carbon (GAC) containing fixed iron oxide. Hydrogen peroxide (H2O2) is amended to the GAC suspension and reacts with the iron, forming hydroxyl radicals (?OH). The radicals react with and oxidize sorbed and soluble contaminants regenerating the carbon surface. Laboratory results are presented in which 2-chlorophenol (2CP) was first adsorbed to GAC and subsequently oxidized via the Fenton-driven mechanism. Transformation of 2CP was indicated by the formation of carboxylic acids and Cl?release. The treatment efficiency of 2CP, defined as the molar ratio of Cl?released to H2O2 consumed, increased with increasing amounts of iron oxide and 2CP on the GAC. The extent of 2CP oxidation increased with H2O2 concentration. Lower treatment efficiency was evident at the highest H2O2 concentration utilized (2.1 M) and was attributed to increased ?OH scavenging by H2O2. Aggressive oxidation procedures used in sequential adsorption∕oxidation cycles did not alter the GAC surface to a degree that significantly interfered with subsequent 2CP adsorption reactions. Although process feasibility has not yet been established beyond bench-scale, experimental results illustrate the potential utility of the adsorption∕oxidation process in aboveground systems or permeable reactive barriers for the treatment of contaminated ground water.     

Effect of Basicity on Persulfate Reactivity

The generation of reactive species in activated persulfate systems under different conditions of basicity was investigated using three probe compounds. Anisole was used to detect both sulfate radical and hydroxyl radical. Nitrobenzene was used to detect hydroxyl radical, and hexachloroethane was used as a reductant probe. Minimal probe compound degradation occurred in persulfate reactions conducted at pH ≤ 10, demonstrating that a low flux of reactants is generated at acidic, neutral, and slightly basic pH regimes. In persulfate reactions at pH?12, sulfate and hydroxyl radical were generated but minimal reductants were produced. Scavenging studies showed that the dominant reactive species at basic pH was hydroxyl radical. The generation of reductants increased at high molar ratios of base to persulfate; however, hydroxyl radical generation rates increased only when molar ratios of base to persulfate were >3∶1. The results of this research demonstrate that the hydroxyl radical is the dominant reactive oxygen species in base-activated persulfate formulations and that overall reactivity increases with increasing base:persulfate ratios.     

Generation of free radicals from hydrogen peroxide and lipid hydroperoxides in the presence of Cr(III)

Free radical generation from H2O2 and lipid hydroperoxides in the presence of Cr(III) was investigated by electron spin resonance (ESR) spin trapping methodology. Incubation of Cr(III) with H2O2 at physiological pH generated hydroxyl (.OH) radical, the yield of which reached saturation level in about 6 min. Deferoxamine reduced the .OH radical yield by only about 20%, diethylenetriamine pentaacetic acid (DTPA) reduced it by about 70%, while cysteine, glutathione, and NADH exhibited no significant effect. The yield of .OH radical formation also depended on the pH being 15 times higher at pH 10 than that at pH 7.2. At pH 3.0, .OH radical generation became nondetectable, and addition of H2O2 to Cr(III) solution did not affect the intensity of the Cr(III) ESR signal while at pH 10, addition of H2O2 reduced the Cr(III) intensity by about 40%, showing that reaction of Cr(III) with H2O2 occurred only at higher pH. Incubation of Cr(III) with the model lipid hydroperoxides, cumene hydroperoxide and t-butyl hydroperoxide, generated lipid hydroperoxide-derived free radicals. Addition of deferoxamine or DTPA had a minor inhibitory effect on that generation. These results show that Cr(III) is capable of producing free radicals from H2O2 and lipid hydroperoxides, which may have significant implications regarding the mechanism of chromium-induced carcinogenesis.     

Kinetics and products of the TiO2 photocatalytic degradation of 2-chlorobiphenyl in water

The light-induced degradation of 2-chlorobiphenyl (2-CB) under simulated solar irradiation has been investigated in aqueous solutions containing TiO2 suspensions as photocatalysts. The apparent quantum yield for an initial 2-CB concentration C0 = 3.8 micrograms/mL at the natural pH was ca. 0.005 The oxidation kinetics of 2-CB follows the Langmuir-Hinshelwood kinetic model at natural pH. The primary degradation of 2-CB follows a pseudo-first-order kinetics. Several reaction intermediates were identified using GC/FTIR/MS and ion chromatography. The products at the initial stage of the reaction were seven isomers of 2-chlorobiphenyl-ol and biphenyl-2-ol. These intermediates underwent further photocatalytic oxidation via aldehydes, ketones, and acids finally into CO2 and HCl. The formation and fate of some of these compounds under irradiation were also investigated. A reaction scheme involving hydroxyl radicals has been proposed.     

Desferrioxamine and vitamin E protect against iron and MPTP-induced neurodegeneration in mice

To elucidate the neuroprotective effects of the iron chelator desferrioxamine (DFO) and the antioxidant vitamin E on excessive iron-induced free radical damage, a chronic iron-loaded mice model was established. The relationship between striatal iron content, oxidized to reduced glutathione ratio, hydroxyl radical (.OH) levels and dopamine concentrations were observed in DFO or vitamin E pretreated iron-loaded/1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated C57BL/6 mice. The results demonstrated that both DFO and vitamin E inhibit the iron accumulation and thus reverses the increase in oxidized glutathione (GSSG), oxidized to reduced glutathione ratios, .OH and lipid peroxidation levels. The striatal dopamine concentration was elevated to normal value. Our data suggested that: (1) iron may induce neuronal damage and thus excessive iron in the brain may contribute to the neuronal loss in PD; (2) iron chelators and antioxidants may serve as potential therapeutic agents in retarding the progression of neurodegeneration.     

Oxidative and Reductive Pathways in Manganese-Catalyzed Fenton’s Reactions

Soluble manganese (II) and amorphous and crystalline manganese (IV) oxides were investigated as catalysts for the Fenton-like decomposition of hydrogen peroxide into oxidants and reductants. 1-Hexanol was used as a hydroxyl radical probe and carbon tetrachloride (CT) was used as a reductant probe. Soluble manganese (II)-catalyzed reactions at acidic pH resulted in >99% degradation of 1-hexanol and no measurable transformation of CT, indicating that hydroxyl radicals were generated but reductants were not. However, when these reactions were conducted at near-neutral pH, an amorphous manganese oxide precipitate formed and 89% of the CT degraded in 60?min, while 1-hexanol degradation was negligible. Using an amorphous manganese oxide synthesized in a separate reactor, CT was rapidly degraded while 1-hexanol oxidation was undetectable. Reactions catalyzed by the crystalline manganese oxide pyrolusite(β-MnO2) at near-neutral pH also resulted in significant CT degradation, indicating that reductants are generated by both the crystalline and amorphous manganese oxide-catalyzed decomposition of H2O2. The presence of manganese oxides in the subsurface and their ability to catalyze the generation of reductants in modified Fenton’s reactions has important implications for hydrogen peroxide stability and contaminant transformation pathways during the in situ Fenton’s treatment of contaminated soils and groundwater.     

In vivo effects of fumonisin B1-producing and fumonisin B1-nonproducing Fusarium moniliforme isolates are similar: fumonisins B2 and B3 cause hepato- and nephrotoxicity in rats

Orellanine, [2,2'-bipyridine]-3,3',4,4'-tetrol-1,1'-dioxide, is the toxin responsible for the lethal nephrotoxicity of some Cortinarius mushrooms. Our present ESR and spin-trapping studies of the redox properties of the system of non-illuminated orellanine, ferrous iron and dioxygen contribute to understanding the molecular mechanism of its toxicity. UV-visible spectrophotometry, cyclic voltammetry and ESR in frozen medium showed the formation of a wine-red tris complex, Fe(III)Or3. This ferric complex is easily reducible (Ep = -565 mV vs Ag/AgCl/3M KCl at pH 7), involving a one-electron reversible process. Spin-trapping using DMPO is employed to detect the generation of superoxide anion and hydroxyl radicals. The instantaneous one-electron oxidation of ferrous ions in the presence of the toxin under air is concomitant with dioxygen consumption as supported by dioxygen consumption. GSH involves the toxin and ferrous ions under air in a redox cycling process resulting in the production of glutathionyl and oxygen free radicals, observed for the first time with an iron complex of a mushroom toxin. In most cases, EDTA is not able to prevent the Fe(III)Or3 and radical formation. The ortho-dihydroxylated groups borne by the di-N-oxidized bipyridine structure and not the bipyridine structure itself, are responsible for the formation of a stable ferric complex at pH 7, as they are for the generation of an apparently stable ortho-semiquinone anion radical. These one-electron mechanisms may play a major role in some of the known toxic effects of orellanine.     

Cobalt-mediated generation of reactive oxygen species and its possible mechanism

Electron spin resonance spin trapping was utilized to investigate free radical generation from cobalt (Co) mediated reactions using 5,5-dimethyl-1-pyrroline (DMPO) as a spin trap. A mixture of Co with water in the presence of DMPO generated 5,5-dimethylpyrroline-(2)-oxy(1) DMPOX, indicating the production of strong oxidants. Addition of superoxide dismutase (SOD) to the mixture produced hydroxyl radical (.OH). Catalase eliminated the generation of this radical and metal chelators, such as desferoxamine, diethylenetriaminepentaacetic acid or 1,10-phenanthroline, decreased it. Addition of Fe(II) resulted in a several fold increase in the .OH generation. UV and O2 consumption measurements showed that the reaction of Co with water consumed molecular oxygen and generated Co(II). Since reaction of Co(II) with H2O2 did not generate any significant amount of .OH radicals, a Co(I) mediated Fenton-like reaction [Co(I) + H2O2-->Co(II) + .OH + OH-] seems responsible for .OH generation. H2O2 is produced from O2.- via dismutation, O2.- is produced by one-electron reduction of molecular oxygen catalyzed by Co. Chelation of Co(II) by biological chelators, such as glutathione or beta-ananyl-3-methyl-L-histidine alters, its oxidation-reduction potential and makes Co(II) capable of generating .OH via a Co(II)-mediated Fenton-like reaction [Co(II) + H2O2-->Co(III) + .OH + OH-]. Thus, the reaction of Co with water, especially in the presence of biological chelators, glutathione, glycylglycylhistidine and beta-ananyl-3-methyl-L-histidine, is capable of generating a whole spectrum of reactive oxygen species, which may be responsible for Co-induced cell injury.     

Free radicals, oxidative stress and antioxidant vitamins

Free radicals having oxidizing properties are produced in vivo. The monoelectronic reduction of dioxygen generates the superoxide radical (.O2-) which, according to the experimental conditions, behaves as a reducing or an oxidizing agent. Its dismutation catalyzed by superoxide dismutases (SODs) produces hydrogen peroxide. The latter reacting with .O2- in the presence of "redox-active" iron produces highly aggressive prooxidant radicals, such as the hydroxyl radical (.OH). This production is prevented through intracellular enzymes (catalase and glutathione peroxidases) which destroy the hydrogen peroxide involved in the biosynthesis of .OH. An increase in SODs activity without parallel enhancement of the enzymes destroying H2O2 may lead to important cellular disturbances. Other enzymes acting with glutathione as substrate (especially glutathione S-transferases) contribute to the antioxidant defence. The same holds true for selenium and zinc which act mainly through their involvement in the structure of both antioxidant enzymes and nonenzymatic proteins. Another line of antioxidant defence is represented by substrates acting as chain-breaking antioxidants in destructive processes linked to prooxidant free radicals, such as lipid peroxidation. The main membranous antioxidant is alpha-tocopherol which is able to quench efficiently lipid peroxyl radicals. Its efficiency would be quickly exhausted if the tocopheryl radical formed during this reaction wouldn't be retransformed into alpha-tocopherol through the intervention of ascorbate and/or glutathione. Ubiquinol and dihydrolipoate also contribute to the membranous antioxidant defence, whereas carotenoids are mainly responsible for the prevention of the deleterious effects of singlet oxygen. An oxidative stress is apparent when the antioxidant defence is insufficient to cope with the prooxidant production.