Redox Disequilibrium Research Articles

Sulfate-mediated Fe(III) mineral reduction accelerates arsenic mobilization by a Desulfovibrio strain isolated from paddy soil

The biogeochemical cycling of arsenic (As) is often intertwined with iron (Fe) and sulfur (S) cycles, wherein Fe(III)- and sulfate-reducing bacteria (SRB) play a crucial role. Here, we isolated strain DS-1, a strictly anaerobic Fe(III)- and sulfate-reducing bacterium, from As-contaminated paddy soil. Using 16S rRNA gene sequence analysis, strain DS-1 was identified as a member of the genus Desulfovibrio. Strain DS-1 utilized energy derived from ferrihydrite reduction to support its cellular growth. Under anoxic sulfate-reducing conditions, the presence of strain DS-1 significantly increased As mobilization compared to sulfate-free conditions. Mechanistically, SRB-produced sulfide reacts with Fe(III) to form FeS, which disrupts Fe(III) minerals, thereby enhancing As release. These findings highlight the critical role of redox disequilibrium in As mobilization and suggest that SRB-produced sulfide may permeate to the rice rhizosphere, increasing As mobilization through Fe(III) reduction.

Arsenic redox disequilibrium in geogenic contaminated groundwater: Bioenergetic insights from organic molecular characterization and gene-informed modeling

Biotransformation of arsenic (As) influences its speciation and mobility, obscuring mechanistic comprehension on spatiotemporal variation of As concentration in geogenic contaminated groundwater. In particular, unresolved processes underlying As redox disequilibrium in comparison to major redox couples discourage practical efforts to rehabilitate the As-contaminated groundwater. Here, quantitative metagenomic sequencing and ultrahigh-resolution mass spectrometry (FT-ICR-MS) were jointly applied to reveal the links between vertical distribution of As metabolic gene assemblages and that of free energy density of dissolved organic matter (DOM) in As-contaminated groundwater of Datong Basin. Observed small excess of Gibbs free energy available by DOM relative to that required for As(V)-to-As(III) reduction exerts thermodynamic constraint on metabolism-mediated redox transformation of As. Accordingly, the vertical distribution of dissolved As(V)/As(III) ratio correlated significantly with that of ars+acr3 and arr encoding As(V) reduction and aio encoding As(III) oxidation in the moderately/strongly reducing groundwater. Further gene-informed biogeochemical modeling suggests that a net effect of these kinetics-restricted bidirectional metabolic pathways leads to co-preservation of As(V) and As(III) even at relatively high rates of ars+acr3 encoded As(V) reduction. This study therefore provides new insights into bioenergetic constraints on As hydrobiogeochemical behavior, with implications for other redox-sensitive contaminants in the groundwater systems.

Oxidative stress, redox status and surfactant metabolism in mechanically ventilated patients receiving different approaches to oxygen therapy (MecROX): An observational study protocol for mechanistic evaluation.

MecROX is a mechanistic sub-study of the UK-ROX trial which was designed to evaluate the clinical and cost-effectiveness of a conservative approach to oxygen therapy for invasively ventilated adults in intensive care. This is based on the scientific rationale that excess oxygen is harmful. Epithelial cell damage with alveolar surfactant deficiency is characteristic of hyperoxic acute lung injury. Additionally, hyperoxaemia (excess blood oxygen levels) may exacerbate whole-body oxidative stress leading to cell death, autophagy, mitochondrial dysfunction, bioenergetic failure and multi-organ failure resulting in poor clinical outcomes. However, there is a lack of in-vivo human models evaluating the mechanisms that underpin oxygen-induced organ damage in mechanically ventilated patients. The aim of the MecROX mechanistic sub-study is to assess lung surfactant composition and global systemic redox status to provide a mechanistic and complementary scientific rationale to the UK-ROX trial findings. The objectives are to quantify in-vivo surfactant composition, synthesis, and metabolism with markers of oxidative stress and systemic redox disequilibrium (as evidenced by alterations in the 'reactive species interactome') to differentiate between groups of conservative and usual oxygen targets. After randomisation into the UK-ROX trial, 100 adult participants (50 in the conservative and 50 in usual care group) will be recruited at two trial sites. Blood and endotracheal samples will be taken at 0, 48 and 72 hours following an infusion of 3 mg/kg methyl-D 9-choline chloride. This is a non-radioactive, stable isotope of choline (vitamin), which has been extensively used to study surfactant phospholipid kinetics in humans. This study will mechanistically evaluate the in-vivo surfactant synthesis and breakdown (by hydrolysis and oxidation), oxidative stress and redox disequilibrium from sequential plasma and bronchial samples using an array of analytical platforms. We will compare conservative and usual oxygenation groups according to the amount of oxygen administered. Trial registration: ISRCTNISRCTN61929838, 27/03/2023 https://doi.org/10.1186/ISRCTN61929838.

Oxidative stress, redox status and surfactant metabolism in mechanically ventilated patients receiving different approaches to oxygen therapy (MecROX): An observational study protocol for mechanistic evaluation

Background MecROX is a mechanistic sub-study of the UK-ROX trial which was designed to evaluate the clinical and cost-effectiveness of a conservative approach to oxygen therapy for invasively ventilated adults in intensive care. This is based on the scientific rationale that excess oxygen is harmful. Epithelial cell damage with alveolar surfactant deficiency is characteristic of hyperoxic acute lung injury. Additionally, hyperoxaemia (excess blood oxygen levels) may exacerbate whole-body oxidative stress leading to cell death, autophagy, mitochondrial dysfunction, bioenergetic failure and multi-organ failure resulting in poor clinical outcomes. However, there is a lack of in-vivo human models evaluating the mechanisms that underpin oxygen-induced organ damage in mechanically ventilated patients. Aim The aim of the MecROX mechanistic sub-study is to assess lung surfactant composition and global systemic redox status to provide a mechanistic and complementary scientific rationale to the UK-ROX trial findings. The objectives are to quantify in-vivo surfactant composition, synthesis, and metabolism with markers of oxidative stress and systemic redox disequilibrium (as evidenced by alterations in the ‘reactive species interactome’) to differentiate between groups of conservative and usual oxygen targets. Methods and design After randomisation into the UK-ROX trial, 100 adult participants (50 in the conservative and 50 in usual care group) will be recruited at two trial sites. Blood and endotracheal samples will be taken at 0, 48 and 72 hours following an infusion of 3 mg/kg methyl-D9-choline chloride. This is a non-radioactive, stable isotope of choline (vitamin), which has been extensively used to study surfactant phospholipid kinetics in humans. This study will mechanistically evaluate the in-vivo surfactant synthesis and breakdown (by hydrolysis and oxidation), oxidative stress and redox disequilibrium from sequential plasma and bronchial samples using an array of analytical platforms. We will compare conservative and usual oxygenation groups according to the amount of oxygen administered. Trial registration: ISRCTN ISRCTN61929838, 27/03/2023 https://doi.org/10.1186/ISRCTN61929838.

A Bioinspired Flexible Sensor for Electrochemical Probing of Dynamic Redox Disequilibrium in Cancer Cells.

Malignant tumors pose a serious risk to human health. Ascorbic acid (AA) has potential for tumor therapy; however, the mechanism underlying the ability of AA to selectively kill tumor cells remains unclear. AA can cause redox disequilibrium in tumor cells, resulting in the release of abundant reactive oxygen species, represented by hydrogen peroxide (H2 O2 ). Therefore, the detection of H2 O2 changes can provide insight into the selective killing mechanism of AA against tumor cells. In this work, inspired by the ion-exchange mechanism in coral formation, a flexible H2 O2 sensor (PtNFs/CoPi@CC) is constructed to monitor the dynamics of H2 O2 in the cell microenvironment, which exhibits excellent sensitivity and spatiotemporal resolution. Moreover, the findings suggest that dehydroascorbic acid (DHA), the oxidation product of AA, is highly possible the substance that actually acts on tumor cells in AA therapy. Additionally, the intracellular redox disequilibrium and H2 O2 release caused by DHA are positively correlated with the abundance and activity of glucose transporter 1 (GLUT1). In conclusion, this work has revealed the potential mechanism underlying the ability of AA to selectively kill tumor cells through the construction and use of PtNFs/CoPi@CC. The findings provide new insights into the clinical application of AA.

The Chains of Ferroptosis Interact in the Whole Progression of Atherosclerosis.

Atherosclerosis (AS), a category of cardiovascular disease (CVD) that can cause other more severe disabilities, increasingly jeopardizes human health. Owing to its imperceptible and chronic symptoms, it is hard to determine the pathogenesis and precise therapeutics for AS. A novel type of programmed cell death called ferroptosis was discovered in recent years that is distinctively different from other traditional cell death pathways in morphological and biochemical aspects. Characterized by iron overload, redox disequilibrium, and accumulation of lipid hydroperoxides (L-OOH), ferroptosis influences endothelial cells, vascular smooth muscle cells (VSMCs), and macrophages, as well as inflammation, partaking in the pathology of many cardiovascular diseases such as atherosclerosis, stroke, ischemia-reperfusion injury, and heart failure. The mechanisms behind ferroptosis are so sophisticated and interwoven that many molecules involved in this procedure are unknown. This review systematically depicts the initiation and modulation of ferroptosis and summarizes the contribution of ferroptosis to AS, which may open a feasible approach for target treatment in the alleviation of AS progression.

Melatonin ameliorates histone modification disorders in mammalian aged oocytes by neutralizing the alkylation of HDAC1

Aging-associated histone modification changes in oocytes have been sporadically reported, but the underlying mechanisms remain elusive. Here, we systematically characterize multiple histone modifications in oocytes during aging. We find that maternal and postovulatory aging markedly alter the status of histone modifications, specifically H4K12ac and H3K4me3, in both mouse and porcine oocytes. Meanwhile, we identify a substantial reduction in HDAC1 (histone deacetylase 1) protein in aged oocytes, which contributes to the changes in H4K12ac and H3K4me3. Moreover, by employing methylglyoxal (MG) and site-directed mutagenesis, we demonstrate that the elevated reactive carbonyl species (RCS) level induces HDAC1 degradation, likely through attacking the cysteine residues, thereby influences histone modification state. Importantly, supplementation of melatonin not only prevents the loss of HDAC1 protein, but also partially corrects the H4K12ac and H3K4me3 status in aged oocytes. To sum up, this study established the link between redox disequilibrium and histone modification alterations during mammalian oocyte aging.

Oxidoreductases and metal cofactors in the functioning of the earth.

Life sustains itself using energy generated by thermodynamic disequilibria, commonly existing as redox disequilibria. Metals are significant players in controlling redox reactions, as they are essential components of the engine that life uses to tap into the thermodynamic disequilibria necessary for metabolism. The number of proteins that evolved to catalyze redox reactions is extraordinary, as is the diversification level of metal cofactors and catalytic domain structures involved. Notwithstanding the importance of the topic, the relationship between metals and the redox reactions they are involved in has been poorly explored. This work reviews the structure and function of different prokaryotic organometallic-protein complexes, highlighting their pivotal role in controlling biogeochemistry. We focus on a specific subset of metal-containing oxidoreductases (EC1 or EC7.1), which are directly involved in biogeochemical cycles, i.e., at least one substrate or product is a small inorganic molecule that is or can be exchanged with the environment. Based on these inclusion criteria, we select and report 59 metalloenzymes, describing the organometallic structure of their active sites, the redox reactions in which they are involved, and their biogeochemical roles.

Constraining Alteration Processes Along the Siccar Point Group Unconformity, Gale Crater, Mars: Results From the Sample Analysis at Mars Instrument

AbstractResults from the Sample Analysis at Mars‐evolved gas analyzer on board the Mars Science Laboratory Curiosity rover constrained the alteration history and habitability potential of rocks sampled across the Siccar Point unconformity in Gale crater. The Glasgow member (Gm) mudstone just below the unconformity had evidence of acid sulfate or Si‐poor brine alteration of Fe‐smectite to Fe amorphous phases, leaching loss of Fe‐Mg‐sulfate and exchange of unfractionated sulfur 34S (δ34S = 2‰ ± 7‰) with enriched 34S (20‰ ± 5‰, Vienna Cañon Diablo Troilite). Carbon abundances did not significantly change (322–661 μgC/g) consistent with carbon stabilization by amorphous Al‐ and Fe‐hydroxide phases. The Gm mudstone had no detectable oxychlorine and extremely low nitrate. Nitrate (0.06 wt.% NO3), oxychlorine (0.13 wt.% ClO4), high C (1,472 μg C/g), and low Fe/Mg‐sulfate concentration (0.24 wt.% SO3) depleted in 34S (δ34S = −27‰ ± 7), were detected in the Stimson formation (Sf) eolian sandstone above the unconformity. Redox disequilibrium through the detections of iron sulfide and sulfate supported limited aqueous processes in the Sf sandstone. Si‐poor brines or acidic fluids altered the Gm mudstone just below the unconformity but did not alter underlying Gm mudstones further from the contact. Chemical differences between the Sf and Gm rocks suggested that fluid interaction was minimal between the Sf and Gm rocks. These results suggested that the Gm rocks were altered by subsurface fluids after the Sf placement. Aqueous processes along the unconformity could have provided habitable conditions and in some cases, C and N levels could have supported heterotrophic microbial populations.

A Connection Between DNA Repair Protein APE1, Alpha‐Synucleinopathy, and Biological Sex in Rodents and Humans

Lewy body disorders are characterized by proteostatic and redox disequilibrium, leading to deposition of α‐synuclein in hallmark inclusions and oxidative damage to DNA. One common pathway for repair of oxidative DNA damage is base excision repair (BER), which involves the coordinated activity of several enzymes, including apurinic/apyrimidinic endonuclease 1 (APE1). The main goal of this study was to assess APE1 in rodents and humans with α‐synucleinopathy, and to test the functional impact of APE1 in the preformed α‐synuclein fibril model. First, we report that knockdown of APE1 with two independent shRNA sequences or inhibition of APE1 DNA repair activity increased inclusions bearing pathologically‐phosphorylated α‐synuclein (pSer129) in preformed fibril‐treated primary hippocampal cultures. Second, we examined APE1 expression in a mouse model of limbic‐centered α‐synucleinopathy, in which α‐synuclein fibrils are infused into the olfactory bulb/anterior olfactory nucleus (OB/AON). Six months later, we observed a fibril‐induced decrease in APE1 expression in the brains of male mice and an increase in females.Similar sex‐opposing patterns were noted for APE1 mRNA expression. Third, we demonstrated that the loss of APE1 in fibril‐infused male mice in vivo is mediated by oxidative stress, as APE1 loss was abolished by dietary administration of the antioxidant N‐acetylcysteine. Fourth, OB/AON tissues harvested from fibril‐infused male mice displayed higher cleavage of synthetic DNA lesions on a biochip than tissues collected in parallel from fibril‐infused female mice. However, OB/AON tissues harvested from fibril‐infused female mice had higher DNA repair activity compared to males. Assessments of open field activity measures and sucrose preference revealed a negative behavioral impact of α‐synuclein fibril infusions in male but not female mice. Fifth, men with Lewy body disorders displayed lower APE1 expression in the OB and amygdala compared to women with Lewy body disorders, similar to fibril‐infused mice. Finally, we infused α‐synuclein fibrils into the OB/AON of transgenic APE1 overexpressing rats and observed a reduction in pSer129 levels in male and female brains compared to fibril‐infused wildtype rats. Preliminary data suggest that APE1 overexpression in fibril‐infused rats improved olfaction and anxiety measures, especially in males. These findings reveal a sex‐biased impact of limbic α‐synucleinopathy on APE1 expression and function but also suggest that APE1 overexpression attenuates α‐synucleinopathy in both sexes.

The case and context for atmospheric methane as an exoplanet biosignature

Methane has been proposed as an exoplanet biosignature. Imminent observations with the James Webb Space Telescope may enable methane detections on potentially habitable exoplanets, so it is essential to assess in what planetary contexts methane is a compelling biosignature. Methane’s short photochemical lifetime in terrestrial planet atmospheres implies that abundant methane requires large replenishment fluxes. While methane can be produced by a variety of abiotic mechanisms such as outgassing, serpentinizing reactions, and impacts, we argue that—in contrast to an Earth-like biosphere—known abiotic processes cannot easily generate atmospheres rich in CH4 and CO2 with limited CO due to the strong redox disequilibrium between CH4 and CO2. Methane is thus more likely to be biogenic for planets with 1) a terrestrial bulk density, high mean-molecular-weight and anoxic atmosphere, and an old host star; 2) an abundance of CH4 that implies surface fluxes exceeding what could be supplied by abiotic processes; and 3) atmospheric CO2 with comparatively little CO.

Aqueous electrochemistry: The toolbox for life's emergence from redox disequilibria

AbstractThe second law of thermodynamics leaves no doubt that life on planet Earth and its inherent substantial decrease in entropy is fundamentally based on mechanisms converting environmental free energy into the spatial and temporal order of metabolic processes. This argument holds for present life as much as it does for its very beginnings some 4 billion years ago. In this contribution, we try to strip down free energy conversion in extant life (known as “bioenergetics” to the biologists) to its basic principles with the aim to potentially retrodict the nature of the pre‐biotic precursor which drove life into existence. We demonstrate that these basic principles are deeply rooted in aqueous electrochemistry and strongly rely on inorganic redox compounds. The question of life's emergence, generally considered to fall into the realm of organic chemistry, should therefore rather be recognized as an electrochemical problem and its ultimate elucidation will need to strongly implicate the community of electrochemical scientists.

Hydrothermal Exploration of the Southern Chile Rise: Sediment‐Hosted Venting at the Chile Triple Junction

AbstractWe report results from a hydrothermal plume survey along the southernmost Chile Rise from the Guamblin Fracture Zone to the Chile Triple Junction (CTJ) encompassing two segments (93 km cumulative length) of intermediate spreading‐rate mid‐ocean ridge axis. Our approach used in situ water column sensing (CTD, optical clarity, redox disequilibrium) coupled with sampling for shipboard and shore based geochemical analyses (δ3He, CH4, total dissolvable iron (TDFe) and manganese, (TDMn)) to explore for evidence of seafloor hydrothermal venting. Across the entire survey, the only location at which evidence for submarine venting was detected was at the southernmost limit to the survey. There, the source of a dispersing hydrothermal plume was located at 46°16.5’S, 75°47.9’W, coincident with the CTJ itself. The plume exhibits anomalies in both δ3He and dissolved CH4 but no enrichments in TDFe or TDMn beyond what can be attributed to resuspension of sediments covering the seafloor where the ridge intersects the Chile margin. These results are indicative of sediment‐hosted venting at the CTJ.

The molecular mechanisms of ferroptosis and its role in cardiovascular disease.

Ferroptosis is a programmed iron-dependent cell death characterized by accumulation of lipid peroxides (LOOH) and redox disequilibrium. Ferroptosis shows unique characteristics in biology, chemistry, and gene levels, compared to other cell death forms. The metabolic disorder of intracellular LOOH catalyzed by iron causes the inactivity of GPX4, disrupts the redox balance, and triggers cell death. Metabolism of amino acid, iron, and lipid, including associated pathways, is considered as a specific hallmark of ferroptosis. Epidemiological studies and animal experiments have shown that ferroptosis plays an important character in the pathophysiology of cardiovascular disease such as atherosclerosis, myocardial infarction (MI), ischemia/reperfusion (I/R), heart failure (HF), cardiac hypertrophy, cardiomyopathy, and abdominal aortic aneurysm (AAA). This review systematically summarized the latest research progress on the mechanisms of ferroptosis. Then we report the contribution of ferroptosis in cardiovascular diseases. Finally, we discuss and analyze the therapeutic approaches targeting for ferroptosis associated with cardiovascular diseases.

Tolerance to NADH/NAD+ imbalance anticipates aging and anti-aging interventions

SummaryRedox couples coordinate cellular function, but the consequences of their imbalances are unclear. This is somewhat associated with the limitations of their experimental quantification. Here we circumvent these difficulties by presenting an approach that characterizes fitness-based tolerance profiles to redox couple imbalances using an in silico representation of metabolism. Focusing on the NADH/NAD+ redox couple in yeast, we demonstrate that reductive disequilibria generate metabolic syndromes comparable to those observed in cancer cells. The tolerance of yeast mutants to redox disequilibrium can also explain 30% of the variability in their experimentally measured chronological lifespan. Moreover, by predicting the significance of some metabolites to help stand imbalances, we correctly identify nutrients underlying mechanisms of pathology, lifespan-protecting molecules, or caloric restriction mimetics. Tolerance to redox imbalances becomes, in this way, a sound framework to recognize properties of the aging phenotype while providing a consistent biological rationale to assess anti-aging interventions.

Forward geochemical modeling as a guiding tool during exploration of Sea Cliff hydrothermal field, Gorda Ridge

Maximizing scientific return is critical to the success of space exploration. During the SUBSEA project, which explored the Sea Cliff vent site aboard the E/V Nautilus as an analog for hydrothermal systems on Ocean Worlds, we used forward geochemical modeling to guide decision-making during the process of exploration. Before the expedition, we performed 1670 reaction-path calculations to simulate water-rock interactions during hydrothermal circulation covering wide ranges of reaction conditions to predict the diversity of possible chemical compositions and energy available for chemosynthetic microorganisms at the Sea Cliff vents. Calculation of the information entropy of predicted concentrations of major solutes and pH allowed us to identify dissolved silica as the chemical species capable of yielding the most information about reaction conditions; as such, the measurement of this parameter was implemented aboard ship for our field program. Using telepresence, results of onboard chemical analyses of fluid samples collected during seafloor Dive n were sent to our shore-based scientific team, who processed the data and used the outcomes to inform the design of Dive n ​+ ​2. Combining data processing with forward modeling revealed, within just two dives, that all the observed fluids venting from 10 °C to 300 ​°C most likely resulted from simple conservative mixing between seawater and a common hydrothermal fluid end-member: the result of reaction of seawater with basalt at ≥350 ​°C. Identification of these reaction conditions early within the cruise allowed additional calculations to be performed to quantify the energy available from redox disequilibria as a function of vent-fluid temperatures as they exited the seafloor. These calculations can help inform and optimize real-time microbiological sampling and culture experiments onboard the ship during field expeditions. The success of our approach coupling forward modeling and onboard ship analyses allowed improved efficiency in completing process studies at the Sea Cliff vent site, providing time for further exploration and sampling of a newly discovered vent site: Apollo. This study demonstrates a novel application of forward and real-time modeling for scientific exploration that allows the time required for result-informed decision making to be reduced from years to hours – an essential breakthrough for future space exploration missions.

Hydrogeochemical Study on Closed-Basin Lakes in Cold and Semi-Arid Climates of the Valley of the Gobi Lakes, Mongolia: Implications for Hydrology and Water Chemistry of Paleolakes on Mars

Previous studies suggested that, generally, the climate of early Mars would have been semi-arid when the surface temperatures were above freezing. On early Mars, closed-basin lakes would have been created; however, the hydrogeochemical cycles of the lake systems are poorly constrained. Here we report results of our field surveys to terrestrial analogs of closed-basin lake systems that developed in cold and semi-arid climates: The Valley of the Gobi Lakes of Mongolia. Our results show that groundwater plays a central role not only in hydrology, but also in geochemical cycles in the lake systems. We find that groundwater predominantly flows into the lakes through local seepage and regional flows in semi-arid climates. Through the interactions with calcite-containing soils, local groundwater seepage provides Ca2+ and HCO3− to the lakes. In the wetland located in between the lakes, high-salinity shallow pools would provide Cl− and Na+ to the groundwater through infiltration. If similar processes occurred on early Mars, local seepage of groundwater would have provided magnesium and alkalinity to the early Jezero lakes, possibly leading to authigenic precipitation of lacustrine carbonates. On early Mars, infiltration of surface brine may have transported salts and oxidants on the surface to lakes via regional groundwater flows. We suggest that inflows of multiple types of groundwater in semi-arid climates could have caused redox disequilibria in closed-basin lakes on early Mars.

Suppressing the Radiation-Induced Corrosion of Bismuth Nanoparticles for Enhanced Synergistic Cancer Radiophototherapy.

The level of tumor killing by bismuth nanoparticles (BiNPs) as radiosensitizers depends strongly on the powerful particle-matter interaction. However, this same radiation leads to the structural damage in BiNPs, consequently weakening their specific physicochemical properties for radiosensitization. Herein, we studied the radiation-induced corrosion behavior of BiNPs and demonstrated that these damages were manifested by the change in their morphology and crystal structure as well as self-oxidation at their surface. Furthermore, artificial heterostructures were created with graphene nanosheets to greatly suppress the radiation-induced corrosion in BiNPs and enhance their radiocatalytic activity for radiotherapy enhancement. Such a nanocomposite allows the accumulation of overexpressed glutathione, a natural hole scavenger, at the reaction interfaces. This enables the rapid removal of radiogenerated holes from the surface of BiNPs and minimizes the self-radiooxidation, therefore resulting in an efficient suppression of radiation corrosion and a decrease of the depletion of reactive oxygen species (ROS). Meanwhile, the radioexcited conduction band electrons react with the high-level H2O2 within cancer cells to yield more ROS, and the secondary electrons are trapped by H2O molecules to produce hydrated electrons capable of reducing a highly oxidized species such as cytochrome c. These radiochemical reactions together with hyperthermia can regulate the tumor microenvironment and accelerate the onset of cellular redox disequilibrium, mitochondrial dysfunction, and DNA damage, finally triggering tumor apoptosis and death. The current work will shed light on radiosensitizers with an enhanced corrosion resistance for controllable and synergistic radio-phototherapeutics.

Trace metals geochemistry for health assessment coupled with adsorption remediation method for the groundwater of Lorong Serai 4, Hulu Langat, west coast of Peninsular Malaysia.

The research study was carried out to evaluate trace metals (Pb, Cd, Se, Al, Mn, Cu, Zn, Fe, As, Ni, Cr, and Ag) concentrations in groundwater of Lorong Serai 4, Hulu Langat, Selangor, Malaysia. Additionally, the research study focused on determining non-carcinogenic and carcinogenic health risks, sources of the contaminants, and effective remediation methods. The results show that the concentration levels of Pb, Cd, Se, Al, Cu, Zn, Ni, Cr, and Ag are lower than their corresponding permissible limits, while Fe, Mn, and As concentrations exceed their acceptable limit. The hazard index of the groundwater in the area exceeded the acceptable limit, showing the rate of carcinogenic and non-carcinogenic health effects associated with the water. The findings also indicate that the lifetime cancer risk is high compared to the maximum limits of lifetime cancer risk from the drinking water (10-6 to 10-4). The groundwater geochemical data of the area are used in establishing the source of Fe, Mn, and As metal ions. Evaluation of Fe2+/Fe3+ and S2-/SO42- redox couples and thermodynamic modelling indicates that the groundwater of the area is in redox disequilibrium. The groundwater samples contain aqueous iron sulphate, which is supersaturated, ferrous carbonate and aluminium sulphate that are saturated. The main state of redox disequilibrium is governed by mineral precipitation and dissolution. Aqueous arsenic and manganese are possibly derived from the dissolution of pyrite (arsenopyrite) and amorphous oxide-hydroxides, respectively. The high concentration of iron in the shallow groundwater in the area is primarily the result of silicate rock weathering of ferroan igneous and metamorphic minerals with a minor contribution from the oxidation of iron sulphides. Magnetite coated with graphene oxide (Fe3O4-GO) nanoparticles (NPs) was synthesized and characterized, and the adsorption preliminary experiments were carried out; and the Fe3O4-GO NPs show enhanced removal (Fe > As > Mn) capacity over graphene oxide (GO).

Oxidative Imbalance and Kidney Damage: New Study Perspectives from Animal Models to Hospitalized Patients.

Chronic kidney disease (CKD) is a major public health problem worldwide and affects both elderly and young subjects. Its main consequences include the loss of renal function, leading to end-stage renal disease, an increased risk of cardiovascular disease, a significant increase in morbidity and mortality, and a decrease in health-related quality of life. This review arose in significant part from work in the authors’ laboratory, complemented by literature data, and was based on a translational approach: we studied the role of many CKD risk factors, such as hypertension, obesity, and oxidative stress/inflammation. The aim was to identify new molecular mechanisms of kidney damage to prevent it through successful behavior modifications. For this purpose, in our studies, both human and animal models were used. In the animal models, we analyzed the mechanisms of renal damage induced by hypertension (spontaneously hypertensive rats) and obesity (cafeteria diet-fed rats), showing that redox disequilibrium in plasma and tissue is extremely important in renal alteration in terms of both oxidative damage (lipid peroxidation, altered expression antioxidant enzymes) and apoptotic pathway (intrinsic/extrinsic) activation. In hemodialysis patients, we explored the correlation between the global oxidative balance and both inflammatory markers and cardiovascular risk, showing a strong correlation between the oxidative index and the blood levels of C-reactive protein and previous cardiovascular events. This multilevel approach allowed us to individually and synergistically analyze some aspects of the complex pathogenic mechanisms of CKD in order to clarify the role of the new amplified risk factors for CKD and to prepare an effective personalized prevention plan by acting on both modifiable and nonmodifiable risk factors.