Superoxide Formation Research Articles

Pengaruh Pemberian Jus Buah Tomat (Solanum Lycopersicum) Terhadap Kadar Antioksidan Pada Ibu Hamil Trimester Ketiga Pascasenam Hamil

Senam merupakan olah raga terbaik yang dapat dilakukan oleh ibu hamil menjelang persalinannya. Salah satu jenis senam yang ditujukan bagi ibu hamil adalah senam hamil. Senam hamil adalah program kebugaran yang diperoleh bagi ibu hamil secara fisik dan mental pada peersalinan cepat, aman dan spontan. Selain untuk meningkat kesehatan ibu hamil, disatu sisi senam hamil dapat bedampak terhadap terbentuknya radikal bebas. Antioksidan (SOD) diperlukan untuk menetralisir radikal bebas ini, salah satu antioksidan eksogen yang dapat diberikan adalah jus buah tomat (Solanum lycopersicum). Penelitian ini bertujuan untuk mengetahui pengaruh pemberian jus buah tomat terhadap kadar antioksidan pada ibu hamil trimester ketiga pascasenam hamil. Background. The changed that occur in anatomically and physiologically in an expectant mother in the third trimester of gestation was a normal occurrence took place. Changed was often followed by complications, if not handled properly, can be harmful to the pregnant woman and the fetus she was carrying. Complications in the third trimester of pregnancy, associated with the presence of oxidative stress, in which the third trimester increased metabolic processes, leading to increased production of free radicals. One way to reduce the complications of pregnancy and childbirth was to do the pregnancy exercise. Pregnancy exercise was the best exercise that can be done by pregnant women in labor. Pregnancy exercise was recommended at 6 months gestation entered into on and have specific movement princioles adapted to the condition of pregnantwomen. By doing pregnancy exercise excessive oxygen or not metabolizer can be used to generate energy. At 4-5% of pregnant women are not rmetabolizer residual oxygen into water and energy. The residual oxygen was the main source of ROS, especially the formation of superoxide, hydroxyl, peroxyl and hydroperoxyl anions. One nonenzimatis natural antioxidants that can be easily obtained are tomatoes. Tomatoes are loaded with vitamin C, vitamin E and beta-carotene and phenolic compounds. Besides tomatoes contain vitamin C also contain lycopene, or often referred to as α-carotene was a carotenoid. Lycopene is a powerful antioxidant that prevents damage to the natural functioning of body cells. Ability to control free radicals 100 times more efficient than vitamin E or 12.500 times that of the gluthation. Method. This study was a randomized experimental study design using pretest posttest control group to see an increase in the levels of enzymatic antioxidants superoxide dismutase (SOD) in pregnant women with gestational age of 25-37 weeks. Samples that meet the inclusion and exclusion criteria consisting of 32 samples, ie 16 person control group who were not given the treatment and the treatment group was given 16 pieces of tomato juice. Result. There were influence of giving tomato juice to the antioxidation and reduced rate of Superoxide Dismutase after given tomato juice (408,39±139,05, p=304,58±79,53). Conclusion. There were side effects from tomato juice and the results of this study showed.

Three-dimensional flower-like multifunctional adsorbents with excellent sorptive removal and colorimetric detection of arsenate

It is highly desirable to construct advanced adsorbents with superb adsorption and visual detectivity of arsenate from complex environmental systems. In this work, a novel kind of iron alkoxide for simultaneous sorptive removal and colorimetric detection of arsenate from environmental water is reported. This adsorbent displays a three-dimensional (3D) flower-like structure with a specific surface area calculated as 93.13 m2 g−1. It is employed to remove arsenate from environmental water based on the specific interaction between arsenate and hydroxyl group on the iron alkoxide. The adsorption experiments show that iron alkoxide possesses strong removal efficiency to arsenate, and its theoretical maximum adsorption capacity is calculated as high as 97.14 mg g−1. Moreover, the anti-interference experiment reveals that iron alkoxide can resist the disturbance of most of co-existing ions. Additionally, the as-prepared iron alkoxide exhibits excellent oxidase-mimicking activity to catalyze the dissolved O2 to form superoxide anion free radical, turning the colorless 3,3′,5,5′-tetramethylbenzidine (TMB) to blue oxidized TMB (TMBox). In the case of the capture of arsenate by iron alkoxide, it results in the mask of active catalytic sites and inhabitation of oxidase-mimicking activity, and a visual quantitative colorimetric assay for detection of arsenate is established. Based on this strategy, visual detectivity of arsenate provides for a linear range from 3.33 to 333.33 µg L−1 and a LOD of 1.57 µg L−1 (S/N = 3). These results demonstrate that iron alkoxide has a very appealing application prospect in the field of sorptive removal and colorimetric detection of arsenate from environmental water.

Do reactive oxygen species or does oxygen itself confer obligate anaerobiosis? The case of Bacteroides thetaiotaomicron.

Bacteroides thetaiotaomicron was examined to determine whether its obligate anaerobiosis is imposed by endogenous reactive oxygen species or by molecular oxygen itself. Previous analyses established that aerated B. thetaiotaomicron loses some enzyme activities due to a high rate of endogenous superoxide formation. However, the present study establishes that another key step in central metabolism is poisoned by molecular oxygen itself. Pyruvate dissimilation was shown to depend upon two enzymes, pyruvate:formate lyase (PFL) and pyruvate:ferredoxin oxidoreductase (PFOR), that lose activity upon aeration. PFL is a glycyl-radical enzyme whose vulnerability to oxygen is already understood. The rate of PFOR damage was unaffected by the level of superoxide or peroxide, showing that molecular oxygen itself is the culprit. The cell cannot repair PFOR, which amplifies the impact of damage. The rates of PFOR and fumarase inactivation are similar, suggesting that superoxide dismutase is calibrated so the oxygen- and superoxide-sensitive enzymes are equally sensitive to aeration. The physiological purpose of PFL and PFOR is to degrade pyruvate without disrupting the redox balance, and they do so using catalytic mechanisms that are intrinsically vulnerable to oxygen. In this way, the anaerobic excellence and oxygen sensitivity of B. thetaiotaomicron are two sides of the same coin.

Влияние обработок препаратом на основе полисульфида кальция на всхожесть семян и урожайность растений пшеницы

Abstract. For the further intensification of the processes of agricultural crop production, the permanent development of new preparations with effective growth-regulating activity in relation to crops and exhibit the ability to suppress phytopathogens and improve the quality of economically valuable products is required. The purpose of the investigation was to study the effect of pre-sowing treatment of wheat seeds with calcium polysulfide (CaS4) preparations on germination, plant productivity parameters, and grain quality. Methods. In laboratory conditions, the effect of calcium polysulfide on the germination of wheat plants was investigated. 0.1; 0.5 and 1 % of CaS4 solutions for incubating the seeds during 1, 2 and 3 hours were used. Fresh and dry mass, shoot and root lengths, as well as the rate of formation of superoxide anion and hydrogen peroxide content, were determined, peroxidase and catalase activity and malondialdehyde (MDA) concentration ware detected. Infield studies seeds were treated with CaS4 solution at a rate of 0.6 l/t, followed by determination of the number of seedlings affected by root rot. Results. As a result of one-hour presowing treatment of seeds with a 0.1% solution in six-day-old seedlings, an increase in leaf length was observed, as well as a beneficial effect of the drug on the redox system of root tissues. The use of CaS4 solution for pre-sowing treatment and during heading in the field increased the yield by 3 quintals/ha and increased the protein content in wheat seeds by 8–9 %. A conclusion is drawn on the effect of calcium polysulfide on the germination of wheat seeds depending on the concentration and time of pre-sowing treatment.

Development of an Analytical Assay for Electrochemical Detection and Quantification of Protein-Bound 3-Nitrotyrosine in Biological Samples and Comparison with Classical, Antibody-Based Methods.

Reactive oxygen and nitrogen species (RONS) cause oxidative damage, which is associated with endothelial dysfunction and cardiovascular disease, but may also contribute to redox signaling. Therefore, their precise detection is important for the evaluation of disease mechanisms. Here, we compared three different methods for the detection of 3-nitrotyrosine (3-NT), a marker of nitro-oxidative stress, in biological samples. Nitrated proteins were generated by incubation with peroxynitrite or 3-morpholino sydnonimine (Sin-1) and subjected to total hydrolysis using pronase, a mixture of different proteases. The 3-NT was then separated by high performance liquid chromatography (HPLC) and quantified by electrochemical detection (ECD, CoulArray) and compared to classical methods, namely enzyme-linked immunosorbent assay (ELISA) and dot blot analysis using specific 3-NT antibodies. Calibration curves for authentic 3-NT (detection limit 10 nM) and a concentration-response pattern for 3-NT obtained from digested nitrated bovine serum albumin (BSA) were highly linear over a wide 3-NT concentration range. Also, ex vivo nitration of protein from heart, isolated mitochondria, and serum/plasma could be quantified using the HPLC/ECD method and was confirmed by LC-MS/MS. Of note, nitro-oxidative damage of mitochondria results in increased superoxide (O2•–) formation rates (measured by dihydroethidium-based HPLC assay), pointing to a self-amplification mechanism of oxidative stress. Based on our ex vivo data, the CoulArray quantification method for 3-NT seems to have some advantages regarding sensitivity and selectivity. Establishing a reliable automated HPLC assay for the routine quantification of 3-NT in biological samples of cell culture, of animal and human origin seems to be more sophisticated than expected.

MitoTEMPO provides an antiarrhythmic effect in aged-rats through attenuation of mitochondrial reactive oxygen species.

The death prevalence from cardiovascular disease is significantly high in elderly-populations, while mitochondrial-aging plays an important in abnormal function of vital organs through high mitochondrial ROS production. Mitochondria have a unique mode of action by providing ATP production and modulating the cytosolic Ca2+-signaling and maintain the redox status of cardiomyocytes. There is an aging-associated impairment in oxidative phosphorylation which causes a marked dysregulation of mitochondrial biogenesis. Therefore, we aimed to examine whether a mitochondria-targeting antioxidant, MitoTEMPO, can directly provide a cardioprotective effect on ventricular cardiomyocyte function under in vitro conditions. The MitoTEMPO-treatment (0.1μM for 4-h) of aged-ventricular cardiomyocytes (from 24-mo-old rats), compared to those of the adults (from 8-mo-old rats) markedly augmented not only the depressed biochemical parameters but also the ultrastructure of mitochondria. It also provided marked protective action against increased mitochondrial superoxide formation and Bnip3 overexpression, which both markedly induce depolarized mitochondrial potential, increase reactive oxygen species, mitochondrial swelling and fission, and accelerate mitochondrial turnover via autophagy. Furthermore, it provided marked protection against spontaneous action potentials, via shortening the prolonged action potential duration, at most, through recovery in depressed K+-channel currents. Moreover, we determined significant recovery in the depressed intracellular Ca2+-changes under electrical stimulation in MitoTEMPO-treated the aged-cardiomyocytes. Overall, we provided important information associated with an antiarrhythmic action, thereby controlling cytosolic and mitochondrial Ca2+-handling, implying its possible protective role of mitochondria-targeting antioxidant-treatment during aging.

Exacerbation of adverse cardiovascular effects of aircraft noise in an animal model of arterial hypertension

Arterial hypertension is the most important risk factor for the development of cardiovascular disease. Recently, aircraft noise has been shown to be associated with elevated blood pressure, endothelial dysfunction, and oxidative stress. Here, we investigated the potential exacerbated cardiovascular effects of aircraft noise in combination with experimental arterial hypertension. C57BL/6J mice were infused with 0.5 mg/kg/d of angiotensin II for 7 days, exposed to aircraft noise for 7 days at a maximum sound pressure level of 85 dB(A) and a mean sound pressure level of 72 dB(A), or subjected to both stressors. Noise and angiotensin II increased blood pressure, endothelial dysfunction, oxidative stress and inflammation in aortic, cardiac and/or cerebral tissues in single exposure models. In mice subjected to both stressors, most of these risk factors showed potentiated adverse changes. We also found that mice exposed to both noise and ATII had increased phagocytic NADPH oxidase (NOX-2)-mediated superoxide formation, immune cell infiltration (monocytes, neutrophils and T cells) in the aortic wall, astrocyte activation in the brain, enhanced cytokine signaling, and subsequent vascular and cerebral oxidative stress. Exaggerated renal stress response was also observed. In summary, our results show an enhanced adverse cardiovascular effect between environmental noise exposure and arterial hypertension, which is mainly triggered by vascular inflammation and oxidative stress. Mechanistically, noise potentiates neuroinflammation and cerebral oxidative stress, which may be a potential link between both risk factors. The results indicate that a combination of classical (arterial hypertension) and novel (noise exposure) risk factors may be deleterious for cardiovascular health.

Electron Scavenging Not Free Radical Scavenging by Fullerene Materials Protects Against Mitochondrial Oxidative Stress in Complex Organisms.

Fullerene materials are often reported to be excellent antioxidants in cells. Usually, direct free radical scavenging mechanisms, as seen in polymer and food industry research, is the proposed antioxidant mechanism. However, free radical scavenging by antioxidants in vivo is kinetically unlikely and conflicts with fullerene material’s molecular properties. Pristine fullerene materials, and many of their derivatives, are pro‐oxidant and form adducts, which are both potentially toxic mechanisms in vivo. Although they are electrophilic, and potentially oxidative molecules with an affinity for electrons, they appear to function like other non‐radical electrophilic antioxidants and stimulate enzymatic oxidative stress management and protection. We approach fullerene material’s antioxidant role from the perspective that they do not act as direct free radical scavengers. Other mechanisms have been previously proposed that are more consistent with fullerene properties, and antioxidant benefits in vivo. Here we discuss fullerene materials as electron scavenging antioxidants rather than free radical scavengers. We propose that fullerene materials scavenge excess electrons in the ETC preventing the formation of superoxide and hydroxyl radicals in the mitochondria. The scavenging of electrons would help in preventing damage to mitochondrial structures and DNA, maintaining optimum NAD+/NADH ratios, as well as in maintaining an oxidized OX/PHOS enzyme system in mitochondrial conditions resulting from excess caloric intake in the absence of cellular energy requirements and progressive mitochondrial dysfunction related to oxidative stress. Further research is needed to evaluate the utilization of fullerene materials for use in metabolic syndromes and neurodegenerative conditions complicated by progressive mitochondrial damage.Support or Funding InformationSupported by Institutional Resources of the University of Science Arts and Technology, Montserrat, BWI, The University of Health and Humanities, BVI and the Einstein Medical Institute, Florida USA.

Copper Modulation and Reactive Oxygen Species Production Across Yeast Lifespan

The mitochondrial electron transport chain (ETC) machinery is the primary site of superoxide formation, a reactive oxygen species (ROS) associated with premature cell aging. A primary defense against ROS in yeast (Saccharomyces cerevisiae) is the enzyme superoxide dismutase (Sod1p). This enzyme requires copper and zinc as metal cofactors in the conversion of superoxide to hydrogen peroxide, a less harmful ROS. How mitochondrial function contributes to yeast chronological lifespan (CLS) is particularly of interest, specifically how essential metals for mitochondrial function and their role in the production of ROS drive the aging process of yeast cells. Our aim is to determine the effect exogenous copper treatment on the CLS of yeast strains lacking Sod1p and its copper chaperone, Lys7p. Our results indicate that low levels of exogenous copper (0.25 mM copper sulfate or less in restricted nutrient media) extend yeast chronological lifespan, especially in cells lacking Lys7p. All cell types see a dramatic reduction in lifespan when exogenous copper levels are increased to 2.0 mM copper sulfate or higher. This indicates that a small increase in the amount of copper in the media is beneficial for yeast in these restricted media conditions. Our current studies are to assess protein levels by western blot and gene expression by qRT‐PCR of various components the yeast ETC machinery, specifically Cox2 and Cox4, to mechanistically understand how exogenous copper in a small dose is contributing to lifespan extension. ROS levels are also being assessed via fluorescent staining. By using biochemical dyes such as Dihydroethidium (DHE) for cytosolic ROS, and MitoSox and mitochondria superoxide production, we are able to monitor ROS production and show localization of these metabolic byproducts with both fluorescent microscopy and FACS at various points of the chronological lifespan yeast.

New and classical methods to compare oxidative stress levels and parameters of vascular function in rat models of hypertension, diabetes and nitrate tolerance

BackgroundOxidative stress was identified as a hallmark of almost all cardiovascular and neurodegenerative diseases. The term oxidative stress describes a condition that is either characterized by increased generation of reactive oxygen and nitrogen species (RONS) and/or dysregulated cellular antioxidant defense mechanisms (e.g. decreased expression of central antioxidant enzymes). Since the transition between oxidative stress and redox signaling is a thin line, the exact knowledge of the identity of formed reactive species, the cellular and subcellular localization of their formation as well as their time duration and concentration are of high clinical and pharmacological importance.Methods and ResultsWith the present studies, we evaluated the specific probe for mitochondrial superoxide formation, mitochondria‐targeted, triphenylphosphonium‐linked hydroethidium (mitoSOX), for its usefulness in the detection of mitochondrial superoxide formation ex vivo/in vivo and compared this HPLC‐based assay with alternative/traditional methods. For this purpose, we used three different animal models with well‐established oxidative stress burden, namely diabetic, hypertensive and nitrate tolerant rats. With our previous work we have stressed that the traditional or old RONS assays are not necessarily inferior as compared to up‐to‐date or even cutting‐edge assays and at least have their specific features and application spectra. Vascular function was assessed by isometric tension methodology and was impaired in the rat models of oxidative stress. Vascular dysfunction correlated with increased mitoSOX oxidation but also classical RONS detection assays as well as typical markers of oxidative stress. Additionally, we successfully applied this method for the mitochondrial superoxide detection in hypertensive (AT‐II induced), aircraft noise exposure mouse model as well as in the combination of these two stressors. The application of this method was also effective in the wild type and Nox2 knockout mice exposed to e‐cigarette vapor over 3 days for 2 h/d.ConclusionIn conclusion, we report that mitoSOX/HPLC indeed represents a suitable method for quantification of mitochondrial superoxide formation in biological samples of animals with cardiometabolic disease, pharmacologically induced cardiovascular complications and cardiovascular diseases induced by novel (environmental/behavioral) stressors. The knowledge on the spatial distribution of RONS formation may be of specific interest for drug development and when it comes to therapy.Support or Funding InformationOur experimental studies were supported by vascular biology research grants from the Boehringer Ingelheim Foundation for the collaborative research group „Novel and neglected cardiovascular risk factors: molecular mechanisms and therapeutic implications”.

Development and validation of an analytical assay for electrochemical detection and quantification of protein‐bound 3‐nitrotyrosine in biological samples and comparison with classical, antibody‐based methods

BackgroundReactive oxygen species (ROS) cause oxidative damage which is associated with endothelial dysfunction and cardiovascular disease. Majority of ROS are formed by mitochondria and NADPH oxidase. Overproduction of ROS leads to oxidative damage and disease progression, therefore, accurate determination of ROS and reactive nitrogen species (like nitric oxide, superoxide and peroxynitrite) is of great importance but also represents a great challenge, since these species are short‐lived and methods that are usually used relay on indirect detection. Here we compared 3 different methods for the detection of 3‐nitrotyrosine, a footprint of peroxynitrite formation in vivo, in biological samples.Methods and ResultsNitrated proteins were generated by incubation with peroxynitrite or 3‐morpholino sydnonimine (SIN‐1) and digested using pronase, a mixture of different proteases. The free 3‐nitrotyrosine was then separated by HPLC and quantified by a coulometric method using the CoulArray system. Concentration‐response‐curves of 3‐nitrotyrosine standards were highly linear (detection limit 50 nM). Concentration‐response‐curves of free 3‐nitrotyrosine obtained from digested nitrated bovine serum albumin standards were also highly linear before reaching a plateau, probably representing nitration of all available tyrosine residues. The presence of 3‐nitrotyrosine in nitrated bovine serum albumin standards was validated by other methods (ELISA and dot blot analysis using specific 3‐nitrotyrosine antibodies), showing a similar pattern as compared to HPLC/ECD detection. Ex vivo nitration of isolated mitochondrial or membranous fractions as well as serum/plasma yielded a concentration‐dependent 3‐nitrotyrosine signal using the HPLC/ECD method. Ongoing studies are dedicated to the quantification of 3‐nitrotyrosine in tissue samples of nitrate‐tolerant, diabetic, hypertensive and septic mice and rats. A major draw‐back seems to be the separation of the 3‐nitrotyrosine peak in complex biological samples, which is currently our main focus.ConclusionsBased on our ex vivo data, the CoulArray quantification method for 3‐nitrotyrosine seems to have some advantages regarding sensitivity and selectivity. In the future, we hope to be able to establish a reliable automated HPLC assay for the routine quantification of 3‐nitrotyrosine in biological samples of cell culture, animal and human origin. Our most recent data show that protein‐bound 3‐nitrotyrosine not only represents a footprint of peroxynitrite formation and marker of oxidative stress but also correlates with increased mitochondrial superoxide formation rates pointing towards self‐propagating oxidative stress vicious circles.Support or Funding InformationVascular biology research grant from the Boehringer Ingelheim Foundation for the collaborative research group „Novel and neglected cardiovascular risk factors: molecular mechanisms and therapeutic implications”

Time‐dependent induction of vascular oxidative stress, inflammation, endothelial dysfunction and high blood pressure by aircraft noise exposure in mice

BackgroundTransportation noise is recognized as an important cardiovascular risk factor. It was shown that traffic noise exposure is associated with cerebro/cardiovascular diseases such as hypertension, myocardial infarction, and stroke. Aircraft noise causes endothelial dysfunction, inflammation and increases cerebral/cardiovascular oxidative stress in mice and traffic noise in general increased stroke mortality in large population studies. Chronic aircraft noise also causes learning and memory impairment in children. We recently studied the effects of different time exposure protocols (sleep versus awake phase) of aircraft noise exposure on C57Bl/6JRj mice and demonstrated that sleep phase noise exposure impairs the circadian clock and causes oxidative stress, endothelial dysfunction and high blood pressure.Methods and ResultsBefore the main study, we ensured that the longest noise exposure did not cause hearing loss in the mice by using audiometry. C57Bl/6JRj mice were exposed to aircraft noise for 4, 7, 14 and 28 days at a maximum sound level of 85 dB(A) and a mean sound pressure level of 72 dB(A) and compared with unexposed control mice. The induction of endothelial dysfunction and elevation of blood pressure was comparable in all exposure groups. Oxidative burst in the whole blood, stimulated with phorbol 12,13‐dibutyrate (PDBu) or zymosan A, was increased in all exposed groups with a maximum at 4 or 7 days. Vascular ROS formation as envisaged by dihydroethidium (DHE) staining was increased in noise‐exposed mice without a significant time response. Noise‐induced aortic, cardiac and cerebral superoxide formation as measured by DHE HPLC analysis increased in dependence of noise exposure duration. Similarly, levels of interleukin‐6 (IL‐6) were time dependently increased by trend in plasma and brain tissue in all noise exposed mice. We also established increased NOX‐2 expression in aortic tissue of noise exposed mice, while levels of P‐VASP were decreased after exposure.ConclusionWe here present novel data on the effects of different aircraft noise exposure protocols (4–28 days) indicating that most adverse vascular effects are established already after 4 days. Importantly, our present data prove that the applied moderate noise levels do not cause induction of hearing loss, even not after long‐term exposures. Thus our present data provide important technical insights in noise exposure protocols for future translational studies in mice with relevance for the human situation.Support or Funding InformationOur experimental studies on noise effects in mice were supported by vascular biology research grants from the Boehringer Ingelheim Foundation for the collaborative research group „Novel and neglected cardiovascular risk factors: molecular mechanisms and therapeutic implications” and Foundation Heart of Mainz

The isoleucic acid triad: distinct impacts on plant defense, root growth, and formation of reactive oxygen species.

Isoleucic acid (ILA), a branched-chain amino acid-related 2-hydroxycarboxylic acid, occurs ubiquitously in plants. It enhances pathogen resistance and inhibits root growth of Arabidopsis. The salicylic acid (SA) glucosyltransferase UGT76B1 is able to conjugate ILA. Here, we investigate the role of ILA in planta in Arabidopsis and reveal a triad of distinct responses to this small molecule. ILA synergistically co-operates with SA to activate SA-responsive gene expression and resistance in a UGT76B1-dependent manner in agreement with the observed competitive ILA-dependent repression of SA glucosylation by UGT76B1. However, ILA also shows an SA-independent stress response. Nitroblue tetrazolium staining and pharmacological experiments indicate that ILA induces superoxide formation of the wild type and of an SA-deficient (NahG sid2) line. In contrast, the inhibitory effect of ILA on root growth is independent of both SA and superoxide induction. These effects of ILA are specific and distinct from its isomeric compound leucic acid and from the amino acid isoleucine. Leucic acid and isoleucine do not induce expression of defense marker genes or superoxide production, whereas both compounds inhibit root growth. All three responses to ILA are also observed in Brassica napus.

Critical Factors Controlling Superoxide Reactions in Lithium–Oxygen Batteries

Superoxide (LiO2) formation on charging is one of the major causes of poor cycle life of Li–O2 batteries. The underlying mechanism controlling LiO2 formation remains elusive. Here, we reveal that t...

Coordination complexes of methimazole with copper: Controlling redox reactions and sulfur extrusion

Sulfur-containing imidazole thiones are of interest for their redox chemistry and tendency to form disulfide bonds reminiscent of biologically active disulfides. Treating copper(II) with redox-active methimazole in the presence of oxygen results in concomitant copper reduction and formation of methimazole disulfide, and ultimately, extrusion of one of the sulfur atoms. Reaction conditions, including stoichiometry, presence of oxygen, and redox state of the metal ion, were varied to examine the mechanistic details that lead to the sulfur extrusion. Six unique products are reported: [Cu(κN,N-MMIMS)2(H2O)2](HSO4)2, [Cu(κN,N-MMIMS)2(H2O)][CH3SO4][HSO4][H2O], [Cu(κN,N-MMIMS)2(H2O)](CH3SO4)2, [Cu(κN,N-MMIMS)(κO,O-SO4)(CH3OH)], [Cu(κN,N-MMIMS)(κO,O-SO4)(DMSO)]∙0.5 DMSO, and [Cu(μ,κO,O,O-SO4)(κN,N-MMIMS)]n[CH3CN] (MMIMS = bis(1-methylimidazol-2-yl)sulfide). In all structures, the HSO4- and CH3SO4- counterions are generated in situ. EPR analysis of the reaction as it proceeds indicates initial formation of a four-coordinate Cu2+-S complex that shifts to square planar or octahedral Cu2+-N coordination over the course of the reaction. Formation of the thiyl radical is also observed by EPR analysis using DMPO as a spin trap. Together, these results establish a complete mechanism for sulfur extrusion that proceeds through copper-methimazole binding and redox, superoxide formation, and nucleophilic attack of water or methanol on sulfur, and subsequent nucleophilic aromatic substitution to yield the sulfur-extruded product. Understanding this mechanism lays the foundation for catalyst development for desulfurization and sulfur-containing polymerization reactions.

Evaluation of physiological and biochemical aberration linked to effect of sodium dodecyl sulphate on barley seedlings

Sodium dodecyl sulphate (SDS) amount in domestic and industrial effluents is consistently increasing since SDS is available in almost all cleaning products. Therefore, it has become one of the potential destructive factors on habitats such as agricultural areas and aquatic environments. This study was carried out to evaluate the SDS-induced changes on barley (Hordeum vulgare L. cv. Olgun) seedlings. Barley seedlings were hydroponically cultivated for nine days at optimal conditions and, then, exposed to five different doses of SDS. After 72 h from SDS addition, root and coleoptile lengths were seriously reduced as compared to control. Also, SDS decreased soluble protein, chlorophyll a, chlorophyll b and carotenoid contents of the barley leaves. Furthermore, the SDS-induced reductive effects on protein profiles of barley leaves were also detected with electrophoresis. SDS caused serious decreases in activities of antioxidant enzymes, including superoxide dismutase, catalase, and ascorbate peroxidase and glutathione reductase except for peroxidase. Moreover, the SDS led to the emergence of oxidative damage symptoms that were manifested by the increased superoxide anion formation, hydrogen peroxide content and lipid peroxidation level of barley seedlings. Eventually, the results of the present study revealed that SDS cause to a severe reduction in the growth of barley seedlings.

Primary Metabolite Responses to Oxidative Stress in Early-Senescing and Paraquat Resistant Arabidopsis thaliana rcd1 (Radical-Induced Cell Death1).

Rcd1 (radical-induced cell death1) is an Arabidopsis thaliana mutant, which exhibits high tolerance to paraquat [methyl viologen (MV)], herbicide that interrupts photosynthetic electron transport chain causing the formation of superoxide and inhibiting NADPH production in the chloroplast. To understand the biochemical mechanisms of MV-resistance and the role of RCD1 in oxidative stress responses, we performed metabolite profiling of wild type (Col-0) and rcd1 plants in light, after MV exposure and after prolonged darkness. The function of RCD1 has been extensively studied at transcriptomic and biochemical level, but comprehensive metabolite profiling of rcd1 mutant has not been conducted until now. The mutant plants exhibited very different metabolic features from the wild type under light conditions implying enhanced glycolytic activity, altered nitrogen and nucleotide metabolism. In light conditions, superoxide production was elevated in rcd1, but no metabolic markers of oxidative stress were detected. Elevated senescence-associated metabolite marker levels in rcd1 at early developmental stage were in line with its early-senescing phenotype and possible mitochondrial dysfunction. After MV exposure, a marked decline in the levels of glycolytic and TCA cycle intermediates in Col-0 suggested severe plastidic oxidative stress and inhibition of photosynthesis and respiration, whereas in rcd1 the results indicated sustained photosynthesis and respiration and induction of energy salvaging pathways. The accumulation of oxidative stress markers in both plant lines indicated that MV-resistance in rcd1 derived from the altered regulation of cellular metabolism and not from the restricted delivery of MV into the cells or chloroplasts. Considering the evidence from metabolomic, transcriptomic and biochemical studies, we propose that RCD1 has a negative effect on reductive metabolism and rerouting of the energy production pathways. Thus, the altered, highly active reductive metabolism, energy salvaging pathways and redox transfer between cellular compartments in rcd1 could be sufficient to avoid the negative effects of MV-induced toxicity.

Reviving reversible anion redox in 3d-transition-metal Li rich oxides by introducing surface defects

The reversible anion redox of O2−/(O2)n− in 3d-transition-metal based Li layered oxides (LLO) has received renewed attention due to its capability of hosting additional redox centers, which can further improve the energy density of Li-ion batteries. However, over-oxidized (O2)n− was found to be unstable upon cycling, resulting in an irreversible crystal structure transformation that lowers long-term cycling stability. Herein, we demonstrated that the anion redox can be tuned through surface defect engineering, which consequently improves the cycling instability. By reconstructing the atomic configuration of the surface, a highly defective surface layer with oxygen vacancies is achieved, substantially enhancing the reversibility of anion redox as well as the stability of bulk crystal structure. The modified LLO expresses a high performances of discharge capacity (94.5%), redox potential (>3.0 V during discharge) and energy density (90.2%) after 100 cycles. Ex-situ XPS measurements confirm a high reversibility of the O2−/(O2)n− redox couple, which is supported by DFT calculations showing that the oxygen vacancies formed at the fully lithiated state of LLO mitigate the over-oxidization of oxygen and the formation of unstable superoxides ((O2)-) through a reductive coupling mechanism.

Lectin-induced oxidative stress in human platelets

Previously we have shown that wheat germ agglutinin (WGA) and, with minor potency, Phaseolus vulgaris agglutinin (PHA), but not lens culinarian agglutinin (LCA), induce platelet aggregation, through the PLCƴ2 activation by the concerted action of src/syk and PI3K/BTK pathways. In this study, we have investigated platelet oxidative stress induced by lectins. Several parameters indicative of oxidative stress, such as reactive oxygen species (ROS), superoxide anion, lipid peroxidation and the efficiency of the aerobic metabolism, have been measured. It was found that ROS, superoxide anion formation and lipid peroxidation are significantly increased upon platelet treatment with WGA and PHA while LCA is ineffective. WGA is always more effective than PHA in all experimental conditions tested. In addition, the involvement of NADPH oxidase 1, syk and PI3K in oxidative stress induced by WGA and PHA has been shown. Concerning the lectins effect on aerobic metabolism, WGA and PHA, but not LCA, act as uncoupling agents, determining an increase of oxygen consumption and a decrease of ATP synthesis, with a consequent decrease of P/O value. These results are confirmed by the impairment of platelets proton gradient formation, evaluated by membrane potential, in platelets treated with WGA and PHA. In conclusion lectins, especially WGA, induce oxidative stress in platelets and decrease energy availability through modifications of membrane structure leading to the inefficiency of the aerobic machinery that steers platelets toward death as suggested by the decreased metabolic activity of platelets and the increased lactic dehydrogenase release.

Investigating the Superoxide Formation and Stability in Mesoporous Carbon Perovskite Solar Cells with an Aminovaleric Acid Additive

AbstractPerovskite solar cells have attracted a great deal of attention thanks to their high efficiency, ease of manufacturing, and potential low cost. However, the stability of these devices is considered their main drawback and needs to be addressed. Mesoporous carbon perovskite solar cells (m‐CPSC), consisting of three mesoporous layers (TiO2/ZrO2/C) infiltrated with CH3NH3PbI3 (MAPI) perovskite, have presented excellent lifetimes of more than 10 000 h when the additive NH2(CH2)4CO2HI (5‐ aminovaleric acid iodide; 5‐AVAI) is used to modify the perovskite structure. Yet, the role of 5‐AVAI in enhancing the stability has yet to be determined. Here, superoxide‐mediated degradation of MAPI m‐CPSC with and without the 5‐AVAI additive is studied using the fluorescence probe dihydroethidium for superoxide detection. In situ X‐ray diffractometry shows that aminovaleric acid methylammonium lead iodide (AVA‐MAPI) perovskite infiltrated in mesoporous layers presents higher stability in an ambient environment under illumination, evidenced by a slower decrease of the MAPI/PbI2 peak ratio. Superoxide yield measurements demonstrate that AVA‐MAPI generates more superoxide than regular MAPI when deposited on glass but generates significantly less when infiltrated in mesoporous layers. It is believed that superoxide formation in m‐CPSC is dependent on a combination of competitive factors including oxygen diffusion, sample morphology, grain size, and defect concentration.