Chemiluminescence from 6-hydroxydopamine: involvement of hydrogen peroxide, the superoxide radical and the hydroxyl radical, a potential role for singlet oxygen.
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Benzoates↗
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Degradation of methyl and ethyl mercury into inorganic mercury by oxygen free radical-producing systems: involvement of hydroxyl radical.
Degradation of methyl mercury (MeHg) and ethyl Hg (EtHg) with oxygen free radicals was studied in vitro by using three well-known hydroxyl radical (.OH)-producing systems, namely Cu2(+)-ascorbate, xanthine oxidase (XOD)-hypoxanthine (HPX)-Fe(III)EDTA and hydrogen peroxide (H2O2)-ultraviolet light B. For this purpose, the direct determination method for inorganic Hg was employed. MeHg and EtHg were readily degraded by these three systems, though the amounts of inorganic Hg generated from MeHg were one half to one third those from EtHg. Degradation activity of XOD-HPX-Fe(III)EDTA system was inhibited by superoxide dismutase, catalase and the .OH scavengers and stimulated by H2O2. Deletion of the .OH formation promoter Fe(III)EDTA from XOD-HPX-Fe(III)EDTA system resulted in the decreased degradation of MeHg and EtHg, which was enhanced by further addition of the iron chelator diethylenetriamine pentaacetic acid. In all these cases, a good correlation was observed between alkyl Hg degradation and deoxyribose oxidation determining .OH. By contrast, their degradation appeared to be unrelated to either superoxide anion (O2-) production or H2O2 production alone. We further confirmed that H2O2 (below 2 mM) itself did not cause significant degradation of MeHg and EtHg. These results suggested that .OH, but not O2- and H2O2, might be the oxygen free radical mainly responsible for the degradation of MeHg and EtHg.
Ascorbic Acid↗
Inhibitory effect of free radical scavenger, MCI-186, in the increase of hydroxyl radical induced by iminodipropionitrile in rats.
Beta,beta'-Iminodipropionitrile (IDPN) is known to produce permanent motor behavioral abnormalities in rats. This behavior syndrome is also termed as "ECC Syndrome", the animal model for Gilles de la Tourette syndrome in humans. Some reports showed that these behavioral abnormalities are caused by monoamine changes. However, there was little research on the relation between IDPN-induced behavioral abnormalities and free radical. 3-Methyl-1-phenyl-2-pyrazolin-5-one (MCI-186), a newly synthesized free radical scavenger, exerts beneficial free radical scavenging and antioxidant characteristics. We investigated that MCI-186 inhibited the process of hydroxyl radical formation induced by IDPN administration in the rat brain. In the group of IDPN administration, hydroxyl radical levels exhibited predominant increase in most parts of the rat brain. In the group of IDPN and MCI-186 administration, hydroxyl radical levels marked significant decrease compared with those in the group of IDPN administration. Therefore, MCI-186 inhibited production of hydroxyl radical and might prove to be effective against ECC syndrome induced by IDPN.
Animals↗
Hydroxyl radical attack on dopamine.
Hydroxyl radicals were generated in the presence of 1 mM dopamine (3,4-dihydroxyphenylethylamine) at pH 7.2 (50 mM phosphate buffer) by the following two mechanisms: 1) a classic Fenton-type reaction between hydrogen peroxide and a ferrous chelate (ferrous diethylenetriaminepentaacetate) and 2) the cyclical redox reactions of iron-EDTA/ascorbate. Three ring-monohydroxylated products of dopamine were detected by high performance liquid chromatography with electrochemical detection: 2-hydroxydopamine, 5-hydroxydopamine, and 6-hydroxydopamine in an approximate ratio of 3:2:1. Scavengers of hydroxyl radicals (dimethyl sulfoxide, mannitol, ethanol) suppressed the yields of products in a concentration-dependent manner. The formation of nonphysiologic hydroxylated forms of dopamine can provide a probe for the formation of hydroxyl radicals in dopamine neurons.
Ascorbic Acid↗
Phenytoin-initiated hydroxyl radical formation: characterization by enhanced salicylate hydroxylation.
Bioactivation of phenytoin and related teratogens by peroxidases such as prostaglandin H synthase (PHS) may initiate hydroxyl radical (.OH) formation that is teratogenic. Salicylate is hydroxylated by .OH at the third and fifth carbon atoms, forming 2,3- and 2,5-dihydroxybenzoic acids (DHBA). In vivo salicylate metabolism produces only the 2,5-isomer, so 2,3-DHBA formation may reflect .OH production. In the present study, we validated the salicylate assay using the known .OH generator paraquat and evaluated .OH production by phenytoin. Female CD-1 mice were treated with paraquat (30 mg/kg, intraperitoneally) given 30 min after acetylsalicylic acid (ASA) (200 mg/kg, intraperitoneally). Blood was collected at 5, 15, and 30 min and 1 and 2 hr after paraquat, and plasma was analyzed for DHBA isomers and glucuronide conjugates by high performance liquid chromatography with electrochemical detection. Paraquat increased 2,3-DHBA formation 19.2-fold, with substantial inter-individual variability in the time of maximal formation (p = 0.0001). The 2,3-DHBA glucuronide conjugates in vivo and in hepatic microsomal studies amounted to approximately 11% and 0.43%, respectively, of total 2,3-DHBA equivalents. To investigate putative .OH production initiated via PHS-catalyzed phenytoin bioactivation, ASA was given 30 min before phenytoin (65 or 100 mg/kg, intraperitoneally), resulting in respective 7.6-fold (p = 0.02) and 14.2-fold (p = 0.003) increases in phenytoin-initiated maximal 2,3-DHBA formation. Maximal 2,3-DHBA formation was 2.1-fold higher when ASA was administered after rather than before the same dose (65 mg/kg) of phenytoin (p = 0.03), indicating ASA inhibition of PHS-catalyzed phenytoin bioactivation. Urinary analysis was much less sensitive, and the 2,5-isomer reflected enzymatic rather than .OH-mediated hydroxylation. The paraquat studies demonstrate the importance of timing in accurately quantifying 2,3-DHBA formation and suggest that glucuronidation does not interfere. The substantial, dose-dependent initiation of 2,3-DHBA formation by phenytoin, and its inhibition by ASA, provide the first in vivo evidence that PHS-dependent .OH formation could contribute to the molecular mechanism of phenytoin teratogenesis.
Animals↗
Photocatalytic degradation of lignin and lignin models, using titanium dioxide: the role of the hydroxyl radical.
The role of hydroxyl radicals on the degradation of lignins during a cellulosic pulp bleaching process including a photocatalytic stage, was assessed using peroxyformic acid lignins EL1 and REL1 and two phenolic niphenyl lignin models 1 and 2. The irradiations were performed in the absence of photocatalyst TiO2 and H2O2 (condition a), in the presence of TiO2 (condition b) and in the presence of H2O2 (condition c). The experiments were conducted in alkaline (pH approximately 11) aqueous ethanol solutions with oxygen bubbling. The relative phenolic content of the irradiated solutions, which is indicative of the involvement of hydroxyl radicals, was determined by ionization absorption spectroscopy. The results obtained show that the catalyzed reaction involves both degradation of the phenolate groups by electron transfer and hydroxylation of the lignin aromatic structure. Benzyl alcohol structural elements in sodium borohydride reduced lignin REL1 and compound 2 were also found as good trapping agents for the hydroxyl radicals. The degradation of EL1 was studied by measuring its fluorescence emission by comparison to the fluorescence of compound 2. The emission spectra indicate that some biphenyl phenolate anions in EL1 are reacting under UV/visible irradiation and some others, probably polyphenolic chromophores emitting less fluorescence, are formed.
Catalysis↗
Dark stained tissues of the epicarp of encore mandarin: interactions with the production of hydroxyl radicals.
The interactions between hydroxyl radical production and the composition of the epicarp cells associated with the dark stained tissues of mature fruits of Encore mandarin were investigated. Phosphatidylinositol content of the cells associated with dark stains was lower in unpitted tissues, whereas the concentration of phosphatidylglycerol, phosphatidylcholine and phosphatidylethanolamine did not vary significantly. In these pitted cells, protein content also showed a 1.59-fold increase. Additionally, the relative proportions of gln, thr, asp, glu and gly increased sharply, while ala and tyr decreased. The polypeptide patterns showed quantitative changes when samples of stained and unstained tissues were compared by SDS-PAGE electrophoresis. Qualitatively, the cells associated with pitted tissues revealed a new polypeptide band with an apparent mol. wt. of 50.4 kDa as well as the disappearance of another one of 10 kDa. Ethylene production in the dark stained tissues was lower than in unpitted tissues and these cells showed significant increases in membrane permeability, hydroxyl radical production, and lipid peroxidation. Furthermore, in these tissues the levels of the carotenoids increased significantly but levels of chlorophyll decreased. It was concluded that in the pitted tissues the significant changes of the membrane composition are closely associated with an increasing acyl lipid peroxidation mediated by hydroxyl radical production. The modulation of this metabolism further indicates an incomplete degradation of fatty acids. The implications of the increasing accumulation of carotenoids in the synthesis of oxy radicals are also discussed.
Carotenoids↗
Influence of dihydralazine on the generation of hydroxyl radicals by human granulocytes.
Hydroxyl radical generation by living human granulocytes was determined by ESR using DMPO as a spin trapping reagent. The influence of dihydralazine and exogenous superoxide dismutase (SOD) on the radical generation was observed. In the presence of dihydralazine the radical production increases distinctly; the higher hydroxyl radical production is observed for the dihydralazine-SOD containing system which is explained by the partial decomposition of the enzyme in the presence of dihydralazine. No effect of dihydralazine on the lipid fluidity of the granulocyte membrane and phase transition in the membrane of living granulocytes was observed.
Cell Membrane↗
Modulation of normobaric pulmonary oxygen toxicity by hydroxyl radical inhibition.
The effects of hydroxyl radical inhibition on an experimental model of normobaric pulmonary oxygen toxicity have been studied. The metal ion chelator, desferrioxamine (which inhibits hydroxyl-radical generation) or the hydroxyl-radical scavenger, dimethylthiourea (DMTU), were administered in an attempt to block hydroxyl-radical-mediated tissue injury. Lung injury was monitored in Sprague-Dawley rats by examining lung histology and bronchoalveolar lavage and by assessing pulmonary capillary permeability using the 125I-albumin lung permeability index and the lung weight:body weight ratio. Control animals had lung permeability indices 0.183 +/- 0.005 and lung weight to body weight ratio of 4.50 +/- 0.10 (all as mean +/- SEM). With increased duration of exposure to hyperoxia, there was a progressive increase in pulmonary inflammation, with thickening of alveolar membranes and atelectasis and a progressive increase in lung permeability indices (0.434 +/- 0.088 at 24 hrs; 0.954 +/- 0.165 at 48 hrs; and 1.55 +/- 0.214 at 60 hrs); and lung weight to body weight ratio (5.28 +/- 0.11 at 24 hrs; 6.54 +/- 0.23 at 48 hrs; and 8.91 +/- 0.51 at 60 hrs). Treatment with desferrioxamine provided significant protection from lung injury after 24 hrs of hyperoxia (eg., lung permeability indices 0.250 +/- 0.018; lung weight to body weight ratio 4.68 +/- 0.14, both p less than 0.025; cf. 24-hr hyperoxia controls) but no reduction in pulmonary injury was observed after 48 and 60 hrs of hyperoxia exposure.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Free radical activity of PM10: iron-mediated generation of hydroxyl radicals.
The purpose of this study was to test the hypothesis that particulate matter < or = 10 microns in aerodynamic diameter (PM10) particles have the ability to generate free radical activity at their surface. We collected PM10 filters from the Edinburgh, United Kingdom, Enhanced Urban Network sampling site, removed particles from the filter, and tested their ability to cause free radical damage to supercoiled plasmid DNA. We found that the PM10 particles did cause damage to the DNA that was mediated by hydroxyl radicals, as shown by inhibition of the injury with mannitol. The PM10-associated hydroxyl radical activity was confirmed using a high-performance liquid chromatography-based assay to measure the hydroxyl radical adduct of salicylic acid. Desferrioxamine abolished the hydroxyl radical-mediated injury, which suggests that iron was involved. Analysis of PM10 filters confirmed the presence of large amounts of iron and leaching studies confirmed that the PM10 samples could release substantial amounts of Fe(III) and lesser amounts of Fe(II). To investigate the size of the particles involved in the hydroxyl radical injury, we centrifuged the suspension of PM10 to clarity, tested the clear supernatant, and found that it had all of the suspension activity. We conclude, therefore, that the free radical activity is derived either from a fraction that is not centrifugeable on a bench centrifuge, or that the radical generating system is released into solution.
Air Pollutants↗
An optical hydroxyl radical sensor.
A hydroxyl radical (.OH) fibre-optic sensor has been developed. An .OH radical-sensitive reagent phase (nitrophenol) was immobilized onto XAD-7 methacrylate beads. Subsequently the beads were attached to the distal end of a polymethylmethacrylate fibre optic. Nitrocatechol, generated from the attack of .OH radical on nitrophenol, exhibits a strong absorption band in the visible region of the electromagnetic spectrum (lambda max = 510 nm). Here, reflectance spectroscopy was employed to monitor the concomitant intensity decrease in the reflectance spectrum upon .OH radical attack. The sensor exhibited excellent stability and linearity of response to .OH generated by a Fenton reaction system (EDTA, Fe(II) and H2O2) with H2O2 over the concentration range of 3.6 x 10(-6)-8.0 x 10(-2) M.
Fiber Optic Technology↗
The reaction of ferrous EDTA with hydrogen peroxide: evidence against hydroxyl radical formation.
Radiolytically generated hydroxyl radicals degrade cytochrome c. In contrast, ferrocytochrome c is oxidized in the Fe-EDTA-H2O2 system, without loss of any cytochrome c. It is concluded that in the latter system no hydroxyl radicals are formed and that oxidation takes place via a FeO(II)EDTA or Fe(II)-H2O2-EDTA complex.
Cytochrome c Group↗
Do humans neutrophils form hydroxyl radical? Evaluation of an unresolved controversy.
Hydroxyl radical is a potent oxidizing agent of potential importance in human pathobiology. Since neutrophilic phagocytes make superoxide and hydrogen peroxide during phagocytosis, it has been proposed that hydroxyl radical is also formed. In this paper we review the literature which supports or refutes formation of hydroxyl radical by neutrophils and the mechanism(s) by which this radical might be formed. We conclude that there is no definitive proof for hydroxyl radical formation by neutrophils. In fact, neutrophil release of lactoferrin and myeloperoxidase appears to limit formation of this radical. Future studies are likely to determine whether superoxide released by neutrophils interacts with target substrates to allow formation of hydroxyl radical.
Free Radicals↗
Cytochrome P-450 mediates tissue-damaging hydroxyl radical formation during reoxygenation of the kidney.
Renal reperfusion injury results from oxygen radical generation. During reoxygenation of hypoxic kidney cells, xanthine oxidase produces superoxide radical, which eventuates in hydroxyl radical formation by the Fenton reaction. This reaction, catalyzed by transition metals such as iron, is particularly important because hydroxyl radical is highly reactive with a wide variety of biomolecules. We tested the hypothesis that this catalytic function is fostered by iron released from the heme moiety of cytochrome P-450. Primary cultures of rat proximal tubule epithelial cells studied in a subconfluent stage were subjected to 60 min of hypoxia and 30 min of reoxygenation. When cells were pretreated with one of three cytochrome P-450 inhibitors (piperonyl butoxide, cimetidine, or ketoconazole), lethal cell injury was attenuated. There was the expected increase in O2-. production during hypoxia/reoxygenation that cytochrome P-450 inhibitors did not prevent; on the other hand, inhibitors did prevent reoxygenation-induced hydroxyl radical formation. Analogously, the increase in catalytic iron (bleomycin-detectable iron) that accompanies hypoxia/reoxygenation did not occur in the presence of cytochrome P-450 inhibitors. In vivo studies confirmed a protective effect of cytochrome P-450 inhibition because glomerular filtration rate was better preserved in rats pretreated with cimetidine and then subjected to renal artery occlusion. In summary, several chemically distinct cytochrome P-450 inhibitors reduced iron release, and thereby, hydroxyl radical formation and reoxygenation-induced lethal cell injury, without inhibiting superoxide radical formation. We conclude that highly labile P-450 may act as an Fe-donating catalyst for Fenton reaction production of HO.-mediated reperfusion injury.
Animals↗
Free radical activity of synthetic vitreous fibers: iron chelation inhibits hydroxyl radical generation by refractory ceramic fiber.
Synthetic vitreous fibers are in widespread use but the parameters that dictate their carcinogenicity are still a matter of scientific debate. The free radical activities of a panel comprising an asbestos sample and five different respirable synthetic vitreous fiber samples were determined, to address the hypothesis that carcinogenic fibers have greater free radical activity than noncarcinogenic fibers. On the basis of recent inhalation studies, the six samples were divided into three carcinogenic fibers-amphibole asbestos, silicon carbide, and refractory ceramic fiber 1 (designated with the abbreviation RCF 1)-and three noncarcinogenic fibers--man-made vitreous fiber 10 (a glass fiber sample designated with the abbreviation MMVF 10), Code 100/475 glass fiber, and RCF4. All experiments were carried out with equal fiber numbers. Of the two assays of free radical activity used, the plasmid assay of DNA scission showed only amosite asbestos to have free radical activity, while the salicylate assay of hydroxyl activity showed that both amosite asbestos and RCF1 release hydroxyl radicals; silicon carbide fibers had no free radical activity in either of the assays. None of the noncarcinogenic fibers demonstrated free radical activity in either of the assays. The differences in the two assays in demonstrating free radical activity with RCF1 may be due to increased release of Fe from RCF1 under the more acid conditions of the salicylate assay, which was confirmed by the fact that soluble iron caused hydroxylation of salicylate. Presence of an iron chelator inhibited the ability of the RCF1 fibers to cause hydroxylation of salicylate, demonstrating that RCF1 generates hydroxyl radical by Fenton chemical reaction in the same way as amphibole asbestos.
Animals↗
RP-HPLC study of the degradation of diclofenac and piroxicam in the presence of hydroxyl radicals.
The effect of hydroxyl radical attack on two non-steroidal anti-inflammatory drugs (NSAIDs) was studied in vitro. Diclofenac and piroxicam were analysed by RP-HPLC after reaction with OH* free radicals to detect newly formed oxidation and/or degradation products. OH* free radicals were obtained by means of ferrous sulphate and ascorbic acid mixtures. During the reaction the mixtures were exposed to irradiation by a tungsten lamp to obtain an increased and more reproducible formation of hydroxyl radicals. The chromatographic profiles showed the formation of several new peaks for both diclofenac and piroxicam due to the presence of a number of degradation/oxidation products formed in the presence of OH* radicals.
Anti-Inflammatory Agents, Non-Steroidal↗
Indole-3-propionate: a potent hydroxyl radical scavenger in rat brain.
The hydroxyl radical scavenging activity of indole-3-propionate was evaluated by kinetic competition studies with the hydroxyl radical trapping reagent 2,2'-azino-bis-(3-ethyl-benz-thiazoline-6-sulfonic acid) (ABTS) and by measuring hydroxyl radical-initiated lipid peroxidation in the rat striatum. Using ABTS, the indole was shown to act as a potent hydroxyl radical scavenger with a rate constant of 7.8x1010 mol l-1 s-1. Hydroxyl radical-initiated lipid peroxidation, determined by measuring tissue malondialdehyde formation, was inhibited dose-dependently both in vitro and in vivo. Indole-3-propionate reacts with hydroxyl radicals at a diffusion controlled rate and can thereby provide on-site protection against the oxidative damage of biomolecules induced by these highly reactive and toxic oxygen intermediates. While it remains to be established if endogenous brain tissue levels of indole-3-propionate are sufficiently high to have a significant impact on total antioxidative capacity, the compound itself or a structurally related agent may be useful as an antioxidant adjuvant to combat hydroxyl radical-mediated oxidative stress.
Animals↗
A comparison of scavenging abilities of antioxidants against hydroxyl radicals.
The reactivities of various antioxidative compounds including catechol derivatives and endogenous radical scavengers toward hydroxyl radical (.OH) were investigated by an electron spin resonance-spin trapping method, thiobarbituric acid method, and DNA strand scission assay. Hydroxyl radical was generated by both the reaction of Cu(II) complex with hydrogen peroxide (H2O2) and ultraviolet (uv) photolysis of H2O2. At physiological pH, catechol derivatives such as protocatechuic acid and catechin greatly suppressed the DNA strand scission by .OH produced from the reaction of Cu(en)2 with H2O2, whereas ascorbic acid and acetylcysteine accelerated DNA strand scission. The former case is due to the chelation of catechol derivatives to Cu(II) ion, forming of Cu(II) complexes being unable to react with H2O2, and the latter case is due to the acceleration of the reduction rate of Cu(II) to Cu(I). On the other hand, all compounds used here suppressed the DNA strand scission by .OH produced from uv photolysis of H2O2. The differences of the reactivities between the reaction system of Cu(en)2-H2O2 and the uv photolysis of H2O2 have been discussed.
Antioxidants↗