Redox Profile Research Articles

Identification of catechin in ethyl acetate phase and determination of redox profile of the Anacardium occidentale L. through electrochemical techniques

Anacardium occidentale L., also known how “cajueiro”, is very used for your pharmacological properties, like: anti-inflammatory, healing, anti-glycemic and others. Their curls have been described as rich in phenolic compounds, powerful natural antioxidants. Thus, the objective of this work was to determine the redox profile of the A. occidentale inner bark extract using electrochemical and spectrophotometric techniques through the DPPH radical sequestration reaction. For this, a phytochemical prospection was made in which steroids, phenols, flavones, flavonoids, saponins, tannins and xanthones were detected in the hydroethanolic extract (HEE) and in the ethyl acetate phase (EAP). Total phenolic content in the EAP was also quantified with values of 848.62 ± 78.18 μg mg-1 ofgallic acid. The DPPH assay showed that the EAP at a concentration of 25μg mL-1, presents the greater sequestration of free radicals (around 90%) with an CE50 value of 16.13 μg mL-1 and an AAI value of 2.48, noting the very strong antioxidant potential of the plant. The EAP High Performance Liquid Chromatography analysis showed a similar behavior to the catechin standard, with a major peak eluted at 3 minutes and 30 seconds with a slightly broad base and a UV absorbance spectrum with a maximum absorbance of 274 nm, identifying (+) - catechin, when compared to the 279 nm UV-Visible scanning spectrum obtained with catechin standard. The EAP voltammograms were similar to the (+) - catechin standard, inferring the catechin involvement with A. occidentale redox activity.

Evaluation of the interaction of a guanylhydrazone derivative with cobalt ferrite nanoparticles and PAMAM electrochemical and UV/visible spectroscopic techniques

Nowadays, scientific research grows a lot around nanotechnology, which connects many areas of knowledge such as electrochemistry and magnetic nanoparticles (MNPs). The study of bioactive substances by electrochemical methods is already very conceptual, and the association of magnetic nanoparticles has emerged as a new bias of this technique. Here, we report the results of the interaction between the molecule LQM10, a derivative of guanylhydrazone, with nanocarriers: cobalt ferrite magnetic nanoparticles (CoFe2O4 MNPs) and polyamidoamine dendrimer (PAMAM), seeking to unite the characteristics of each nanocarrier to benefit LQM10. The electrochemical system was composed of 3 electrodes, Ag/AgCl/Cl− saturated (reference), platinum (auxiliary), and modified glassy carbon (GCE) (work) with CoFe2O4 MNPs alone and with PAMAM G3, in buffered medium pH 7.03 with or without a co-solvent (analytical grade ethanol). UV-visible spectroscopic studies were carried out in aqueous-ethanolic medium in different concentrations of PAMAM G3 and CoFe2O4 MNPs. The magnetic properties of CoFe2O4 MNPs and each nanocarriers were confirmed by vibrating sample magnetometer and by field effect calorimetry. LQM10, which has a redox profile in oxidative potentials, showed good interaction with all tested electrodes and revealed considerable values of formation constant (KF), highlighting the GCE modified with CoFe2O4 MNPs (KF = 1.92 × 106 L/mol) and PAMAM G3, corroborating with the results of UV-visible data (Kb = 7.60 × 105 L/mol). The generation of heat by magnetic hyperthermia of CoFe2O4 MNPs in the presence of PAMAM G3 and LQM10 was determined (SAR = 0.72 W/g). Therefore, we demonstrated the association of promising nanocarriers (PAMAM G3 and CoFe2O4 MNPs) with anticancer substances and their applicability as magnetic hyperthermia.

Effect of cassava flour on the lipidic and redox profile of Wistar rats with dyslipidemia.

One of the major risk factors for cardiovascular disease is high total cholesterol. It is known that some foods can reduce plasma cholesterol, such as oats. Cassava flour has a similar amount of fiber when compared to oats. The objective of this study was to evaluate the hypocholesterolemic potential of cassava flour. Thirty Wistar rats (eight weeks old) were divided into three groups: control, high-cholesterol diet, high-cholesterol diet+cassava flour, and were treated for 8weeks. The weight and food consumption of the animals were evaluated weekly. After euthanasia, analyzes of biochemical and oxidative stress profiles were performed, besides the histological analysis of the liver. Cassava flour protected animals from lipoperoxidation, according to thiobarbituric acid-reactive substances results and improved superoxide dismutase activity and thiol content; however, failed to improve the lipid profile and catalase. Cassava flour was possibly able to slow the progression of NASH according to liver histology. PRACTICAL APPLICATIONS: Lifestyle and nutritional habits have been considered important factors associated with the development of dyslipidemia and other chronic diseases. Medicines for chronic diseases are often expensive and have present side effects, and therefore, it is preferable to prevent them through food. Cassava flour is a food widely consumed by Brazilians, which is inexpensive and contains no gluten. Understanding more about one of the most used foods in Brazil is important for health professionals to be able to prescribe it for the correct purposes.

Tuberculosis latent infection in health care workers: oxidative stress and Quantiferon-TB Plus

Abstract Background This study moves from recent evidences highlighting: 1) the high sensitivity of Mycobacterium tuberculosis (MT) to perturbation of redox homeostasis induced by oxidative stress; 2) the improvement of Tuberculosis (TB) diagnosis following the introduction of Quantiferon-TB Plus (QFT-Plus) assay. Methods The QFT-Plus diagnostic performance and the blood antioxidant capacity, expressed as ratio between oxidized (GSSG) and reduced (GSH) forms of glutathione, were determined on three selected populations (40 Health care workers (HCWs) controls, 63 latent TB HCWs, 8 active TB patients). Quantitative Real Time PCR analysis on leukocytes of active TB patients was also performed, in order to identify “redox profiles” of genes mainly involved in the antioxidant response. Results 1) The glutathione homeostasis was shifted towards an oxidative status in active TB patients respect to controls, as evidenced by the significant decrease of the ratio between free and total GSH, an indirect index of oxidative stress. More reducing conditions were observed in latent TB subjects. 2) The expression profiles of antioxidant genes confirmed the major susceptibility of active TB patients to oxidative stress compared to controls, and highlighted a great individual variability. 3) The diagnostic performance of QFT-Plus test present a moderate concordance with QFT-GIT one, in this preliminary phase. Conclusions Glutathione has anti-mycobacterial effects in its reduced form GSH, thus the quantification of Free/Total GSH ratio may represent a systemic marker of TB infection and be useful in developing combined therapies. Moreover, the identification of personalized redox profiles will additionally provide an individual antioxidant response to the infection. This project was funded by the Ministry of Health (RF 2016) Key messages LTBI management represents an objective of primary importance in the field of occupational medicine in order to define a personalized prevention in HCW. A new approach that combines biochemical determinations of redox biomarkers and gene expression in blood will be a novel biomarkers of tuberculosis.

Effects of Fine Sediment on Seagrass Meadows: A Case Study of Zostera muelleri in Pāuatahanui Inlet, New Zealand

Seagrass meadows are vulnerable to fine sediment (mud) pollution, with impacts usually attributed to reduction in submerged light. Here we tested two non-exclusive hypotheses, that mud particles (<63 µm) impact seagrasses through both (1) the light climate and (2) changes in substrate physico-chemistry. We tested these hypotheses in Pāuatahanui Inlet, New Zealand, by comparing seagrass presence, abundance, and health, together with light climate and substrate physico-chemistry at contrasting habitats where (1) seagrass used to thrive but no longer grows (historical seagrass), (2) seagrass still persists (existing seagrass) and (3) seagrass has been present recently, but not currently (potential seagrass). Historical seagrass substrate had significantly higher mud (35% average), bulk density (1.5 g cm−3), porewater ammonium concentration (65 µM), and a more reduced redox profile (negative redox at only 2 cm soil depth) as well as a lower light availability when submerged compared to other habitats, while total daily light exposure differed little between habitats. This suggests that failure of seagrass to recolonize historical seagrass habitat reflects substrate muddiness and consequent unfavorable rhizosphere conditions. Our results provide evidence for the multi-stressor effects of fine sediment on seagrasses, with substrate suitability for seagrass being detrimentally affected even where light exposure seems sufficient.

Metabolt: An In-Situ Instrument to Characterize the Metabolic Activity of Microbial Soil Ecosystems Using Electrochemical and Gaseous Signatures.

Metabolt is a portable soil incubator to characterize the metabolic activity of microbial ecosystems in soils. It measures the electrical conductivity, the redox potential, and the concentration of certain metabolism-related gases in the headspace just above a given sample of regolith. In its current design, the overall weight of Metabolt, including the soils (250 g), is 1.9 kg with a maximum power consumption of 1.5 W. Metabolt has been designed to monitor the activity of the soil microbiome for Earth and space applications. In particular, it can be used to monitor the health of soils, the atmospheric-regolith fixation, and release of gaseous species such as N2, H2O, CO2, O2, N2O, NH3, etc., that affect the Earth climate and atmospheric chemistry. It may be used to detect and monitor life signatures in soils, treated or untreated, as well as in controlled environments like greenhouse facilities in space, laboratory research environments like anaerobic chambers, or simulating facilities with different atmospheres and pressures. To illustrate its operation, we tested the instrument with sub-arctic soil samples at Earth environmental conditions under three different conditions: (i) no treatment (unperturbed); (ii) sterilized soil: after heating at 125 °C for 35.4 h (thermal stress); (iii) stressed soil: after adding 25% CaCl2 brine (osmotic stress); with and without addition of 0.5% glucose solution (for control). All the samples showed some distinguishable metabolic response, however there was a time delay on its appearance which depends on the treatment applied to the samples: 80 h for thermal stress without glucose, 59 h with glucose; 36 h for osmotic stress with glucose and no significant reactivation in the pure water case. This instrument shows that, over time, there is a clear observable footprint of the electrochemical signatures in the redox profile which is complementary to the gaseous footprint of the metabolic activity through respiration.

Resistance training improves sleep quality, redox balance and inflammatory profile in maintenance hemodialysis patients: a randomized controlled trial

Patients in maintenance hemodialisys (HD) present sleep disorders, increased inflammation, unbalanced redox profiles, and elevated biomarkers representing endothelial dysfunction. Resistance training (RT) has shown to mitigate the loss of muscle mass, strength, improve inflammatory profiles, and endothelial function while decreasing oxidative stress for those in HD. However, the relation between those factors and sleep quality are inadequately described. The aim of this study was to verify the effects of 3 months of RT on sleep quality, redox balance, nitric oxide (NO) bioavailability, inflammation profile, and asymmetric dimethylarginine (ADMA) in patients undergoing HD. Our primary goal was to describe the role of RT on sleep quality. Our secondary goal was to evaluate the effect of RT on NO, metabolism markers, and inflammatory and redox profiles as potential mechanisms to explain RT—induced sleep quality changes. Fifty-five men undergoing maintenance hemodialysis were randomized into either a control (CTL, n = 25) and RT group (RTG; n = 30). Participants in the RT group demonstrated an improvement in sleep pattern, redox, inflammatory profiles, and biomarkers of endothelial function (NO2− and ADMA). This group also increased muscle strength (total workload in RT exercises of upper and lower limbs). These findings support that RT may improve the clinical status of HD patients by improving their sleep quality, oxidative and inflammatory parameters.

Accelerated ageing profile in inflammatory arthritis is unique and tissue compartment specific.

Rheumatoid arthritis is prevalent in more than 1% of the global population, with the highest occurrence between ages 35 and 50, which places a huge burden on the economy. Drug discovery for the prevention of this chronic disease is; therefore, a priority. It is known that subclinical progression of many chronic non-communicable diseases is exacerbated via accelerated ageing, a pro-inflammatory phenotype shift. However, rheumatoid arthritis additionally has significant humoral immune activation, inflammatory signalling-and thus the accelerated ageing profile-may differ from other chronic inflammatory diseases. The current study simulated inflammatory arthritis onset in a collagen-induced arthritis (CIA) rodent model, to characterise the redox and inflammatory profile at the onset of clinical symptoms, in different tissues, in the presence and absence of preventative antioxidant treatment. The data illustrate that an increased free radical level are evident already very early on in RA disease progression. Furthermore, oxidative stress seems to somewhat precede a significant pro-inflammatory state, perhaps due to humoral immune activation. Our data across different compartments further suggest that the compensatory increase in endogenous antioxidant activity is gradually exhausted at a different pace, with the liver showing the first signs of oxidant damage, even before significant evidence exist in circulation. The current data further suggest that preventative antioxidant intervention may have a sparing effect on endogenous antioxidant mechanisms and preserve telomere length to delay disease progression-or at least the accelerated ageing known to exacerbate RA symptoms-although it did not seem to have a significant direct effect on the autoimmune activity.

Electronic Consequences of Ligand Substitution at Heterometal Centers in Polyoxovanadium Clusters: Controlling the Redox Properties through Heterometal Coordination Number.

The rational control of the electrochemical properties of polyoxovanadate‐alkoxide clusters is dependent on understanding the influence of various synthetic modifications on the overall redox processes of these systems. In this work, the electronic consequences of ligand substitution at the heteroion in a heterometal‐functionalized cluster was examined. The redox properties of [V5O6(OCH3)12FeCl] (1‐[V5FeCl]) and [V5O6(OCH3)12Fe]X (2‐[V5Fe]X; X=ClO4, OTf) were compared in order to assess the effects of changing the coordination environment around the iron center on the electrochemical properties of the cluster. Coordination of a chloride anion to iron leads to an anodic shift in redox events. Theoretical modelling of the electronic structure of these heterometal‐functionalized clusters reveals that differences in the redox profiles of 1‐[V5FeCl] and 2‐[V5Fe]X arise from changes in the number of ligands surrounding the iron center (e.g., 6‐coordinate vs. 5‐coordinate). Specifically, binding of the chloride to the sixth coordination site appears to change the orbital interaction between the iron and the delocalized electronic structure of the mixed‐valent polyoxovanadate core. Tuning the heterometal coordination environment can therefore be used to modulate the redox properties of the whole cluster.

Whey protein boosts the antioxidant profile of rats by enhancing the activities of crucial antioxidant enzymes in a tissue-specific manner

Whey protein, a by-product of cheese industry, is harmful for the environment (i.e., surface and subterranean waters, soil) and, therefore, for humans due to its high polluting burden. Concomitantly, it has been reported that it is a mixture with potent antioxidant action since it is rich in cysteine residues, which are necessary for glutathione synthesis in vivo. On this basis, this study intended to examine the role of whey protein on the intensification of tissue antioxidant arsenal. To this end, a dose of sheep/goat whey protein equal to 1 g/kg of body weight/day dissolved in drinking water was administered to rats for 28 consecutive days. According to our findings, whey protein improved the antioxidant profile of liver, small intestine, lung and muscle whereas it did not affect the redox state of kidney. Our results were based on the alterations found in the protein expression of glutamate cysteine ligase, catalase and superoxide dismutase-1 measured in all tissues and the activity of glutathione S-transferase evaluated in muscle. Although tissue-specific, it is obvious that the action of whey protein is biologically beneficial and could serve as a biofunctional constituent for foods able to improve redox profile when administered against redox-related diseases.

CRGD mediated redox and pH dual responsive poly(amidoamine) dendrimer-poly(ethylene glycol) conjugates for efficiently intracellular antitumor drug delivery

To improve antitumor efficiency of chemotherapy and reduce side effect, according to the physiological characteristics of tumor tissues and tumor intracellular microenvironment, a multifunctional drug delivery system with properties of long circulation, active targeting, redox and pH triggered drug release was established based on the Generation 4 polyamidoamine dendrimer (PAMAM). First, the redox cleavable disulfide bonds (SS) were introduced for linking polyethylene glycol (PEG) with PAMAM to form PAMAM-S-S-PEG (PSSP). Then cRGD peptide was applied to the PEG end of PSSP to construct RGD-PSSP conjugates. Finally, encapsulating the antitumor chemotherapy drug doxorubicin (DOX) into the hydrophobic cavity of RGD-PSSP conjugates constructed the RGD-PSSP/DOX drug delivery system. The in vitro experiments displayed that RGD-PSSP/DOX NPs showed obviously redox and pH dual sensitive drug release profile. MTT and cell uptake observation elucidated cRGD modification could increase the cytotoxicity, and promote the uptake of B16 cells and HUVEC cells both overexpressing integrin ανβ3on cell membrane. Cell uptake mechanism investigation further revealed that RGD-PSSP/DOX interacted with plasma membrane via specific recognition of cRGD peptide with integrin ανβ3, and was subsequently internalized mainly through clathrin- and caveolin-mediated endocytosis. Remarkably, RGD-PSSP/DOX presented superior anticancer activity and lower heart and kidney toxicity in vivo, which could be regarded as a potential candidate for efficient antitumor chemotherapy drug delivery.

Influence of Long-Term Fasting on Blood Redox Status in Humans.

Fasting is increasingly practiced to improve health and general well-being, as well as for its cytoprotective effects. Changes in blood redox status, linked to the development of a variety of metabolic diseases, have been recently documented during calorie restriction and intermittent fasting, but not with long-term fasting (LF). We investigated some parameters of the blood redox profile in 109 subjects before and after a 10-day fasting period. Fasting resulted in a significant reduction in body weight, improved well-being and had a beneficial modulating effect on blood lipids and glucose regulation. We observed that fasting decreased lipid peroxidation (TBARS) and increased total antioxidant capacity (TAC) in plasma, concomitant with a uric acid elevation, known to be associated with fasting and did not cause gout attacks. Reduced glutathione (GSH), glutathione reductase (GR), glutathione peroxidase (GPx) and catalase in erythrocytes did not show significant changes. In addition, reduction in body weight, waist circumference, and glucose levels were associated to a reduced lipid peroxidation. Similar results were obtained by grouping subjects on the basis of the changes in their GSH levels, showing that a period of 10 days fasting improves blood redox status regardless of GSH status in the blood.

P1143REDOX PROFILING IN MESOTHELIAL CELLS IN EXPERIMENTAL PERITONEAL DIALYSIS

Abstract Background and Aims PD-fluids lead to generation of reactive oxygen species (ROS) in the peritoneal cavity. The caused oxidative stress, defined as a cellular oxidant-antioxidant imbalance impairs not only peritoneal cell viability but also contributes to progression of local and systemic PD-related pathomechanisms. We aim to analyze the impact and specific targets of ROS during PD and the anti-oxidative mechanism of supplementation of PD-fluid with alanyl-glutamine (AlaGln) on a global proteome-wide level. Method To establish a redox-proteomics workflow for studying oxidative stress in peritoneal mesothelial cells we used a gold-standard model of redox-stress (H2O2) and PD-fluid induced stress. Levels of oxidative stress were first validated by increased intracellular ROS and superoxide dismutase activity with PD-fluid and H2O2 treatment and a reduction of these parameters by the addition of AlaGln. To detect alterations of the redox proteome, cysteine residues were either directly or indirectly labeled with fluorescent dyes (redox-2D-DiGE) or isobaric tags (iodo-TMT). Results: The gel-based approach allowed global visualization of the reduced and oxidized cysteines and revealed redox profiles of 540 protein spots. Compared to control, we found an increase in oxidized and decrease in reduced cysteines in all PD treatments. The development of a highly sensitive LC/MS-based redox proteomics workflow allowed identification of ∼950 proteins affected by redox-stress in mesothelial cells and confirmed the quantitative levels seen on cysteine oxidation. The addition of AlaGln reduced the overall redox status (intracellular ROS and superoxide dismutase activity) but further showed different proteins to be affected by redox modifications. Conclusion: Redox proteomics of peritoneal cells could represent a novel approach for the identification of mediators of PD-induced pathomechanisms, but also to evaluate effects of novel anti-oxidant therapeutical or pharmacological interventions.

The Bacterial Toxin CNF1 Protects Human Neuroblastoma SH-SY5Y Cells against 6-Hydroxydopamine-Induced Cell Damage: The Hypothesis of CNF1-Promoted Autophagy as an Antioxidant Strategy.

Several chronic neuroinflammatory diseases, including Parkinson’s disease (PD), have the so-called ‘redox imbalance’ in common, a dynamic system modulated by various factors. Among them, alteration of the mitochondrial functionality can cause overproduction of reactive oxygen species (ROS) with the consequent induction of oxidative DNA damage and apoptosis. Considering the failure of clinical trials with drugs that eliminate ROS directly, research currently focuses on approaches that counteract redox imbalance, thus restoring normal physiology in a neuroinflammatory condition. Herein, we used SH-SY5Y cells treated with 6-hydroxydopamine (6-OHDA), a neurotoxin broadly employed to generate experimental models of PD. Cells were pre-treated with the Rho-modulating Escherichia coli cytotoxic necrotizing factor 1 (CNF1), before the addition of 6-OHDA. Then, cell viability, mitochondrial morphology and dynamics, redox profile as well as autophagic markers expression were assessed. We found that CNF1 preserves cell viability and counteracts oxidative stress induced by 6-OHDA. These effects are accompanied by modulation of the mitochondrial network and an increase in macroautophagic markers. Our results confirm the Rho GTPases as suitable pharmacological targets to counteract neuroinflammatory diseases and evidence the potentiality of CNF1, whose beneficial effects on pathological animal models have been already proven to act against oxidative stress through an autophagic strategy.

Anti-inflammatory exosomes mediate the beneficial effect of mesenchymal stem cell therapy on lung preservation

Background & Aim Mesenchymal stem cell (MSCs) therapy protects donor lungs against ischemic-reperfusion injury. We recently reported that local infusion of human umbilical cord-derived MSCs during donor lung ablation significantly conserved lung function. The anti-inflammatory effect of MSCs is mainly exerted through a paracrine mechanism. Thus, in the present study, we investigated whether the preservation capacity of MSCs is related to the secretion of anti-inflammatory exosomes. Methods, Results & Conclusion The rat lung preservation model settled before consisted on: cardiac arrest, warm ischemia (2h) in which cells were administered at 1h via the pulmonary artery (1 × 10^6 cells or vehicle), cold ischemia, and normothermic ex-vivo lung perfusion with ventilation. Here, we assessed 3 experimental groups right after the warm ischemia period (2h): vehicle, MSCs, and exosomes (released by 1 × 10^6 cells). Exosomes were chromatographically purified from MSCs conditioned medium and their anti-inflammatory activity was evaluated, in vitro, based on their ability to suppress the acquisition of M1 phenotype in LPS-stimulated RAW264.7 cells. Physiologic data (pressure-volume curves) were acquired right after the cardiac arrest and at the end of the warm ischemia time and lung biopsies were taken to study edema formation, neutrophil infiltration, redox profile, and inflammatory molecular markers. As expected, exosomes were positive for human-specific CD63 and CD81, and showed the tipical size and morphology by electron microscopy. Exosomes also exposed their anti-inflammatory activity by significantly reducing IL-6 secretion in LPS-stimulated macrophages by 60%. Previously, in the complete lung preservation model (4.5h), we observed that MSCs administration facilitated organ preservation by significantly reducing the drop on lung compliance (∼50% vs vehicle treated group, p Taking in consideration our previous data and these new results we conclude that MSCs-derived exosomes have a key role in lung preservation mediated by MSCs. Consequently, we postulate that exosomes may represent an innovative cell free therapy for organ preservation.

Mesenchymal Stem Cell therapy maximizes lung preservation by preventing ischemic organ injury

Background & Aim Recently, we reported that local infusion of human umbilical cord-derived mesenchymal stem cells (MSCs) during donor lung ablation may increase lung availability by improving organ preservation. We found that MSCs protect donor lungs against ischemic injury by reducing oxidative damage and neutrophil extravasation. Pre-conditioning has emerged as a strategy to improve MSC-based therapies. Here, we studied whether the preservation capacity of MSCs may be enhanced by their pre-activation into an anti-inflammatory phenotype with TNF-alpha (TNF-a). Methods, Results & Conclusion We settled a lung preservation model in rats that mimics the different phases by which donor organs must undergo before implantation which consist on: cardiac arrest, warm ischemia (2h at room temperature), cold ischemia (1.5h at 4°C, with Perfadex), and normothermic lung perfusion with ventilation (Steen solution, 1h). After 1h of warm ischemia, 1 × 10^6 cells (MSCs, or TNF-a treated cells) or vehicle were infused via the pulmonary artery. Physiologic data (pressure-volume curves) were acquired right after the cardiac arrest and at the end of the perfusion. Lung biopsies were taken at the end of the perfusion to study edema formation, neutrophil infiltration, redox profile, etc. Interestingly, although the TNF-a treated cells showed an anti-inflammatory phenotype in vitro, we did not register a significant change in their preservation capacity. In this line, lung compliance decreased 39% and 35% in the MSCs- and TNF-a-treated groups, respectively, while the vehicle group showed a stronger reduction (72%, p These results suggest that, in this therapeutic conditions, the anti-inflammatory effect of non-activated MSCs is strong enough to conserve the functionality of the lung during ischemia, and reaffirm the notion that cell therapy is a novel tool for organ preservation.

A magma ocean origin to divergent redox evolutions of rocky planetary bodies and early atmospheres

Magma oceans were once ubiquitous in the early solar system, setting up the initial conditions for different evolutionary paths of planetary bodies. In particular, the redox conditions of magma oceans may have profound influence on the redox state of subsequently formed mantles and the overlying atmospheres. The relevant redox buffering reactions, however, remain poorly constrained. Using first-principles simulations combined with thermodynamic modeling, we show that magma oceans of Earth, Mars, and the Moon are likely characterized with a vertical gradient in oxygen fugacity with deeper magma oceans invoking more oxidizing surface conditions. This redox zonation may be the major cause for the Earth’s upper mantle being more oxidized than Mars’ and the Moon’s. These contrasting redox profiles also suggest that Earth’s early atmosphere was dominated by CO2 and H2O, in contrast to those enriched in H2O and H2 for Mars, and H2 and CO for the Moon.

2-methoxy-isobutyl-isonitrile-conjugated gold nanoparticles improves redox and inflammatory profile in infarcted rats

The tissue response to acute myocardial infarction (AMI) is key to avoiding heart complications due to inflammation, mitochondrial dysfunction, and oxidative stress. Antioxidant and anti-inflammatory agents can minimize the effects of AMI. This study investigated the role of 2-methoxy-isobutyl-isonitrile (MIBI)-associated gold nanoparticles (AuNP) on reperfusion injury after ischemia and its effect on cardiac remodeling in an experimental AMI model. Three-month-old Wistar rats were subjected to a temporary blockade of the anterior descending artery for 30 min followed by reperfusion after 24 h and 7 days by intraventricularly administering 0.4, 1.3, and 3 mg/kg AuNP-MIBI. The cardiac toxicity and renal and hepatic function levels were determined, and the infarct and peri-infarct regions were surgically removed for histopathology, analysis of inflammation from oxidative stress, and echocardiography. MIBI-conjugated AuNP promoted changes in oxidative stress and inflammation depending on the concentrations used, suggesting promising applicability for therapeutic purposes.

Super Kinetically Pseudocapacitive MnCo2S4 Nanourchins toward High‐Rate and Highly Stable Sodium‐Ion Storage

AbstractImproving surface morphology profiles, i.e., surface area and porosity, by nanostructure/surface engineering is effective in accommodating sodium's ionic and kinetic inadequacies. However, this strategy is limited to only activating the extrinsic pseudocapacitance in terms of improving surface‐based reactions. Herein, it is aimed to improve the sodiation performance by enhancement from both intrinsic and extrinsic pseudocapacitance to maximize sodiation potential of materials. A rarely reported but highly functional spinel MnCo2S4 (MCS), is introduced and systematically analyzed using first‐principles investigations, which exhibits energetically favorable charge‐transfer states and strong Na‐ions adsorption kinetics as well as diffusion channels (−3.65 and 0.40 eV respectively). The overall electrochemical redox profiles of the MCS nanostructure is revealed by in situ techniques, which disclose the commencing of partial and then a full conversion‐type sodiation at low discharge potentials (0.52 V vs Na/Na+) with fast Na‐ions diffusivity. Assisted by surface engineering technology on the intrinsically pseudocapacitive MCS, the urchin‐like morphology is instrumental in boosting and realizing sodium storage performance, especially the surface capacitive behavior (from 73.4% to 94.1%), prolonged cycling stability (>800 cycles), and high‐rate capability (416 mAh g−1 at 10 A g−1), as well as exhibiting remarkable full cell capability (high rate at 2 A g−1, >200 cycles at 200 mA g−1).

Developmental programming: intrauterine caloric restriction promotes upregulation of mitochondrial sirtuin with mild effects on oxidative parameters in the ovaries and testes of offspring.

According to the developmental origins of health and disease (DOHaD) hypothesis, changes in the maternal environment are known to reprogram the metabolic response of offspring. Known for its redox modulation, caloric restriction extends the lifespan of some species, which contributes to diminished cellular damage. Little is known about the effects of gestational caloric restriction, in terms of antioxidant parameters and molecular mechanisms of action, on the reproductive organs of offspring. This study assessed the effects of moderate (20%) caloric restriction on redox status parameters, molecular expression of sirtuin (SIRT) 1 and SIRT3 and histopathological markers in the ovaries and testes of adult rats that were subjected to gestational caloric restriction. Although enzyme activity was increased, ovaries from female pups contained high levels of oxidants, whereas testes from male pups had decreased antioxidant enzyme defences, as evidenced by diminished glyoxalase I activity and reduced glutathione content. Expression of SIRT3, a deacetylase enzyme related to cellular bioenergetics, was increased in both ovaries and testes. Previous studies have suggested that, in ovaries, diminished antioxidant metabolism can lead to premature ovarian failure. Unfortunately, there is little information regarding the redox profile in the testis. This study is the first to assess the redox network in both ovaries and testes, suggesting that, although intrauterine caloric restriction improves molecular mechanisms, it has a negative effect on the antioxidant network and redox status of reproductive organs of young adult rats.