Redox-sensitive Processes Research Articles

Redox regulation of chromatin remodelling in plants.

Changes in the cellular redox balance that occur during plant responses to unfavourable environmental conditions significantly affect a myriad of redox-sensitive processes, including those that impact on the epigenetic state of the chromatin. Various epigenetic factors, like histone modifying enzymes, chromatin remodelers, and DNA methyltransferases can be targeted by oxidative posttranslational modifications. As their combined action affects the epigenetic regulation of gene expression, they form an integral part of plant responses to (a)biotic stress. Epigenetic changes triggered by unfavourable environmental conditions are intrinsically linked with primary metabolism that supplies intermediates and donors, such acetyl-CoA and S-adenosyl-methionine, that are critical for the epigenetic decoration of histones and DNA. Here, we review the recent advances in our understanding of redox regulation of chromatin remodelling, dynamics of epigenetic marks, and the interplay between epigenetic control of gene expression, redox signalling and primary metabolism within an (a)biotic stress context.

The effect of rice residue management on rice paddy Si, Fe, As, and methane biogeochemistry

Rice production results in residues of straw and husk, and the management of these residues has implications for the sustainability of the rice agroecosystem. Rice straw is typically incorporated into soil either as fresh residue or is burned prior to incorporation. Rice husk is not typically returned to rice fields. However, rice husk contains high levels of silicon, which has been shown to decrease rice accumulation of arsenic. In this work, we studied the resulting biogeochemical changes in rice paddy soils when paddies were amended with either straw or burned straw and either no husk, husk, or burned husk over two years. Using a full-factorial design, we observed that the higher lability of rice straw carbon controlled redox-sensitive processes despite the application of husk and straw at similar carbon rates. Amending paddies with straw, rather than burned straw, increased porewater Fe and As, plant As, and methane emissions regardless of husk amendment. Husk addition provided insignificant Si to the plant despite its high concentration of Si, suggesting limited short-term mobility of Si and that long-term additions of husk or higher rates may need to be studied.

A reversible mitochondrial complex I thiol switch mediates hypoxic avoidance behavior in C. elegans

C. elegans react to metabolic distress caused by mismatches in oxygen and energy status via distinct behavioral responses. At the molecular level, these responses are coordinated by under-characterized, redox-sensitive processes, thought to initiate in mitochondria. Complex I of the electron transport chain is a major site of reactive oxygen species (ROS) production and is canonically associated with oxidative damage following hypoxic exposure. Here, we use a combination of optogenetics and CRISPR/Cas9-mediated genome editing to exert spatiotemporal control over ROS production. We demonstrate a photo-locomotory remodeling of avoidance behavior by local ROS production due to the reversible oxidation of a single thiol on the complex I subunit NDUF-2.1. Reversible thiol oxidation at this site is necessary and sufficient for the behavioral response to hypoxia, does not respond to ROS produced at more distal sites, and protects against lethal hypoxic exposure. Molecular modeling suggests that oxidation at this thiol residue alters the ability for NDUF-2.1 to coordinate electron transfer to coenzyme Q by destabilizing the Q-binding pocket, causing decreased complex I activity. Overall, site-specific ROS production regulates behavioral responses and these findings provide a mechanistic target to suppress the detrimental effects of hypoxia.

Arsenic fate in upper Indus river basin (UIRB) aquifers: Controls of hydrochemical processes, provenances and water-aquifer matrix interaction

Major river basins of the Himalayas contain a significant amount of arsenic (As) in the geological matrix, which tends to contaminate the groundwater at a local and regional scale. Although As enrichment in Quaternary deposits has been linked to primary provenances (Himalayan orogeny), limited studies have reported As enrichment in bedrock aquifers. In the present study, the hard rock and groundwater samples were collected across the upper Indus river basin (UIRB), Ladakh to assess the hydrogeochemical processes and environments responsible for As mobilization and release. The higher As concentrations were found in Khardung volcanics followed by Ophiolitic melange, Dras volcanics, Nindam sandstone, and Nindam Shale. The variability in As concentration among different rock samples is largely governed by the presence of felsic minerals and the type of magmatic setting. The groundwater is less mineralized, with moderate electrical conductivity (EC), and weakly acidic to alkaline in nature. The results indicated that mineral weathering, dissolution, and active cation exchange reactions have a strong influence on the major ion chemistry of the groundwater. Redox-sensitive processes are influencing the As mobilization and release under reducing environmental conditions. As in groundwater poses a serious threat to human health hence awareness is urgent towards achieving sustainable As mitigation globally. The study provided a significant dataset to better understand the processes and environmental conditions responsible for hydrogeochemical evolution, sources of solutes, and As mobilization and release in groundwater which will help in sustainable water resource management policies and ecosystem restoration across the Himalayas.

Dominant geochemical reactions and hazardous metal contamination status in the Kabul’s aquifers, Afghanistan

Water is an essential resource for all people, particularly those who live in arid areas, such as Kabul city, Afghanistan. In last decade, development of academic communities and contribution from international organizations have provided opportunities for researchers to address the environmental issues, including problems related to drinking water in Kabul city. Although most of these researches focused on the capital, due to shortage of financial support for water quality studies as well as security concerns, there are in fact very limited publications in that area of interest. Based on an extensive literature search and comprehensive review, four major processes have been identified as controlling factors for water quality in the studied area, which include mineral weathering, redox-sensitive processes, role of adsorption/desorption, and effects of NO3 influx. Among these factors, the most important one was the redox-sensitive processes that have considerable impacts on the chemical composition of water reserves in the Kabul area. Even though there are significant inputs of domestic sewage that released protons into the aquifers, the presence of carbonates with a great buffering capacity has prevented the dissolution of most pH-sensitive minerals; in most cases, these minerals contain hazardous metals. In terms of metal contamination in the Kabul Basin, three metals have displayed elevated levels above the World Health Organization guidelines: uranium, arsenic, and nickel. Based on the literature review, the origin of these toxic metals has revealed, and the associated weathering reactions are presented.

Abstract MP31: Peripheral Vascular Dysfunction In A Model Of Small Vessel Disease Of The Brain (CADASIL) Involves Impaired Redox-sensitive Cyclic GMP/PKG Signaling

CADASIL, a monogenic condition due to Notch3 mutations, is a very aggressive small vessel disease of the brain resulting in premature vascular dementia and stroke. Changes in cerebral vessels include vascular dysfunction and narrowing, and accumulation of granular osmiophilic material (GOM). It is not clear whether small peripheral arteries undergo similar damage. Therefore, our aim is to assess vascular dysfunction and associated mechanisms in mesenteric resistance arteries from CADASIL mice. Mesenteric arteries (MA) from male CADASIL-causing Notch3 mutation (TgNotch3 R169C ) and wildtype (TgNotch3 WT ) mice (6 months old) were investigated. GOM deposits in MA from CADASIL mice were identified by electron microscopy. mRNA expression of Notch3 (WT: 2.0±0.5 vs. 6.0±1.3) and its downstream target HeyL (WT: 1.1±0.4 vs. 2.9±0.6) was augmented in CADASIL mice (p<0.01), suggesting increased Notch3 activation. CADASIL mice exhibited endothelial-dependent (Emax 109.9±7.4 vs. 81.3±5.4) and -independent dysfunction (pD 2 7.8±0.1 vs. 6.8±0.3); effects associated with increased eNOS inhibition (p-Thr 495 ) (1.8-fold increase) and decreased cGMP levels (1.2±0.2 vs. 0.59±0.2) (p<0.05). Plasma lipid peroxidation (0.8±0.1 vs. 2.0±0.3; p<0.05) and vascular reactive oxygen species (ROS) production (7.2±1.9 vs. 75.4±35.0; p<0.05) were increased in TgNotch3 R169C mice; processes associated with upregulation of soluble guanylate cyclase (sGC) oxidation and decreased sGC activity. H 2 O 2 levels were decreased in TgNotch3 R169C mice (1.9±0.2 vs. 1.1±1.9; p<0.05), which was associated with reduced activation of protein kinase G (PKG). Observations in TgNotch3 R169C mice were recapitulated in human CADASIL, where ROS levels (0.8±0.1 vs. 4.1±2.7; p<0.05) and sGC oxidation were also increased. Our findings demonstrate that the vasculopathy associated with a CADASIL Notch3 gain-of-function mutation in peripheral small vessels involves reduction in eNOS activation and redox-sensitive processes leading to impaired sGC/cGMP signalling pathway. We identify a potential new therapeutic target in CADASIL, for which there are no disease-specific treatments.

Tin stable isotopes in magmatic-affected coal deposits: Insights in the geochemical behavior of tin

Tin (Sn) is a redox-sensitive element and geochemically incompatible that accumulates in evolved magmas and associated hydrothermal fluids. Here, a Sn stable isotope approach is used to characterize sources and geochemical behaviors of Sn in magmatic intruded coal deposits by combining with petrographic and elemental analysis. Sn isotope ratios of twelve coal samples with various magmatic-affected degrees show a δ120/118Sn variation from −0.06 to 0.22‰ (2σ of 0.07‰, relative to NIST 3161a). Basing on Sn isotope data and geochemical characteristics of the samples, we suggest binary source mixing and redox state related isotope shift as two mechanisms accounting for the isotope variations. The first mechanism is an admixture of magmatic-hydrothermal fluids, characterized by high δ120/118Sn, into coal deposits with low δ120/118Sn. A binary mixing model is used to estimate Sn contributions of the two end-members. The second process results in a positive isotope shift caused by an oxidation of sample states when they are affected by magmatic intrusions. In fact, magmatic intrusions could trigger the oxidation of Sn, resulting in heavy Sn isotope enrichment in the magmatic affected samples. The change in coal redox-state is supported by a concomitant change of redox proxies, such as V/(V + Ni), Mn/Cr and V/Cr. The enrichment of heavy Sn isotopes in samples impacted by magmatic hydrothermal fluids compared to normally-deposited coals could be explained by the conversion of dominant Sn species from Sn (II)–S to Sn (IV)–O under the influence of oxidative magma, which favors the enrichment of heavier Sn isotopes in Sn (IV)–O due to its shorter bond length. This study shows that Sn isotope ratios are useful tools for investigating Sn geochemical behavior in different Earth reservoirs and during redox sensitive processes.

The Redox Theory of Development.

Significance: The geological record shows that as atmospheric O2 levels increased, it concomitantly coincided with the evolution of metazoans. More complex, higher organisms contain a more cysteine-rich proteome, potentially as a means to regulate homeostatic responses in a more O2-rich environment. Regulation of redox-sensitive processes to control development is likely to be evolutionarily conserved. Recent Advances: During early embryonic development, the conceptus is exposed to varying levels of O2. Oxygen and redox-sensitive elements can be regulated to promote normal development, defined as changes to cellular mass, morphology, biochemistry, and function, suggesting that O2 is a developmental morphogen. During periods of O2 fluctuation, embryos are "reprogrammed," on the genomic and metabolic levels. Reprogramming imparts changes to particular redox couples (nodes) that would support specific post-translational modifications (PTMs), targeting the cysteine proteome to regulate protein function and development. Critical Issues: Major developmental events such as stem cell expansion, proliferation, differentiation, migration, and cell fate decisions are controlled through oxidative PTMs of cysteine-based redox nodes. As such, timely coordinated redox regulation of these events yields normal developmental outcomes and viable species reproduction. Disruption of normal redox signaling can produce adverse developmental outcomes. Future Directions: Furthering our understanding of the redox-sensitive processes/pathways, the nature of the regulatory PTMs involved in development and periods of activation/sensitivity to specific developmental pathways would greatly support the theory of redox regulation of development, and would also provide rationale and direction to more fully comprehend poor developmental outcomes, such as dysmorphogenesis, functional deficits, and preterm embryonic death.

The Proteomic Landscape of Cysteine Oxidation That Underpins Retinoic Acid-Induced Neuronal Differentiation.

The initial phases of neuronal differentiation are key to neuronal function. A particularly informative model to study these initial phases are retinoic acid-stimulated SH-SY5Y cells. Although these progressions are associated with redox-sensitive processes, it is largely undefined how the cellular proteome underpins redox dynamics and the management of reactive oxygen species. Here, we map the global cysteine-based redox landscape of SH-SY5Y cells using quantitative redox proteomics. We find evidence that redox alterations occurred early in differentiation and affect the expression of neuronal marker proteins and the extension of neurites. The spatiotemporal analysis of reactive oxygen species suggests a NOX2-dependent peak in cytoplasmic superoxide anions/hydrogen peroxide generation 2 h after retinoic acid stimulation. At the same time point, 241 out of 275 proteins with an altered cysteine redox state are reversibly oxidized in response to retinoic acid. Our analyses pinpoint redox alterations of proteins involved in the retinoic acid homeostasis and cytoskeletal dynamics.

Field and Laboratory Studies Linking Hydrologic, Geochemical, and Microbiological Processes and Enhanced Denitrification during Infiltration for Managed Recharge.

We present linked field and laboratory studies investigating controls on enhanced nitrate processing during infiltration for managed aquifer recharge. We examine how carbon-rich permeable reactive barriers (PRBs) made of woodchips or biochar, placed in the path of infiltrating water, stimulate microbial denitrification. In field studies with infiltration of 0.2-0.3 m/day and initial nitrate concentrations of [NO3-N] = 20-28 mg/L, we observed that woodchips promoted 37 ± 6.6% nitrate removal (primarily via denitrification), and biochar promoted 33 ± 12% nitrate removal (likely via denitrification and physical absorption effects). In contrast, unamended soil at the same site generated <5% denitrification. We find that the presence of a carbon-rich PRB has a modest effect on the underlying soil microbial community structure in these experiments, indicating that existing consortia have the capability to carry out denitrification given favorable conditions. In laboratory studies using intact cores from the same site, we extend the results to quantify how infiltration rate influences denitrification, with and without a carbon-rich PRB. We find that the influence of both PRB materials is diminished at higher infiltration rates (>0.7 m/day) but can still result in denitrification. These results demonstrate a quantitative relationship between infiltration rate and denitrification that depends on the presence and nature of a PRB. Combined results from these field and laboratory experiments, with complementary studies of denitrification during infiltration through other soils, suggest a framework for understanding linked hydrologic and chemical controls on microbial denitrification (and potentially other redox-sensitive processes) that could improve water quality during managed recharge.

Economic phosphorite from the Ediacaran Doushantuo Formation, South China, and the Neoproterozoic-Cambrian Phosphogenic Event

Phosphorite of the Ediacaran Doushantuo Formation accumulated in the central Guizhou province during the Neoproterozoic-Cambrian Phosphogenic Event, producing the first true phosphorite giant in Earth history. Deposition is interpreted to have occurred on a wave-dominated epeiric platform along the northern margin of the Qianzhong Uplift. Lithofacies stacking patterns and two paleokarst surfaces record phosphogenesis through at least two sea-level cycles. As in younger Phanerozoic epeiric sea phosphorites, the delivery of upwelled phosphorus is interpreted to have stimulated phosphogenesis in a range of shallow-water environments.Ten phosphatic and associated lithofacies are recognized in the Doushantuo Formation. Wavy and horizontal laminated pristine facies were the locus of phosphogenesis and reflect the authigenic precipitation of francolite in accumulating fine sediment. Granular, cross-stratified phosphorite is interpreted to have been produced through storm-wave winnowing of pristine facies and the subsequent transport, redeposition, and concentration of phosphatic peloids into economic beds. Beds with the highest concentration of phosphorus formed in shallow, wave-agitated environments around paleo-topographic highs. Paragenetic analysis suggests that secondary meteoric processes further enriched the phosphorus content (>35 wt%) of these granular beds during sea-level lowstands.Such aerially extensive, upwelling-related phosphorite contrasts Paleoproterozoic and Neoproterozoic phosphatic deposits. Throughout much the Proterozoic francolite precipitation was restricted to shallow-water, photosynthetic oxygen oases where redox sensitive phosphogenic processes were focused in the sediment. The Doushantuo Formation is interpreted to record the oxygenation of the water column and concomitant expansion of phosphogenic environments during the Neoproterozoic Oxygenation Event. This progressive ventilation of the deep ocean forever changed the biogeochemical cycling of phosphorus in the marine realm and set the stage for the deposition of phosphorite giants that punctuate the Phanerozoic stratigraphic record.

VEGFR (Vascular Endothelial Growth Factor Receptor) Inhibition Induces Cardiovascular Damage via Redox-Sensitive Processes.

Although VEGF (vascular endothelial growth factor) inhibitors (VEGFIs), are effective anticancer therapies, they cause hypertension through unknown mechanisms. We questioned whether changes in vascular redox state may be important, because VEGF signaling involves nitric oxide (NO) and reactive oxygen species. Molecular mechanisms, including NOS, NADPH oxidase (Nox)-derived reactive oxygen species, antioxidant systems, and vasoconstrictor signaling pathways, were probed in human endothelial cells and vascular smooth muscle exposed to vatalanib, a VEGFI. Vascular functional effects of VEGFI were assessed ex vivo in mouse arteries. Cardiovascular and renal in vivo effects were studied in vatalanib- or gefitinib (EGFI [epidermal growth factor inhibitor])-treated mice. In endothelial cells, vatalanib decreased eNOS (Ser1177) phosphorylation and reduced NO and H2O2 production, responses associated with increased Nox-derived O2- and ONOO- formation. Inhibition of Nox1/4 (GKT137831) or Nox1 (NoxA1ds), prevented vatalanib-induced effects. Nrf-2 (nuclear factor erythroid 2-related factor 2) nuclear translocation and expression of Nrf-2-regulated antioxidant enzymes were variably downregulated by vatalanib. In human vascular smooth muscles, VEGFI increased Nox activity and stimulated Ca2+ influx and MLC20 phosphorylation. Acetylcholine-induced vasodilatation was impaired and U46619-induced vasoconstriction was enhanced by vatalanib, effects normalized by N-acetyl-cysteine and worsened by L-NAME. In vatalanib-, but not gefitinib-treated mice vasorelaxation was reduced and media:lumen ratio of mesenteric arteries was increased with associated increased cardiovascular and renal oxidative stress, decreased Nrf-2 activity and downregulation of antioxidant genes. We demonstrate that inhibition of VEGF signaling induces vascular dysfunction through redox-sensitive processes. Our findings identify Noxs and antioxidant enzymes as novel targets underling VEGFI-induced vascular dysfunction. These molecular processes may contribute to vascular toxicity and hypertension in VEGFI-treated patients.

224 Vascular endothelial growth factor receptor inhibition induces vascular dysfunction via redox-sensitive processes

Vascular endothelial growth factor (VEGF)/VEGF receptor (VEGFR) inhibitors, used as anti-angiogenic drugs to treat cancer, induce severe hypertension. Molecular mechanisms whereby VEGF inhibitors cause hypertension are unclear, but nitric oxide...

Redox Regulation of the Superoxide Dismutases SOD3 and SOD2 in the Pulmonary Circulation.

When evaluating the role of redox-regulating signaling in pulmonary vascular diseases, it is intriguing to consider the modulation of key antioxidant enzymes like superoxide dismutase (SOD) because SOD isoforms are regulated by redox reactions, and, in turn, modulate downstream redox sensitive processes. The emerging field of redox biology is built upon understanding the regulation and consequences of tightly controlled and specific reduction-oxidation reactions that are critical for diverse cellular processes including cell signaling. Of relevance, both the site of production of specific reactive oxygen and nitrogen species and the site of the antioxidant defenses are highly compartmentalized within the cell. For example, superoxide is generated during oxidative phosphorylation in the mitochondria as well as by a number of enzymatic sources within the cytosol and at the cell membrane. In the pulmonary circulation, these sources include the mitochondrial electron transport chain, NADPH oxidases (NOX1-4, Duox1,2), nitric oxide synthases, and xanthine oxidase; this important topic has been thoroughly reviewed recently [1]. In parallel with these different cellular sites of superoxide production, the three SOD isoforms are also specifically localized to the cytosol (SOD1), mitochondria (SOD2) or extracellular compartment (SOD3). This chapter focuses on the role of redox mechanisms regulating SOD2 and SOD3, with an emphasis on these processes in the setting of pulmonary hypertension.

PS 01-14] SYNDECAN-1 IS INVOLVED IN OSTEOPROTEGERIN-INDUCED REACTIVE OXYGEN SPECIES PRODUCTION AND VASCULAR INJURY

Objective: Increased levels of osteoprotegerin (OPG), an antiosteogenic factor, is used as a biomarker of vascular dysfunction and cardiovascular risk in metabolic diseases, suggesting pleiotropic effects independent of regulation of vascular calcification. Syndecan-1 (SDC1) may be involved in OPG-induced vascular responses, as it is involved in OPG-induced inflammation. We assessed whether OPG, through SDC1 and redox sensitive processes, regulates vascular function and injury. Design and Method: Vascular reactivity of resistance vessels from WKY rats was studied by wire myography in the presence or absence of OPG (50 ng/mL) and/or synstatin (SSNT - 10–6 M - syndecan-1 inhibitor). Rat endothelial cells (EC) and vascular smooth muscle cells (VSMC) were used. Reactive oxygen species (ROS) were measured by chemiluminescence and Amplex Red. Results: Exposure of resistance arteries to OPG induced endothelial (decreased relaxation to acetylcholine) and VSMC (decreased relaxation to sodium nitroprusside - SNP) dysfunction, as well as, increased contraction to phenylephrine. All responses were blocked by SSNT. OPG-induced ROS production in VSMCs (1.5 fold increase, p < 0.05) was blocked by SDC1 signalling inhibitors such as SSNT, chondroitinase/heparinase (removal of SDC1 sulfate chains), γ-secretase inhibitor (SDC1 intracellular domain) and MMP2/MMP9 inhibitor (SDC1 extracellular domain). In ECs, OPG decreased H2O2 (0.5 fold) and NO (0.5 fold) production/release. In VSMCs, OPG increased ONOO- (0.5 fold) levels, protein oxidation (0.5 fold), Rho kinase (1.5 fold) and myosin light chain activation (1 fold) (p < 0.05) through SDC1. OPG increased mRNA levels of IL6 (2 fold), IL-1β (2 fold), MMP2 (1 fold) and MMP9 (2 fold) in vascular cells; all inhibited by SSNT. Conclusions: In conclusion, vascular dysfunction/damage elicited by OPG is mediated by syndecan-1 and ROS. Identification of syndecan-1 as the upstream effector of OPG-induced vascular injury suggests that membrane proteoglycans may be potential targets for the treatment of vascular diseases, where the protective role of OPG is preserved.

Abstract P096: Vascular Protein Oxidation and Redox Proteomics in Human Hypertension

Oxidative stress has been implicated in the pathophysiology of hypertension (HTN) through redox-sensitive processes that cause vascular damage. Despite recent advances in the field of vascular redox signalling in HTN, it still remains unclear exactly how ROS cause vascular injury. We hypothesise that regulation of redox-sensitive protein tyrosine phosphatases (PTP) through post-translational oxidative modification, is impaired in HTN where ROS levels are increased. Vascular smooth muscle cells (VSMC) from small arteries of normotensive (NT) and hypertensive (HT) individuals were stimulated with AngII (10-7 M) and ET-1 (10-7 M). Irreversible oxidation of proteins and PTPs was assessed by oxyblot and immunoblotting, respectively. Differential gel electrophoresis (DiGE) and CyDye thiol labelling were employed for screening of reversibly oxidised proteome. Irreversible protein oxidation was not affected by AngII or ET-1 in VSMCs from NT and HT subjects. PTP hyperoxidation tended to increase in VSMCs from NT upon stimulation with AngII (FC=2.12 at 60min) and ET-1 (FC=1.60 at 60min), whereas a similar trend was observed only after AngII treatment (FC=1.38 at 60min) in HTN (p&gt;0.05). Proteomic data, filtered for FC&gt;2, detected 2051 spots with 1899 (92.5%) being equally oxidised between NT and HT. In addition, oxidation of 57 (2.9%) spots was increased, while 95 (4.6%) were decreased in HT. Candidate proteins exhibiting consistent changes across three experimental replicates included β-actin (FC=-2.86), annexin A1 (-2.23), galectin-1 (-1.67), FK506 binding protein (-2.35) and polymerase I and transcript release factor (PTRF, -1.92). Stimulation with AngII altered the redox status in 2-3% of proteins, both in HT and NT. However, vimentin was the only target changing consistently across the replicates (FC=2.48). Our findings indicate that pro-hypertensive agents may not impact significantly on irreversible protein and PTP oxidation in health and disease, but may have effects on reversible oxidation. Our proteomic data, in agreement with our previous rat studies, support decreased reversible thiol oxidation in HTN. Moreover, these novel findings identify differentially oxidised proteins which may contribute to oxidative vascular injury in HTN.

Neoproterozoic peritidal phosphorite from the Sete Lagoas Formation (Brazil) and the Precambrian phosphorus cycle

AbstractThe Neoproterozoic Sete Lagoas Formation (ca 610 Ma) of the São Francisco Basin, Brazil, is a succession of siltstone, limestone and phosphorite. Phosphorite forms part of a previously unrecognized 150 to 200 m thick, unconformity bounded depositional sequence. Lithofacies stacking patterns indicate that deposition was punctuated by higher order fluctuations in base level that produced aggradational parasequences. These shallowing‐upward cycles record the progradation of phosphate‐rich intertidal flats over shallow subtidal deposits as accommodation filled. The presence of mudcracks, authigenic chert nodules, lack of coarse terrigenous clastics and the abundance of silt with fine, abraded quartz grains suggests accumulation along an arid coastline with significant aeolian input. Delivery of phosphorus adsorbed on aeolian Fe‐(oxyhydr)oxide and clay is interpreted as having stimulated phosphogenesis in peritidal environments. Lithofacies associations indicate that windblown phosphorus promoted the establishment of cyanobacterial communities along the coast, which produced photosynthetic oxygen and the suboxic conditions necessary for the precipitation of authigenic carbonate fluorapatite. As in other Precambrian phosphatic systems, nearshore oxygen oases were a prerequisite for phosphorite accumulation because redox sensitive phosphogenic processes were pushed into the sediment to concentrate phosphorus. In more distal, anoxic environments phosphorite could not form because these biotic and abiotic processes were suspended in the water column, which cycled phosphorus in sea water rather than at the sediment–water interface. Such shallow‐water phosphorite is unlike larger, younger Neoproterozoic–Phanerozoic phosphatic deposits inferred to have formed in deeper‐upwelling related environments. The increasing size of phosphatic deposits through the latest Precambrian is interpreted as reflecting the progressive ventilation of the oceans during the Neoproterozoic Oxygenation Event, and resultant expansion of phosphogenic environments into distal settings. The widespread cycling of bioavailable phosphorus at the sea floor not only produced the first true phosphorite giants, but may have also been an important precondition for the evolution of multicellular animals.

Effects of drying on phosphorus uptake in re-flooded lake sediments.

Sediment drying associated with large water level fluctuations is an increasingly common feature of temporary streams and lakes worldwide. Drying-induced sediment aeration and re-flooding periodically alter redox conditions, and therefore stimulate redox-sensitive processes influencing phosphorus (P) binding forms. We experimentally tested the effects of drying on P binding forms, and the P sorption potential, by drying and re-flooding lake sediments in the laboratory. Wet and dried fine sediments were re-flooded in columns, and the overlying water was continuously re-stocked to a constant P concentration. We measured changes in P forms, P uptake rates, and the pore water dynamics in each column over 36 weeks. Drying decreased the fraction of stable P, stimulated the mineralization of organic P, and increased the proportion of labile and reductant-soluble forms. Drying of sediment furthermore reduced its P sorption affinity and capacity by up to 32% in batch equilibrium experiments, and led to a fourfold increase in sediment compaction which increased P uptake rates by a factor of 1.7 in sediment column experiments. Compaction due to drying also induced the development of a sharp gradient below which P was mobilized. These results indicate that in fine sediments, a single drying event can result in the transformation of P components into more labile forms which accumulate in the uppermost sediment layer, therefore raising the potential for a pulsed P release under reducing conditions.

Variations in Fe3+/∑Fe of Mariana Arc Basalts and Mantle Wedge fO2

Arc basalts are more oxidized than mid-ocean ridge basalts, but it is unclear whether this difference is due to differentiation processes in the Earth’s crust or to a fundamental difference in the oxygen fugacity of their mantle sources. Distinguishing between these two hypotheses is important for understanding redox-sensitive processes related to arc magmatism, and thus more broadly how Earth materials cycle globally. We present major, volatile, and trace element concentrations in combination with Fe^(3+)/∑Fe ratios determined in olivine-hosted glass inclusions and submarine glasses from five Mariana arc volcanoes and two regions of the Mariana Trough. For single eruptions, Fe^(3+)/∑Fe ratios vary along liquid lines of descent that are either slightly oxidizing (olivine + clinopyroxene + plagioclase fractionation, CO_2 ± H_2O degassing) or reducing (olivine + clinopyroxene + plagioclase ± magnetite fractionation, CO_2 + H_2O + S degassing). Mariana samples are consistent with a global relationship between calc-alkaline affinity and both magmatic H_2O and magmatic oxygen fugacity, where wetter, higher oxygen fugacity magmas display greater affinity for calc-alkaline differentiation. We find, however, that low-pressure differentiation cannot explain the majority of variations observed in Fe^(3+)/∑Fe ratios for Mariana arc basalts, requiring primary differences in magmatic oxygen fugacity. Calculated oxygen fugacities of primary mantle melts at the pressures and temperatures of melt segregation are significantly oxidized relative to mid-ocean ridge basalts (∼QFM, where QFM is quartz–fayalite–magnetite buffer), ranging from QFM + 1·0 to QFM + 1·6 for Mariana arc basalts, whereas back-arc related samples record primary oxygen fugacities that range from QFM + 0·1 to QFM + 0·5. This Mariana arc sample suite includes a diversity of subduction influences, from lesser influence of a homogeneous H_2O-rich component in the back-arc, to sediment melt- and fluid-dominated influences along the arc. Primary melt oxygen fugacity does not correlate significantly with sediment melt contributions (e.g. Th/La), nor can it be attributed to previous melt extraction in the back-arc. Primary melt oxygen fugacity correlates strongly with indices of slab fluids (e.g. Ba/La) from the Mariana Trough through the Mariana arc, increasing by 1·5 orders of magnitude as Ba/La increases by a factor of 10 relative to mid-ocean ridge basalts. These results suggest that contributions from the slab to the mantle wedge may be responsible for the elevated oxygen fugacity recorded by Mariana arc basalts and that slab fluids are potentially very oxidized.

About the dangers, costs and benefits of living an aerobic lifestyle.

The era in which ROS (reactive oxygen species) were simply the 'bad boys of biology' is clearly over. High levels of ROS are still rightfully considered to be toxic to many cellular processes and, as such, contribute to disease conditions and cell death. However, the high toxicity of ROS is also extremely beneficial, particularly as it is used to kill invading micro-organisms during mammalian host defence. Moreover, a transient, often more localized, increase in ROS levels appears to play a major role in signal transduction processes and positively affects cell growth, development and differentiation. At the heart of all these processes are redox-regulated proteins, which use oxidation-sensitive cysteine residues to control their function and by extension the function of the pathways that they are part of. Our work has contributed to changing the view about ROS through: (i) our characterization of Hsp33 (heat-shock protein 33), one of the first redox-regulated proteins identified, whose function is specifically activated by ROS, (ii) the development of quantitative tools that reveal extensive redox-sensitive processes in bacteria and eukaryotes, and (iii) the discovery of a link between early exposure to oxidants and aging. Our future research programme aims to generate an integrated and system-wide view of the beneficial and deleterious effects of ROS with the central goal to develop more effective antioxidant strategies and more powerful antimicrobial agents.