Low Concentrations Of H2O2 Research Articles

The p66shc-mediated Regulation of Hepatocyte Senescence Influences Hepatic Steatosis in Nonalcoholic Fatty Liver Disease.

BackgroundRecent studies have suggested that hepatocyte senescence could contribute to hepatic steatosis and its progression in nonalcoholic fatty liver disease (NAFLD). However, the underlying mechanism causing hepatocyte senescence in this pathological condition is still unclear. A thorough understanding of the mechanism could provide a new target for therapeutic intervention. The purpose of this study was to investigate the role of p66shc in hepatocyte senescence and hepatocyte damage in NAFLD progression.Material/MethodsWe examined the expression levels of hepatic p66shc and senescence markers in rats and humans with NAFLD, and we assessed the effect of p66shc knockdown or overexpression on senescence and steatosis in human liver cells.ResultsIn this study, we showed that increased hepatic p66shc expression was consistent with upregulated expression of the following senescence markers in NAFLD rats: heterochromatin protein-1-beta (HP1β), p16, p21, and p53. Furthermore, senescence and steatosis could be induced in hepatoblastoma cell line (HepG2) cells when cells were stimulated with a low concentration of H2O2, and this effect was significantly alleviated by knockdown of p66shc. However, overexpression of p66shc could promote senescence and steatosis in L02 cells. Finally, increased hepatic p66shc protein levels correlated with enhanced expression of the senescence marker p21 and mirrored the degree of disease severity in NAFLD patients.ConclusionsOur findings indicated that the increase in hepatocyte senescence and steatosis in NAFLD may be caused by the upregulation of p66shc expression, implying that strategies for p66shc-mediated regulation of hepatocyte senescence may provide new therapeutic tools for NAFLD.

Protection from hydrogen peroxide stress relies mainly on AhpCF and KatA2 in Stenotrophomonas maltophilia

BackgroundAerobically-grown bacteria can be challenged by hydrogen peroxide stress from endogenous aerobic metabolism and exogenously generated reactive oxygen species. Catalase (Kat), alkyl hydroperoxidase (Ahp), and glutathione peroxidase (Gpx) systems are major adaptive responses to H2O2 stress in bacteria. Stenotrophomonas maltophilia is a ubiquitous Gram-negative bacterium equipped with four Kats (KatA1, KatA2, KatMn, and KatE), one Ahp (AhpCF), and three Gpxs (Gpx1, Gpx2, and Gpx3). Here, we systematically investigated how the eight H2O2 scavenging genes differentially contribute to the low-micromolar levels of H2O2 generated from aerobic metabolism and high-millimolar levels of H2O2 from exogenous sources.MethodsGene expression was assessed and quantified by reverse transcription-PCR (RT-PCR) and real time quantitative PCR (qRT-PCR), respectively. The contribution of these enzymes to H2O2 stress was assessed using mutant construction and functional investigation.ResultsOf the eight genes, katA2, ahpCF, and gpx3 were intrinsically expressed in response to low-micromolar levels of H2O2 from aerobic metabolism, and the expression of katA2 and ahpCF was regulated by OxyR. AhpCF and KatA2 were responsible for alleviating aerobic growth-mediated low concentration H2O2 stress and AhpCF played a critical role for stationary-phase cells. KatA2 was upregulated to compensate for AhpCF in the case of ahpCF inactivation. After exposure to millimolar levels of H2O2, katA2 and ahpCF were upregulated in an OxyR-dependent manner. KatA2 was the critical enzyme for dealing with high concentration H2O2. Loss-of-function of KatA2 increased bacterial susceptibility to high concentration H2O2.ConclusionsAhpCF and KatA2 are key enzymes protecting S. maltophilia from hydrogen peroxide stress.

The synthesis of strigolactone is affected by endogenous ascorbic acid in transgenic rice for l-galactono-1, 4-lactone dehydrogenase suppressed or overexpressing

Rice tillering, which determines the panicle number per plant, is an important agronomic trait for grain production. In higher plants, ascorbic acid (Asc) plays a major role in ROS-scavenging activity. l-Galactono-1, 4-lactone dehydrogenase (GalLDH, EC1.3.2.3) is an enzyme that catalyzes the last step of Asc biosynthesis in plants. Previously, we have reported that homozygous L-GalLDH-suppressed transgenic rice plants (GI) display a reduced tiller number and a lower level of foliar carotenoids (Car) compared with wild type. Strigolactones (SL), which play an important role in the suppression of shoot branching, are synthesized in the roots of rice plant using Car as substrates. In this paper, the relationship between Asc, SL, the accumulation of H2O2, changes in antioxidant capacity, enzyme activities, and gene transcriptions related to the synthesis of SL were analyzed in transgenic rice plants for L-GalLDH suppressed (GI-1 and GI-2) and overexpressing (GO-2). The results showed that the altered level of Asc in the L-GalLDH transgenic rice plants leads to a change in redox homeostasis, resulting in a marked accumulation of H2O2 and decreased antioxidant capacity in GI-1 and GI-2, but lower H2O2 content and increased antioxidant capacity in GO-2. Meanwhile, the altered level of Asc also leads to altered enzyme activities and gene transcript abundances related to SL synthesis in L-GalLDH transgenics. These observations support the conclusion that Asc influences tiller number in the L-GalLDH transgenics by affecting H2O2 accumulation and antioxidant capacity, and altering those enzyme activities and gene transcript abundances related to SL synthesis.

Photosynthesis is sensitive to nitric oxide and respiration sensitive to hydrogen peroxide: Studies with pea mesophyll protoplasts

Reports on the effect of nitric oxide (NO) or reactive oxygen species (ROS) on photosynthesis and respiration in leaf tissues are intriguing; therefore, the effects of exogenous addition of sodium nitroprusside (SNP, releases NO) or H2O2 on the photosynthetic O2 evolution and respiratory O2 uptake by mesophyll protoplasts in pea (Pisum sativum) were evaluated in the present study. Low concentrations of SNP or H2O2 were used to minimize nonspecific effects. The effects of NO or H2O2 on respiration and photosynthesis were different. The presence of NO decreased the rate of photosynthesis but caused a marginal stimulation of dark respiration. Conversely, externally administered H2O2 drastically decreased the rate of respiration but only slightly decreased photosynthesis. The PS I activity was more sensitive to NO than PS II. On the other hand, 100 μM H2O2 had no effect on the photochemical reactions of either PS I or PS II. The sensitivity of photosynthesis to antimycin A or SHAM (reflecting the interplay between chloroplasts and mitochondria) was not affected by NO. By contrast, H2O2 markedly decreased the sensitivity of photosynthesis to antimycin A and SHAM. It can be concluded that chloroplasts are the primary targets of NO, while mitochondria are the primary targets of ROS in plant cells. We propose that H2O2 can be an important signal to modulate the crosstalk between chloroplasts and mitochondria.

Antioxidant Activity of Compounds Isolated from Elaeagnus umbellata Promotes Human Gingival Fibroblast Well-Being.

Four new triterpenoid bidesmosidic saponins (1–4) and a sesquiterpenoid glucoside (5), together with nine known phenolic compounds (6–14), were isolated from the fruits of Elaeagnus umbellata. Their structures were elucidated using 1D and 2D NMR spectroscopy and mass spectrometry data. The antioxidant capability of the isolated compounds was evaluated in human gingival fibroblasts. Compound 6 decreased ROS production and promoted cell proliferation. It also counteracted the cell cycle blockade induced by a low concentration of H2O2 decreasing the expression of p21 and CDKN2A (p16INK4A). Compound 6 decreased the expression of inflammatory cytokines (IL-6 and IL-8) in response to inflammatory stimuli, supporting its possible use in periodontitis lesions.

Enhanced heterogeneous Fenton-like degradation of nuclear-grade cationic exchange resin by nanoscale zero-valent iron: experiments and DFT calculations.

Nanoscale zero-valent iron (nZVI) was prepared and used as a heterogeneous Fenton-like catalyst for the degradation of nuclear-grade cationic exchange resin. The properties of nZVI before and after reaction were characterized by scanning electron microscopy (SEM), X-ray diffraction (XRD), and Brunauer-Emmett-Teller (BET) surface area analysis. The results showed that nZVI-H2O2 system exhibited the enhanced degradation of cationic resins, compared with Fe2+-H2O2, Cu0-H2O2, and Fe0/Cu0-H2O2 systems. The effects of initial temperature, nZVI dose, and H2O2 concentration were studied, and the higher temperature and nZVI dose with relatively low H2O2 concentration brought faster degradation rate. The degradation of cationic resins followed the pseudo-first-order kinetics with the apparent activation energy of 53.29kJ/mol. According to the experimental and calculated infrared and UV-visible spectra, the carbon skeleton of cationic resins was broken with the detachment of benzene ring and the desulfonation of resin polymer by hydroxyl radicals (•OH), generating long-chain alkenes. These intermediates were further oxidized through the hydroxyl substitution, hydrogen abstraction, ring cleavage, or carbonylation reactions, finally forming carboxylic acids remained in solution.

New insights into the resistance of four citrus genotypes to Xanthomonas citri subsp. citri

The resistance of different citrus genotypes to citrus canker, caused by Xanthomonas citri subsp. citri (Xcc), is quite different. In this study, four citrus genotypes with different resistance, including resistant kumquat ‘Luofu’ (Fortunella margarita), moderately resistant Ponkan ‘18–1-10’ (Citrus reticulata), moderately susceptible sweet orange ‘Newhall’ (C. sinensis) and susceptible grapefruit ‘Duncan’ (C. paradisi) were used to elucidate the resistance mechanism. The antibacterial analysis in vitro showed low concentration of H2O2 promoted growth of Xcc, whereas high concentration inhibited growth. In addition, NADPH oxidases, also known as respiratory burst oxidase homologues (rbohs), are required for H2O2 burst during infection. Subsequently, Xcc accumulation, H2O2 production and expression of CsrbohD was measured to elucidate their roles in citrus-Xcc interaction. Through the Spearman correlation and multiple linear regression analysis, we found all three factors were significantly correlated with variety resistance, which was significantly affected by H2O2 content and expression of CsrbohD. Taken together, these data indicate a feedback regulation of CsrbohD and H2O2 in citrus. When the H2O2 content was lower than the threshold, it was not sufficient to suppress Xcc growth, and more Xcc populations suppressed H2O2 production, thus forming a vicious circle. By contrast, it can suppress Xcc growth, then CsrbohD was suppressed to reduce the oxidative damage.

Expression and functional analysis of the hydrogen peroxide biosensors HyPer and HyPer2 in C2C12 myoblasts/myotubes and single skeletal muscle fibres

Hydrogen peroxide (H2O2) is generated in cells and plays an important role as a signalling molecule. It has been reported that H2O2 is involved in physiological and pathological processes in skeletal muscle. However, H2O2 detection in cells with traditional techniques produces frequent artefacts. Currently, the HyPer biosensor detects intracellular H2O2 specifically in real time using fluorescence microscopy. The aim of this study was to develop and optimize approaches used to express the HyPer biosensor in different models of skeletal muscle cells, such as the C2C12 myoblast/myotube cell line and mature skeletal muscle fibres isolated from C57BL/6J mice, and to measure intracellular H2O2 in real time in these cells. The results show that the expression of the HyPer biosensor in skeletal muscle cells is possible. In addition, we demonstrate that HyPer is functional and that this biosensor detects changes and fluctuations in intracellular H2O2 in a reversible manner. The HyPer2 biosensor, which is a more advanced version of HyPer, presents improved properties in terms of sensitivity in detecting lower concentrations of H2O2 in skeletal muscle fibres. In conclusion, the expression of the HyPer biosensor in the different experimental models combined with fluorescence microscopy techniques is a powerful methodology to monitor and register intracellular H2O2 specifically in skeletal muscle. The innovation of the methodological approaches presented in this study may present new avenues for studying the role of H2O2 in skeletal muscle pathophysiology. Furthermore, the methodology may potentially be adapted to yield other specific biosensors for different reactive oxygen and nitrogen species or metabolites involved in cellular functions.

Combination of tert-butyl hydroperoxide with vorinostat induces cell death of Acanthamoeba through cell cycle arrest

Safety precautions prior to contact lens usage is essential for preventing Acanthamoeba keratitis. Contact lens disinfecting solutions containing 3% hydrogen peroxide (H2O2) are known to exert amoebicidal effect against Acanthamoeba. Yet, these solutions need to be neutralized to prevent ocular irritation, which consequently may result in incomplete disinfection. In this study, amoebicidal effect of tert-butyl hydroperoxide (tBHP) was investigated and its efficacy was compared to those of hydrogen peroxide (H2O2). H2O2 and tBHP showed dose dependent amoebicidal effect, however high concentration of these compounds demonstrated cytotoxicity in human corneal epithelial (HCE) cells. To reduce their cytotoxicity, the concentrations of both compounds were diluted to 50 μM and subsequently combined with 10 μM vorinostat to enhance amoebicidal effect. Addition of vorinostat induced high amoebicidal effect against Acanthamoeba trophozoites, even at low concentrations of H2O2 or tBHP. Cellular damage induced by combined treatment of H2O2 or tBHP with vorinostat in Acanthamoeba were determined by assessing cell cycle arrest and apoptosis via FACS analysis. While 50 μM H2O2 combined with 10 μM vorinostat showed 36.26% cytotoxicity on HCE cells during 24 h exposure, 50 μM tBHP with 10 μM vorinostat did not show cytotoxicity on HCE cells. These findings suggest that the application of tBHP and vorinostat for Acanthamoeba keratitis treatment and contact lens disinfection system is highly plausible.

Oxidative stress induces transcription of telomeric repeat-containing RNA (TERRA) by engaging PKA signaling and cytoskeleton dynamics

Long non-coding RNAs transcribed from telomeres, known as TERRA (telomeric repeat-containing RNA), are associated with telomere and genome stability. TERRA abundance responds to different cell stresses; however, no studies have focused on oxidative stress, condition that damages biomolecules and is involved in aging and disease. Since telomeres are prone to oxidative damage leading to their dysfunction, our objective was to characterize TERRAs and the mechanisms that control their expression. TERRA increased in cells exposed to H2O2 and reverted by antioxidant treatment. TERRAs are also induced in brown adipose tissue of mice exposed to cold, which raises mitochondrial ROS. In cells exposed to H2O2, ChIP showed that chromatin landscape was modified favoring telomere transcription. TERRAs interacted with HP1α/γ, proteins that were found recruited to subtelomeres. Since HP1γ interacts with the transcriptional machinery, TERRAs may stimulate their own expression by recruiting HP1γ to subtelomeres. TERRA induction reverted within 2 h after removal of H2O2 from culture medium, suggesting they have protective functions. This was supported by rapid TERRA induction following a second H2O2 challenge. PKA inhibitors H89 and PKI blocked TERRA increase by H2O2 or IBMX+Forskolin treatment, suggesting PKA signaling regulates TERRA induction. Treatment of cells with drugs that disturb cytoskeleton integrity or growing cells on surfaces of different stiffness known to generate differential cytoskeleton tension also modified TERRA levels and sensitized cells to lower H2O2 concentrations. In summary, we show that TERRAs are induced in response to oxidative stress and are regulated by PKA as well as by changes in cytoskeleton dynamics.

Cycling system for decomposition of gaseous benzene by hydrogen peroxide with naturally Fe-containing activated carbon.

For the removal of volatile organic compounds (VOCs) from environmental systems, gaseous benzene, a model VOC, was adsorbed on naturally Fe-containing activated carbon and subsequently, decomposed in the presence of de-ionized water, and low (0.03%, pH 6.5) and high (30%, pH 2.5) concentration H2O2 solutions. The intermediates produced during benzene decomposition were analyzed and compared using gas chromatography-mass spectrometry. After the decomposition process, the activated carbon sample was air dried. Three cycles were carried out with de-ionized water and low and high concentration H2O2 solutions as oxidants. The adsorption capacity of the activated carbon sample treated with DI water gradually decreased as the number of cycles increased. On the other hand, the benzene adsorption capacity of the activated carbon samples treated with the H2O2 solutions was improved due to the relatively higher specific surface areas of these samples. After treatment with the low-concentration H2O2 solution, intermediates such as glyoxylic acid, oxalic acid, phenol, malonic acid, and pyrocatechol were observed. After treatment with high-concentration H2O2 solution, intermediates such as glyoxylic acid, formic acid, and acetic acid were formed. With increasing H2O2 concentration, the number and the molecular weight of the intermediate formed by the oxidative degradation of benzene, simultaneously decreased. The Fenton reaction induced by naturally Fe-containing activated carbon and H2O2 could lead to more efficient decomposition of benzene.

Relationship between Optical Redox Status and Reactive Oxygen Species in Cancer Cells

Shifted NAD(H) redox status and enhanced reactive oxygen species (ROS) scavenging systems have been observed in cancers. However, how such redox shift is related to the ROS level in cancer cells is less clear. Based on collecting the intrinsic fluorescence of oxidized flavoproteins (Fp containing flavin adenine dinucleotide) and reduced nicotinamide adenine dinucleotide (NADH), optical redox imaging (ORI) provides a quantitative measure of the mitochondrial redox state by the optical redox ratio, Fp/(NADH+Fp), a surrogate marker of the NAD+-coupled redox state NAD+/NADH. Our study aims to explore the relationship between NAD(H) redox status and ROS by imaging NADH, Fp, and ROS levels using cultured breast cancer cell models. By manipulating either ROS levels via application of exogenous H2O2 or redox status via metabolic perturbation compounds, we found that: (1) oxidation of NAD(H) redox status correlates with ROS levels at lower H2O2 concentrations (up to ~700 μM), but not necessarily at higher concentrations; (2) an elevated ROS level diminishes NADH and reduces redox ratio plasticity; (3) either more oxidized or more reduced status can correlate to an increased ROS level; and (4) sometimes, a more oxidized status can correlate to a decreased ROS level depending on cell lines. These observations indicated that cellular NAD(H) redox state and ROS are intricately related but can also change separately. This study can benefit cancer research as both NAD(H) redox status and ROS have been implicated in cancer transformation and progression.

Oxidants in Physiological Processes.

A number of diseases and conditions have been associated with prolonged or persistent exposure to non-physiological levels of reactive oxygen species (ROS). Similarly, ROS underproduction due to loss-of-function mutations in superoxide or hydrogen peroxide (H2O2)-generating enzymes is a risk factor or causative for certain diseases. However, ROS are required for basic cell functions; in particular the diffusible second messenger H2O2 that serves as signaling molecule in redox processes. This activity sets H2O2 apart from highly reactive oxygen radicals and influences the approach to drug discovery, clinical utility, and therapeutic intervention. Here we review the chemical and biological fundamentals of ROS with emphasis on H2O2 as a signaling conduit and initiator of redox relays and propose an integrated view of physiological versus non-physiological reactive species. Therapeutic interventions that target persistently altered ROS levels should include both selective inhibition of a specific source of primary ROS and careful consideration of a targeted pro-oxidant approach, an avenue that is still underdeveloped. Both strategies require attention to redox dynamics in complex cellular systems, integration of the overall spatiotemporal cellular environment, and target validation to yield effective and safe therapeutics. The only professional primary ROS producers are NADPH oxidases (NOX1-5, DUOX1-2). Many other enzymes, e.g., xanthine oxidase (XO), monoamine oxidases (MAO), lysyl oxidases (LO), lipoxygenase (LOX), and cyclooxygenase (COX), produce superoxide and H2O2 secondary to their primary metabolic function. Superoxide is too reactive to disseminate, but H2O2 is diffusible, only limited by adjacent PRDXs or GPXs, and can be apically secreted and imported into cells through aquaporin (AQP) channels. H2O2 redox signaling includes oxidation of the active site thiol in protein tyrosine phosphatases, which will inhibit their activity and thereby increase tyrosine phosphorylation on target proteins. Essential functions include the oxidative burst by NOX2 as antimicrobial innate immune response; gastrointestinal NOX1 and DUOX2 generating low H2O2 concentrations sufficient to trigger antivirulence mechanisms; and thyroidal DUOX2 essential for providing H2O2 reduced by TPO to oxidize iodide to an iodinating form which is then attached to tyrosyls in TG. Loss-of-function (LoF) variants in TPO or DUOX2 cause congenital hypothyroidism and LoF variants in the NOX2 complex chronic granulomatous disease.

Suppressing Cyanobacteria with Hydrogen Peroxide Is More Effective at High Light Intensities.

Hydrogen peroxide (H2O2) can be used as an emergency method to selectively suppress cyanobacterial blooms in lakes and drinking water reservoirs. However, it is largely unknown how environmental parameters alter the effectiveness of H2O2 treatments. In this study, the toxic cyanobacterial strain Microcystis aeruginosa PCC 7806 was treated with a range of H2O2 concentrations (0 to 10 mg/L), while being exposed to different light intensities and light colors. H2O2 treatments caused a stronger decline of the photosynthetic yield in high light than in low light or in the dark, and also a stronger decline in orange than in blue light. Our results are consistent with the hypothesis that H2O2 causes major damage at photosystem II (PSII) and interferes with PSII repair, which makes cells more sensitive to photoinhibition. Furthermore, H2O2 treatments caused a decrease in cell size and an increase in extracellular microcystin concentrations, indicative of leakage from disrupted cells. Our findings imply that even low H2O2 concentrations of 1–2 mg/L can be highly effective, if cyanobacteria are exposed to high light intensities. We therefore recommend performing lake treatments during sunny days, when a low H2O2 dosage is sufficient to suppress cyanobacteria, and may help to minimize impacts on non-target organisms.

A possible new oxidation marker for hair adulteration: Detection of PTeCA (1H-pyrrole-2,3,4,5-tetracarboxylic acid) in bleached hair.

Hair analysis has become a valuable tool in forensic toxicology to assess drug or alcohol abstinence. Yet, hair adulteration by cosmetic products presents a major challenge for forensic hair analysis. Oxidative treatments, e.g. bleaching, may lead to analyte loss and thereby to false negative results. Currently, the eumelanin degradation product 1H-pyrrole-2,3,5-tricarboxylic acid (PTCA) serves as a marker for oxidative hair treatment, but requires the definition of cut-off values. To investigate further eumelanin degradation products as markers for oxidative hair treatment, hair samples with and without in vitro bleaching (hydrogen peroxide (H2 O2 ) concentrations 1.9% up to 12%; incubation times 15 min, 30 min, 60 min) were analyzed by liquid chromatography coupled to high-resolution time of flight mass spectrometry (HPLC-HRMS). The distribution of eumelanin degradation products along the hair shaft was investigated for routine applicability after segmentation of cosmetically untreated hair samples and authentically treated hair samples. The signals of the eumelanin degradation products PTCA, 1H-pyrrole-2,3,4-tricarboxylic acid (isoPTCA), and 1H-pyrrole-2,3,4,5-tetracarboxylic acid (PTeCA) were found to be significantly elevated after in vitro bleaching already with low H2 O2 concentrations and after short incubation times. In contrast to PTCA and isoPTCA, PTeCA was not detectable in cosmetically untreated segments up to 12 cm from hair root and was only formed through the oxidation process. The results of the study show that the detection of PTeCA within the proximal 3 to 6 cm segment can be applied to reliably detect hair adulteration attempts through hair bleaching.

Hydrogen Peroxide Sensors Based on Fluorescence Quenching of the 2-AminobenzimidazoleFluorophore.

The fluorescence emission of the parent 2-aminobenzimidazole (ABZ, 1), the mono- and disubstituted derivatives (2, 3), 2-aminonaphthoimidazole (4), and 4-amino dinaphthodiazepine 5 (λem = 315-400 nm) is strongly quenched in the presence of aqueous hydrogen peroxide. The quenching process is dual: for diazepine 5, quenching is dynamic at lower H2O2 concentrations with linear reduction of the fluorescence lifetime from 4.3 to 2.6 ns. At higher H2O2 concentrations, a second species appears in the absorption and emission spectra with fluorescence lifetimes of 1.3 ns, indicating the formation of a new (ground-state) hydrogen-bonded ABZ-H2O2 complex (static quenching). Sensors 1 and 2 show also dual quenching that fits with a static 1:1 and 1:2 model with K1:1 = 8(11) M-1 and K1:2 = 21(147) M-1 for 1(2). The formation of a 1:2 complex (1:(H2O2)2) is also supported by density functional theory (DFT) calculations and spectra simulations.

High-pressure jet-induced hydrodynamic cavitation as a pre-treatment step for avoiding cyanobacterial contamination during water purification

Due to specific physical properties, hydrodynamic cavitation (HC) is assigned to the powerful technologies for treating the biotic contamination in water including cyanobacteria. Contaminated water stream (CWS) can be cavitated directly by passing through some HC device, or indirectly when high-pressure jet stream (HPJS) is directed against its flow. Relatively small HPJS stream can thus treat a big volume of CWS in a short time or even work in continuous mode. Cyanobacteria floating in the CWS are forced to flow through the mixing cavitation zone. Within 2 h after single HC treatment, cyanobacterial cell suspensions showed disintegration of larger colonies and enhanced biomass sedimentation. Additional pre-treatment of CWS with low amounts of hydrogen peroxide (H2O2; 33, 66 and 99 μmol/L) enhanced the effect of HC and led to further inhibition of cyanobacterial photosynthesis (maximum quantum yield of photosystem II decreased by up to 60%). The number of cyanobacterial cells in the treated CWS decreased continuously over 48 and 72 h, though some cells remained alive and were able to recover photosynthetic activity. The technique proposed (direction of a HPJS against a CWS and pre-treatment with low H2O2 concentrations) provides (i) effective removal of cells from the water column, and (ii) reduced contamination by organic compounds released from the cells (especially cyanotoxins) as the cell membranes are not destroyed and the cells remain alive. This process shows potential as an effective pre-treatment step in water purification processes related to cyanobacterial contamination.

Photo-Fenton process at natural conditions of pH, iron, ions, and humic acids for degradation of diuron and amoxicillin.

Effect of ferric ions at concentrations typically found in natural waters (0.05 to 1.06mgL-1) and low H2O2 concentrations (between 0.5 and 17.9mgL-1) on simulated sunlight-induced (300Wm-2) photo-Fenton degradation at initial neutral pH (7.0) of amoxicillin and diuron in Milli-Q water was studied using an rotatable central composite experimental design 22 with a central and two axial points. H2O2 concentration was the parameter playing the key role on the degradation of both pollutants. Despite that initial pH was 7.0 in Milli-Q water, this latter decreased rapidly in the first minutes, reaching values of 3.5 and 5.0 for diuron and amoxicillin respectively after 15min of simulated sunlight irradiation. In contrast, in presence of bicarbonate/carbonate (HCO3-/CO3=), fluoride (F-), and humic acids (HAs) at concentrations found often in surface and well waters with ferric ion and H2O2 concentrations of 0.3 and 9.7 and 15.2mgL-1 respectively, both pollutants exhibited a strong degradation keeping the circumneutral pH. Amoxicillin and diuron degradation byproducts found by HPLC/MS were compatible with HO• and/or CO3-• radical attack. Several photo-induced processes such as photo-Fenton (by dissolved ferric-HA complexes), heterogeneous photocatalysis (by colloidal iron), UV-B H2O2 photolysis, irradiated-dissolved organic matter, and their reactions with pollutants would be the main oxidative route responsible of degradations. These findings demonstrated that it could be possible using iron concentrations often found in natural waters to oxidize via photo-Fenton processes among other events, organic pollutants at natural pH conditions.

Loss of function of Arabidopsis NADP-malic enzyme 1 results in enhanced tolerance to aluminum stress.

In acidic soils, aluminum (Al) toxicity is a significant limitation to crop production worldwide. Given its Al-binding capacity, malate allows internal as well as external detoxification strategies to cope with Al stress, but little is known about the metabolic processes involved in this response. Here, we analyzed the relevance of NADP-dependent malic enzyme (NADP-ME), which catalyzes the oxidative decarboxylation of malate, in Al tolerance. Plants lacking NADP-ME1 (nadp-me1) display reduced inhibition of root elongation along Al treatment compared with the wild type (wt). Moreover, wt roots exposed to Al show a drastic decrease in NADP-ME1 transcript levels. Although malate levels in seedlings and root exudates are similar in nadp-me1 and wt, a significant increase in intracellular malate is observed in roots of nadp-me1 after long exposure to Al. The nadp-me1 plants also show a lower H2 O2 content in root apices treated with Al and no inhibition of root elongation when exposed to glutamate, an amino acid implicated in Al signaling. Proteomic studies showed several differentially expressed proteins involved in signal transduction, primary metabolism and protection against biotic and other abiotic stimuli and redox processes in nadp-me1, which may participate directly or indirectly in Al tolerance. The results indicate that NADP-ME1 is involved in adjusting the malate levels in the root apex, and its loss results in an increased content of this organic acid. Furthermore, the results suggest that NADP-ME1 affects signaling processes, such as the generation of reactive oxygen species and those that involve glutamate, which could lead to inhibition of root growth.

The mechanisms of alteration of a homogeneous U0.73Pu0.27O2 MOx fuel under alpha radiolysis of water

An homogeneous MOx fuel with 24 wt% of plutonium was leached in a carbonated water (10−2 M) under argon ([O2] < 1 vppm) for one year in order to assess the leaching behaviour of U–Pu oxide solid solutions and more specifically to simulate the behaviour of Pu enriched agglomerates characteristic of heterogeneous Mimas MOx fuel. The alpha activity of the pellets was 2.2 × 109 Bq. g−1. Two successive dissolution regimes were observed: an initial dissolution with a uranium release rate of 1.2 × 10−4 molU.m−2. d−1, and then, a long-term dissolution regime with a rate of 7.6 × 10−6 molU.m−2. d−1. The H2O2 concentration was under the detection limit of 1 × 10−7 mol L−1. Pu concentration in the homogeneous solution was constant around 10−9 mol L−1 throughout the duration of the experiment, in accordance with a thermodynamic equilibrium controlled by an amorphous Pu(OH)4 phase. SEM – WDS analysis confirmed a Pu-enriched layer at the surface of the pellets with Pu contents up to 39 wt%. This Pu-enriched layer becomes more resistant against leaching than the pristine surface. Despite this Pu enrichment, H2O2 concentration remained very low in the homogeneous solution. Different mechanisms of consumption can be considered, such as the oxidative dissolution of the pellet, the precipitation of U or Pu peroxides or the catalytic disproportionation. As the precipitation of peroxides at the surface was discarded by Raman spectroscopy and the oxidative dissolution was very limited, the low H2O2 concentration was likely due to a higher catalytic disproportionation of H2O2 by the Pu-enriched layer. Mass balance calculation showed that H2O2 disproportionation represented 99% of the H2O2 consumption for the homogeneous MOx, against 86% for UO2 pellets. These results shed new light on the Pu stabilizing mechanisms against the oxidative dissolution that can be applied to model the behaviour of different MOx fuels under long-term disposal conditions.