Oxidative Chain Reactions Research Articles

ChemInform Abstract: Aromatic Hydroxylations by Flavins: Evidence on Direct Attack of Phenylalanine by Flavin Radical Species.

Abstract In 0.05–12.0 N acidic solutions, the 5-ethyl-3-methyllumiflavosemiquinone 5 (and/or 5H + ) spontaneously arose from the corresponding flavinium cation 4 . Raising the temperature from 20 to 50°C, considerably increased the reaction rates with no significant changes in the yields of 5 ( 5H + ). The spontaneous one-electron reduction of 4 requires a coupling with a one-electron oxidation of another flavin such as 5-ethyl-4 a -hydroxy-3-methyl-4 a ,5-dihydroflavin pseudobase 1 . The latter, being in equilibrium with 4 , can be oxidized to give the transient 5-ethyl-4 a -hydroxy-3-methyllumiflavin radical 2 . This is the protonated form of a flavinoxy radical 3 a,b , a product of a homolysis of the OO bond in a dihydroflavin hydroperoxide. As an alternative to the homolysis mentioned, the one-electron oxidation of 1 provides the principle to develop a new hydroxylating model system that does not require a dihydroflavin hydroperoxide as a starting compound. Using phenylalanine as a test substrate, the anaerobic formation of tyrosine and its o - and m -hydroxyphenylalanine isomers was established. This achievement is a strong experimental support for the hypothesis that flavin radical species like 2 may directly attack an aromatic. Evidence was obtained on some accumulation of an intermediate that is not a hydroxycyclohexadienyl radical. It was shown to react in a secondary, oxidative chain reaction, remarkably increasing the yields of aromatic hydroxylation without any further supply of flavin.

The Effects of Microwave Frying on Physicochemical Properties of Frying and Sunflower Oils

AbstractDeep fat frying is a method of food preparation which has been popular for quite a number of years. During deep frying, the quality of oil and the finished product decreases as the result of heat treatment of the oil exposed to air at high temperature. Application of heat by microwave as an alternative to the conventional method of frying has become popular in recent years. In this research, the effects of microwave frying on the changes in the quality indices of used oil have been investigated. To achieve this, potato slices were fried in both frying and sunflower oils by application of medium power microwave (550 W) for 20 min, three times a day, for five consecutive days, and oils were sampled for analysis. The results obtained from the chemical tests demonstrated that used frying oil had lower polar compounds, a higher induction period, and more saturated fatty acids than sunflower oil. The interesting point observed was that peroxides formed as the result of oxidation chain reactions were not broken down and were built up due to the lower temperature and shorter period of frying. Therefore microwave frying might be considered as a suitable alternative to the conventional frying due to less degradation of the oil and consequently a lower production of artifacts.

Reactive oxygen and nitrogen species induce protein and DNA modifications driving arthrofibrosis following total knee arthroplasty

BackgroundArthrofibrosis, occurring in 3%-4% of patients following total knee arthroplasty (TKA), is a challenging condition for which there is no defined cause. The hypothesis for this study was that disregulated production of reactive oxygen species (ROS) and nitrogen species (RNS) mediates matrix protein and DNA modifications, which result in excessive fibroblastic proliferation.ResultsWe found increased numbers of macrophages and lymphocytes, along with elevated amounts of myeloperoxidase (MPO) in arthrofibrotic tissues when compared to control tissues. MPO expression, an enzyme that generates ROS/RNS, is usually limited to neutrophils and some macrophages, but was found by immunohistochemistry to be expressed in both macrophages and fibroblasts in arthrofibrotic tissue. As direct measurement of ROS/RNS is not feasible, products including DNA hydroxylation (8-OHdG), and protein nitrosylation (nitrotyrosine) were measured by immunohistochemistry. Quantification of the staining showed that 8-OHdg was significantly increased in arthrofibrotic tissue. There was also a direct correlation between the intensity of inflammation and ROS/RNS to the amount of heterotopic ossification (HO). In order to investigate the aberrant expression of MPO, a real-time oxidative stress polymerase chain reaction array was performed on fibroblasts isolated from arthrofibrotic and control tissues. The results of this array confirmed the upregulation of MPO expression in arthrofibrotic fibroblasts and highlighted the downregulated expression of the antioxidants, superoxide dismutase1 and microsomal glutathione S-transferase 3, as well as the significant increase in thioredoxin reductase, a known promoter of cell proliferation, and polynucleotide kinase 3'-phosphatase, a key enzyme in the base excision repair pathway for oxidative DNA damage.ConclusionBased on our current findings, we suggest that ROS/RNS initiate and sustain the arthrofibrotic response driving aggressive fibroblast proliferation and subsequent HO.

Antioxidant properties of resveratrol: A structure–activity insight

Resveratrol, a natural product, is known to affect a broad range of intracellular mediators. In the present study, we clarified the antioxidant activity of resveratrol by employing various in vitro antioxidant assays such as DPPH•, ABTS•+, DMPD•+, O2•− and H2O2 scavenging activities, total antioxidant activity, reducing abilities, and Fe2+ chelating activities. Resveratrol inhibited 89.1% of the lipid peroxidation of linoleic acid emulsion at 30 µg/mL concentration. On the other hand, BHA, BHT, α-tocopherol, and trolox exhibited inhibitions of 83.3, 82.1, 68.1, and 81.3% against peroxidation of linoleic acid emulsion at the same concentration, respectively. In addition, resveratrol had effective DPPH•, ABTS•+, DMPD•+, O2•− and H2O2 scavenging activities, reducing power, and Fe2+ chelating activities. The present study found that resveratrol had effective in vitro antioxidant and radical scavenging activity. It can be used in pharmacological and food industry due to its antioxidant properties. Antioxidants are often added to foods to prevent the radical chain reactions of oxidation and they act by inhibiting the initiation and propagation step leading to the termination of the reaction and delay the oxidation process. At the present time, the most commonly used antioxidants are BHA, BHT, propylgallate and tert-butyl hydroquinone. Besides that BHA and BHT are restricted by legislative rules because of doubts over their toxic and carcinogenic effects. Therefore, there is a growing interest on natural and safer antioxidants in food applications, and a growing trend in consumer preferences for natural antioxidants, all of which has given more impetus to explore natural sources of antioxidants. A variety of foods and beverages of vegetable origin contain several nonflavonoid classes of phenolic compounds synthesized by plants. Among them, resveratrol has been identified as the major active compound of stilbene phytoalexins and is presumed to be beneficial for human health. Resveratrol is naturally occurring in the fruits and leaves of edible plants, peanuts, mulberries, grapes and red wine. Resveratrol is currently in the limelight all over the world due to their beneficial effects on the human body. Resveratrol can be used for minimizing or preventing lipid oxidation in pharmaceutical products, retarding the formation of toxic oxidation products, maintaining nutritional quality and prolonging the shelf life of food products and pharmaceuticals instead of BHA and BHT and other antioxidant compounds because of their safer usage.

Peptides as antioxidants and carbonyl quenchers in biological model systems

Subjecting selected peptides to in vitro analyses covering their ability to interfere with the lipid oxidation chain reaction as well as to protect proteins from direct and indirect oxidation has provided the basis for a more detailed understanding of peptide-mediated protection in biological systems. The efficiency of peptides as radical scavengers and chain-breaking antioxidants in oxidizing lipid membranes was found to be low. Previous studies on antioxidative activity of peptides tend not to include comparisons with efficiencies of more well-documented antioxidants and/or use irrelevantly high dosages of peptides. The present study demonstrates that the effect of the investigated peptides towards oxidation in biological membrane systems is mainly a protection of vital proteins from being oxidatively modified. This protection is obtained through a prevention of lipid oxidation derived carbonylation (indirect protein oxidation) and through interference with aqueous radical species (direct protein oxidation), and it is only achieved if the peptides are present in high concentrations as sacrificial antioxidants.

KIMIA OKSIGEN SINGLET: SENSITISER, CAHAYA DAN REAKTIVITASNYA TERHADAP ASAM LEMAK TAK JENUH

Singlet oxygen chemistry and photooxidation reaction, in general, often require one or more criticalreaction steps that involve a sensitizer and light for photochemistry production of singlet oxygen from atriplet state. Singlet oxygen can be formed chemically, enzimatically, and photochemically. However, themost well documented formation mechanism for singlet oxygen is photochemistry using sensitizers.Chlorophyll, riboflavin, myoglobin, porphyrins, erythrosine, rose bengal, methylene blue, bilirubin andretinal are well-known photosensitizer and can absorb energy from light and transfer it to triplet oxygen toform singlet oxygen. Photooxidation provides an important way to produced hydroperoxides fromunsaturated fatty acids in presence of oxygen, light energy and photosensitizer. Hydroperoxide are themajor initiation products of lipid oxidation chain reactions. Singlet oxygen participated in the initiation stepof oil oxidation and the reaction rate of singlet oxygen with oleic, linoleic acid and linolenic are about30.000, 1450 and 900 times greater than that of triplet oxygen. Therefore, this review discusses twoimportant singlet oxygen mechanisms, the formation of singlet oxygen and double bond reaction inunsaturated fatty acid system Key word: Singlet oxygen, sensitizer, unsaturated fatty acids, hydroperoxides

Transmission of oxLDL-derived lipid peroxide radicals into membranes of vascular cells is the main inducer of oxLDL-mediated oxidative stress

Oxidatively modified LDL is generally accepted to be an important elicitor of pro-mitotic, pro-inflammatory, and atherogenic effects in vascular cells. The uptake of oxLDL and concomitant activation of the O2-producing NAD(P)H oxidase and/or oxLDL as a self-contained emitter of O2 are believed to trigger these malfunctions. The following observations allowed reinvestigating the mode of oxLDL-induced stress: (1) we observed that artery smooth muscle primary cells internalize fluorescently labelled oxidized or acetylated LDL considerably less efficient than endothelial cells. (2) Both types of cells, however, displayed an oxLDL concentration dependent level of oxidative stress as monitored by the oxidation of carboxy-H2DCFDA to fluorescent carboxy-DCF. A dose dependent decrease of dihydroethidine oxidation to oxyethidine implied an oxLDL-induced depletion of the cellular energy pool. The release of O2 by exogenous oxLDL, as postulated above, did not sufficiently explain intracellular stress because the fluorescence was only marginally blocked by antioxidative enzymes (SOD, catalase) or substances (l-NAME, DMSO, DMHP, DMTU). We were able to reveal a third mode of oxLDL-induced stress by showing with the help of a fluorescent, oxidizable lipid analogue (BODIPY™ 581/591 C11) that oxLDL-derived lipid peroxides and radicals migrate into cellular membranes giving rise to a chronic inoculation of the vascular cells with oxidative chain reactions. The novel data may help to design adequate therapeutic strategies against oxLDL-induced cardiovascular diseases.

Effect of Group II Metal Cations on Catecholate Oxidation

The unexpected effects of Ca(2+) on the free-radical chain reactions of dopamine, norepinephrine, isoproterenol, and pyrocatechol oxidation are studied using oxygen consumption measurements, EPR-spectroscopy, UV/VIS spectrophotometry, and by potentiometric titration. It is found that the formation of Ca(2+)-catecholate complexes is accompanied by an increase in the dissociation constants (K(ai) ) of their phenolic hydroxyls. At pH>pK(ai) and in the presence of alkaline-earth metal cations, the rate of catecholate oxidation increases (Ca(2+), Mg(2+)> Sr(2+), Ba(2+)), whereas on addition of Zn ions the rate decreases. The effects of Group II metal cations on catecholate autoxidation are concomitant with a transient increase of the EPR signal for metal-semiquinonate complexes. Therefore, the effects of Ca(2+) and other alkaline-earth metal cations on catecholate autoxidation can be defined as 1) additional deprotonation of catechol OH-groups involved in the formation of M(2+)-catecholate complexes, the latter exceeding catechols in the susceptibility to dioxygen-induced oxidation and 2) formation of relatively stable free-radical intermediates responsible for chain propagation.

Metal free in situ formation of phthalimide N-oxyl radicals by light-induced homolysis of N-alkoxyphthalimides

Irradiation of N-triphenylmethyloxy- or N-diphenylmethyloxy phthalimide is reported to result in the formation of phthalimide N-oxyl radical (PINO), which is able to initiate and propagate oxidative radical chain reactions of hydrocarbons.

Heme of consumed red meat can act as a catalyst of oxidative damage and could initiate colon, breast and prostate cancers, heart disease and other diseases

Dietary epidemiological studies indicate correlations between the consumption of red meat and/or processed meat and cancer of the colon, rectum, stomach, pancreas, bladder, endometrium and ovaries, prostate, breast and lung, heart disease, rheumatoid arthritis, type 2 diabetes and Alzheimer's disease. The correlation of all these major diseases with dietary red meat indicates the presence of factors in red meat that damage biological components. This hypothesis will focus on the biochemistry of heme compounds and their oxidative processes. Raw red meat contains high levels of oxymyoglobin and deoxymyoglobin and oxyhemoglobin and deoxyhemoglobin and cytochromes in muscle and other tissues. Cooked and processed meat contain hemichromes and hemochromes. After being eaten heme proteins are hydrolyzed to amino acids and peptides and the heme group which is coordinated with strong ligands. The iron of heme coordinates to the sulfur, nitrogen or oxygen of amino acids and peptides and other biological components. The coordinated heme groups are absorbed and transported by the blood to every organ and tissue. Free and coordinated heme preferentially catalyze oxidative reactions. Heme catalyzed oxidations can damage lipids, proteins, DNA and other nucleic acids and various components of biological systems. Heme catalysis with hydroperoxide intermediates can initiate further oxidations some of which would result in oxidative chain reactions. Biochemical and tissue free radical damage caused by heme catalyzed oxidations is similar to that resulting from ionizing radiation. Oxidative biochemical damage is widespread in diseases. It is apparent that decreasing the amount of dietary red meat will limit the level of oxidative catalysts in the tissues of the body. Increasing consumption of vegetables and fruits elevates the levels of antioxidative components, for example, selenium, vitamin E, vitamin C, lycopene, cysteine-glutathione and various phytochemicals. These detrimental processes of heme catalysis of oxidative damage hypothesized here are not well recognized. More investigative studies in this field need to be done.

Aging of Black Filled Rubber under Deformation

Abstract Prolonged dynamic deformation of a rubber is found to significantly accelerate oxidative crosslinking due to mechanochemical oxidative crosslinking. The extent of acceleration is larger at lower temperatures and increases with increasing strain. The activation energy of the rate of oxidative crosslinking decreases with increasing strain toward the highest value among the unit reactions of oxidative chain reaction cycle or the value of diffusion of oxygen, which is much smaller than that of static aging. On the other hand, static deformation is also found to accelerate oxidative crosslinking but to considerably lesser extents. Mechanochemical acceleration can be noticed only in the early stage of prolonged deformation. The degree of acceleration in prolonged deformation increased with increasing strain without change in the activation energy. The acceleration observed in prolonged static deformation is considered to arise from the increased area of exposure to the oxidizing atmosphere. It appears that mechanochemical acceleration is merely spent to compensate the loss in crosslink density upon deformation in this case.

Kinetic regularities of solid-phase formation in the branching chain reaction of dichlorosilane oxidation in rf plasma at low pressures and 293 K

In studies of the initiated ignition of dichlorosilane−oxygen mixtures it has been shown that rf discharge applied before ignition leads to an increase in the lifetime of aerosol particles in the reactor volume, in contrast to direct current discharge which markedly decreases the amount of aerosol particles formed in ignition. Ordered structures of the type of ‘liquid dust crystal’ have been detected in rf plasma of branching-chain heterophaseous reaction.

Free radicals, antioxidants, and soil organic matter recalcitrance

SummaryHighly reactive, and potentially damaging, free radicals are readily generated in our oxygen‐rich environment, and are ubiquitous in biological systems. However, plants and animals have evolved protection against them with a range of antioxidant molecules, such as vitamins C and E, many of which are phenolic compounds. These stop the destructive chain reaction of free radical formation by being transformed into unreactive, stable free radicals. The biodegradation of food involves oxidation by free radicals, and is retarded by antioxidants. Similarly, the biodegradation of plant residues in soils involves free radicals; so the questions arise: (i) do soils have antioxidants, and (ii) what function might they have? The evidence suggests that they probably do have antioxidants. First, plant and animal remains added to soils will contain antioxidants. These are likely to persist for a time, particularly tannins, which are polyphenolic compounds with known antioxidant properties and which are relatively resistant to degradation. Second, studies using electron spin resonance spectroscopy have shown that humic materials contain stable semiquinone free radicals, and that their concentration increases as humification progresses. These semiquinone species are most likely to be derived from the reaction of phenolic compounds with reactive radicals. If this is the case, the phenolics are acting as antioxidants, because they are scavenging the reactive free radicals and terminating the oxidative chain reaction responsible for soil organic matter (SOM) degradation. Thus the soil's antioxidant capacity could control the rate of breakdown of organic matter in the more labile pools and could provide a chemical mechanism for the recalcitrance of SOM. Current available evidence for the nature of the recalcitrant pool in SOM is discussed in the light of this hypothesis, and the experimental approaches necessary for testing it are outlined.

Balancing the generation and elimination of reactive oxygen species

Fossil records suggest that bacteria developed the ability to photosynthesize ≈3,500 million years ago (mya), initiating a very slow accumulation of atmospheric oxygen (1). Recent geochemical models suggest that atmospheric oxygen did not accumulate to levels conducive for aerobic life until 500–1,000 mya (2, 3). The oxygenation of Earth's atmosphere resulted in the emergence of aerobic organisms followed by a great diversification of biological species and the eventual evolution of humans. Although oxygen is thought to have been responsible for the expansion of life on Earth, there are two sides to this molecule: life giving and life taking. Oxygen in the air we breathe is a relatively nonreactive chemical (4). However, when oxygen is exposed to high-energy or electron-transferring chemical reactions, it can be converted to various highly reactive chemical forms (Fig. 1) collectively designated “reactive oxygen species” (ROS; ref. 5). ROS are toxic to biological organisms because they oxidize lipids, proteins, DNA, and carbohydrates, resulting in the breakdown of normal cellular, membrane, and reproductive functions. Ultimately, toxic levels of ROS cause a chain reaction of cellular oxidation, resulting in disease and lethality (5–7). ROS are unavoidable byproducts of biochemical pathways, such as glycolysis and photosynthesis, that are central to energy production and storage …

ANTIOXIDANT CAPACITY OF BERRY CROPS, CULINARY HERBS AND MEDICINAL HERBS

ANTIOXIDANT CAPACITY OF BERRY CROPS, CULINARY HERBS AND MEDICINAL HERBS

Mitochondrial formation of reactive oxygen species.

The reduction of oxygen to water proceeds via one electron at a time. In the mitochondrial respiratory chain, Complex IV (cytochrome oxidase) retains all partially reduced intermediates until full reduction is achieved. Other redox centres in the electron transport chain, however, may leak electrons to oxygen, partially reducing this molecule to superoxide anion (O2-*). Even though O2-* is not a strong oxidant, it is a precursor of most other reactive oxygen species, and it also becomes involved in the propagation of oxidative chain reactions. Despite the presence of various antioxidant defences, the mitochondrion appears to be the main intracellular source of these oxidants. This review describes the main mitochondrial sources of reactive species and the antioxidant defences that evolved to prevent oxidative damage in all the mitochondrial compartments. We also discuss various physiological and pathological scenarios resulting from an increased steady state concentration of mitochondrial oxidants.

Mitochondrial formation of reactive oxygen species

The reduction of oxygen to water proceeds via one electron at a time. In the mitochondrial respiratory chain, Complex IV (cytochrome oxidase) retains all partially reduced intermediates until full reduction is achieved. Other redox centres in the electron transport chain, however, may leak electrons to oxygen, partially reducing this molecule to superoxide anion (O2−•). Even though O2−• is not a strong oxidant, it is a precursor of most other reactive oxygen species, and it also becomes involved in the propagation of oxidative chain reactions. Despite the presence of various antioxidant defences, the mitochondrion appears to be the main intracellular source of these oxidants. This review describes the main mitochondrial sources of reactive species and the antioxidant defences that evolved to prevent oxidative damage in all the mitochondrial compartments. We also discuss various physiological and pathological scenarios resulting from an increased steady state concentration of mitochondrial oxidants.

An Electroanalytical Investigation on the Redox Properties of Calcium Antagonist Dihydropyridines

AbstractThe antioxidant capacity of some calcium antagonists and one calcium agonist 1,4‐dihydropyridines (DHPs) was evaluated by a competitive kinetic procedure. With the exception of Amlodipine, all the calcium antagonist DHPs display an unambiguous antioxidant capacity, while for the calcium agonist DHP (Bay K 8644) no measurable reactivity towards peroxyl radicals could be detected. The finding was corroborated by an electroanalytical investigation of the redox properties of DHPs compounds to get an insight about both the thermodynamic constraints of their oxidation process and reaction pattern. The oxidation potentials decrease with both antioxidant capacity and increasing basic character, thus suggesting the relevance of the electron density on the DHP ring. For all the compounds investigated, the overall oxidation process takes place through a primary one‐electron step accompanied by a fast proton release and the formation of a neutral radical undergoing a second much easier one‐electron step. The protonated form of the parent pyridine derivative is thus generated as the final product. This pattern is relevant for the antioxidant effect, since the radical intermediate is much more prone to be oxidized than to be reduced, thus fully preventing the propagation of the oxidative chain reaction. In the case of calcium antagonist DHPs, the above release of protons complicates the overall oxidation process by introducing a parasitic side reaction where a coupling between protons and the starting species takes place. This DHP self‐protonation subtracts part of the original species from the electrode process because the parent cationic species is no longer electroactive. Conversely, the calcium agonist DHP, which is more difficult to be oxidized, turned out to be such a weak base as to be unable to undergo the self‐protonation reaction. The combined effect of oxidation potentials and proton binding capacity of DHPs is a key element for the redox transition, which could support their antioxidant effect and should be considered to some extent in accounting for the calcium antagonist vs calcium agonist effect.

Dark reactions of free radicals trapped in densely crosslinked polymer networks after photopolymerization

AbstractDifunctional methacrylate monomers containing stiff or flexible spacers were combined with a vinylcyclopropane derivate in a copolymerization to form densely crosslinked networks. The high rate of visible light photoinitiation at 20–22°C was used for starting the polymerization. By switching off the light after 40 s, the long‐lived free radicals, trapped in the polymer network, retain radical processes, however, at substantially retarded rates. The postcuring development of the network structure in the investigated samples lasting at least 12 weeks was proved by the increasing density of the crosslinks, by the increasing amount of the gel fraction, and by the decreasing of the residual unsaturation. The relaxation spectra from dynamic mechanical thermal analyses (DMTA) show curves with two evident maxima. The first one belonged the glass transition (Tg) of original network and increases in the postcuring period. The second one belonged to the final structure to which the crosslinked polymer approaches slowly during aging. The final state develops fast during a DMTA thermal scan to 200°C. All procedures proceeded in the dark, but in the presence of air oxygen. The chemiluminescence (CL) response of the postcured samples proved the accumulation of hydroperoxides. The oxidation chain reaction took place in the postcuring time and competed with the building up of additional crosslinks. The majority of postcuring changes were observed during the first 3 weeks of aging. Nine weeks later, the long‐lived radicals were still present in the network and maintained the sensibility of the crosslinked polymer to free‐radical reactions. © 2003 Wiley Periodicals, Inc. J Appl Polym Sci 89: 579–588, 2003

Effect of vitamin E treatment on the oxidative damage occurring in Henoch‐Schönlein purpura

Aim: To evaluate the role of reactive oxygen molecules (ROMs) in the pathogenesis of Henoch‐Schonlein purpura and the effect of vitamin E on oxidative damage. ROMs have been suggested to contribute in many pathological conditions including renal diseases and vasculitis. Methods: The activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH‐Px) as antioxidant enzymes were measured, and the level of malondialdehyde (MDA) as an indicator of lipid peroxidation in 27 children with Henoch‐Schönlein purpura at the onset of the disease and during the remission period. The results of this study were compared with those of 11 healthy children studied as a control group. Results: With regard to all the oxidative damage parameters such as SOD, GSH‐Px and MDA, significant differences were detected between the patients and the control group in both the acute and remission periods. But no such differences were detected between patients with and those without renal involvement. In 15 patients receiving vitamin E treatment, oxidative damage parameters and clinical course showed no improvement despite significant increases in plasma vitamin E levels. Conclusion: Oxidative damage and lipid peroxidation may play an important part in the pathogenesis of Henoch‐Schonlein purpura but vitamin E given after initiation of lipid peroxidation, which is the last phase of cellular damage, is of no use in breaking down the oxidative chain reactions that have already been triggered.