Oxygen Fluctuations Research Articles

Simulation Tool for the Development of a Staged Combustion Pellet Stove Controller

Optimizing the combustion control concepts on a pellet stove with very low heat output is time-consuming and costly. In order to shorten the required laboratory test time, a 0-D transient tool was developed within the ERA-NET project “LowEmi-MicroStove”, which simulates a 4 kW pellet stove with staged combustion and heat transfer. This approach was chosen in order to greatly simplify the description of the combustion processes and so reduce the computational complexity and simulation time. The combustion of a bed of pellets is modeled as a superposition of the combustion cycles of individual pellets, assuming no interactions between pellets. A test setup was developed and used to determine the ignition and burning cycle of individual pellets. The description of the CO emissions behavior is based upon an empirically grounded relation which is in turn based on the air/fuel ratio and the combustion chamber temperature. For the validation of the 0-D simulation results, a test rig for a 4 kW pellet stove was built. Despite its simplistic approach, good agreement was found between the simulation and 4 kW pellet stove test results for the mean values and temporal fluctuations of flue gas temperature and oxygen and carbon monoxide content during start up, stable operation and load changes. The simulation could thus be used to quantify the effect of air flow rates and distribution as well as load changes on performance and draw conclusions regarding different process control strategies. A control strategy which can operate the stove at high temperatures near the air stoichiometric limit with acceptable CO emissions has been proven to be the most promising. Additionally, the model can be used to quantify the effects of variations in other process parameters, for example the impact of fluctuations in the pellet feed. Due to its effectiveness and simplicity, this model approach can be applied for the development of control strategies for other staged, pellet combustion systems.

Magnetic resonance imaging of the dopamine system in schizophrenia - A scoping review.

For decades, aberrant dopamine transmission has been proposed to play a central role in schizophrenia pathophysiology. These theories are supported by human in vivo molecular imaging studies of dopamine transmission, particularly positron emission tomography. However, there are several downsides to such approaches, for example limited spatial resolution or restriction of the measurement to synaptic processes of dopaminergic neurons. To overcome these limitations and to measure complementary aspects of dopamine transmission, magnetic resonance imaging (MRI)-based approaches investigating the macrostructure, metabolism, and connectivity of dopaminergic nuclei, i.e., substantia nigra pars compacta and ventral tegmental area, can be employed. In this scoping review, we focus on four dopamine MRI methods that have been employed in patients with schizophrenia so far: neuromelanin MRI, which is thought to measure long-term dopamine function in dopaminergic nuclei; morphometric MRI, which is assumed to measure the volume of dopaminergic nuclei; diffusion MRI, which is assumed to measure fiber-based structural connectivity of dopaminergic nuclei; and resting-state blood-oxygenation-level-dependent functional MRI, which is thought to measure functional connectivity of dopaminergic nuclei based on correlated blood oxygenation fluctuations. For each method, we describe the underlying signal, outcome measures, and downsides. We present the current state of research in schizophrenia and compare it to other disorders with either similar (psychotic) symptoms, i.e., bipolar disorder and major depressive disorder, or dopaminergic abnormalities, i.e., substance use disorder and Parkinson’s disease. Finally, we discuss overarching issues and outline future research questions.

Hypoxic stress and hypoxia-inducible factors in leukemias.

To cope with hypoxic stress, ancient organisms have developed evolutionally conserved programs centered on hypoxia-inducible transcriptional factors (HIFs). HIFs and their regulatory proteins have evolved as rheostats to adapt cellular metabolism to atmospheric oxygen fluctuations, but the amplitude of their transcriptional programs has tremendously increased along evolution to include a wide spectrum of physiological and pathological processes. The bone marrow represents a notable example of an organ that is physiologically exposed to low oxygen levels and where basal activation of hypoxia signaling appears to be intrinsically wired within normal and neoplastic hematopoietic cells. HIF-mediated responses are mainly piloted by the oxygen-labile α subunits HIF1α and HIF2α, and current literature suggests that these genes have a functional specification that remains to be fully defined. Since their identification in the mid 90s, HIF factors have been extensively studied in solid tumors, while their implication in leukemia has lagged behind. In the last decades however, many laboratories have addressed the function of hypoxia signaling in leukemia and obtained somewhat contradictory results. Suppression of HIFs expression in different types of leukemia has unveiled common leukemia-promoting functions such as stimulation of bone marrow neoangiogenesis, maintenance of leukemia stem cells and chemoresistance. However, genetic studies are revealing that a definition of HIF factors as bona fide tumor promoters is overly simplistic, and, depending on the leukemia subtype, the specific oncogenic event, or the stage of leukemia development, activation of hypoxia-inducible genes may lead to opposite consequences. With this article we will provide an updated summary of the studies describing the regulation and function of HIF1α and HIF2α in blood malignancies, spanning from acute to chronic, lymphoid to myeloid leukemias. In discussing these data, we will attempt to provide plausible explanations to contradictory findings and point at what we believe are areas of weakness in which further investigations are urgently needed. Gaining additional knowledge into the role of hypoxia signaling in leukemia appears especially timely nowadays, as new inhibitors of HIF factors are entering the clinical arena for specific types of solid tumors but their utility for patients with leukemia is yet to be determined.

Hypoxia Effects on Trypanosoma cruzi Epimastigotes Proliferation, Differentiation, and Energy Metabolism

Trypanosoma cruzi, the causative agent of Chagas disease, faces changes in redox status and nutritional availability during its life cycle. However, the influence of oxygen fluctuation upon the biology of T. cruzi is unclear. The present work investigated the response of T. cruzi epimastigotes to hypoxia. The parasites showed an adaptation to the hypoxic condition, presenting an increase in proliferation and a reduction in metacyclogenesis. Additionally, parasites cultured in hypoxia produced more reactive oxygen species (ROS) compared to parasites cultured in normoxia. The analyses of the mitochondrial physiology demonstrated that hypoxic condition induced a decrease in both oxidative phosphorylation and mitochondrial membrane potential (ΔΨm) in epimastigotes. In spite of that, ATP levels of parasites cultivated in hypoxia increased. The hypoxic condition also increased the expression of the hexokinase and NADH fumarate reductase genes and reduced NAD(P)H, suggesting that this increase in ATP levels of hypoxia-challenged parasites was a consequence of increased glycolysis and fermentation pathways. Taken together, our results suggest that decreased oxygen levels trigger a shift in the bioenergetic metabolism of T. cruzi epimastigotes, favoring ROS production and fermentation to sustain ATP production, allowing the parasite to survive and proliferate in the insect vector.

Body mass and cell size shape the tolerance of fishes to low oxygen in a temperature-dependent manner.

Aerobic metabolism generates 15–20 times more energy (ATP) than anaerobic metabolism, which is crucial in maintaining energy budgets in animals, fueling metabolism, activity, growth and reproduction. For ectothermic water‐breathers such as fishes, low dissolved oxygen may limit oxygen uptake and hence aerobic metabolism. Here, we assess, within a phylogenetic context, how abiotic and biotic drivers explain the variation in hypoxia tolerance observed in fishes. To do so, we assembled a database of hypoxia tolerance, measured as critical oxygen tensions (P crit) for 195 fish species. Overall, we found that hypoxia tolerance has a clear phylogenetic signal and is further modulated by temperature, body mass, cell size, salinity and metabolic rate. Marine fishes were more susceptible to hypoxia than freshwater fishes. This pattern is consistent with greater fluctuations in oxygen and temperature in freshwater habitats. Fishes with higher oxygen requirements (e.g. a high metabolic rate relative to body mass) also were more susceptible to hypoxia. We also found evidence that hypoxia and warming can act synergistically, as hypoxia tolerance was generally lower in warmer waters. However, we found significant interactions between temperature and the body and cell size of a fish. Constraints in oxygen uptake related to cellular surface area to volume ratios and effects of viscosity on the thickness of the boundary layers enveloping the gills could explain these thermal dependencies. The lower hypoxia tolerance in warmer waters was particularly pronounced for fishes with larger bodies and larger cell sizes. Previous studies have found a wide diversity in the direction and strength of relationships between P crit and body mass. By including interactions with temperature, our study may help resolve these divergent findings, explaining the size dependency of hypoxia tolerance in fish.

Hypoxic preconditioning induces neuroprotection against oxidative stress

Brain is an oxyregulator organ, however extremely vulnerable to oxygen. Both high and low oxygen concentrations generate free radicals and may cause oxidative stress and damage because of an insufficient response of the antioxidant system. Hypoxic preconditioning (HP) exerts neuroprotective effects and may be a protecting tool against oxygen fluctuations, thus preventing neuronal damage in events such as ischaemia, acute hypoxia, stroke, or traumatic brain injury, among others. This review aims to discuss the molecular mechanisms involved in the neuroprotective action of HP against oxidative stress and subsequently upon the brain under pro-oxidant conditions. Activation of the antioxidant defences represents the first line to neutralize oxidative stress and is characterized by low reactive oxygen species, reduced oxidative damage biomarkers, and increased level of reduced glutathione. These protective mechanisms decrease cell death activating anti-apoptotic signalling pathways and reducing neuroinflammation by the inactivation of microglia and astroglia cells. HP could be considered a new approach to reduce oxidative stress derived damage caused by a great variety of brain pathologies. Despite our intriguing findings, further experiments are needed for a better understanding of the molecular mechanisms involved in the neuroprotective actions of HP.

NADPH-Oxidase Derived Hydrogen Peroxide and Irs2b Facilitate Re-oxygenation-Induced Catch-Up Growth in Zebrafish Embryo.

Oxygen deprivation induces multiple changes at the cellular and organismal levels, and its re-supply also brings another special physiological status. We have investigated the effects of hypoxia/re-oxygenation on embryonic growth using the zebrafish model: hypoxia slows embryonic growth, but re-oxygenation induces growth spurt or catch-up growth. The mitogen-activated kinase (MAPK)-pathway downstream insulin-like growth factor (IGF/Igf) has been revealed to positively regulate the re-oxygenation-induced catch-up growth, and the role of reactive oxygen species generated by environmental oxygen fluctuation is potentially involved in the phenomenon. Here, we report the role of NADPH-oxidase (Nox)-dependent hydrogen peroxide (H2O2) production in the MAPK-activation and catch-up growth. The inhibition of Nox significantly blunted catch-up growth and MAPK-activity. Amongst two zebrafish insulin receptor substrate 2 genes (irs2a and irs2b), the loss of irs2b, but not its paralog irs2a, resulted in blunted MAPK-activation and catch-up growth. Furthermore, irs2b forcedly expressed in mammalian cells allowed IGF-MAPK augmentation in the presence of H2O2, and the irs2b deficiency completely abolished the somatotropic action of Nox in re-oxygenation condition. These results indicate that redox signaling alters IGF/Igf signaling to facilitate hypoxia/re-oxygenation-induced embryonic growth compensation.

Contrasting resistance and resilience to light variation of the coupled oxic and anoxic components of an experimental microbial ecosystem.

Understanding how microbial communities of aquatic ecosystems respond to environmental change remains a critical challenge in microbial ecology. In this study, we used light‐dependent oxic–anoxic micro‐ecosystems to understand how the functioning and diversity of aerobic and anaerobic lake analog communities are affected by a pulse light deprivation. Continuous measurements of oxygen concentration were made and a time series of full‐length 16S rRNA sequencing was used to quantify changes in alpha‐ and beta diversity. In the upper oxic layer, oxygen concentration decreased significantly under light reduction, but showed resilience in daily mean, minimum, and maximum after light conditions were restored to control level. Only the amplitude of diurnal fluctuations in oxygen concentrations did not recover fully, and instead tended to remain lower in treated ecosystems. Alpha diversity of the upper oxic layer communities showed a delayed increase after light conditions were restored, and was not resilient in the longer term. In contrast, alpha diversity of the anoxic lower layer communities increased during the light reduction, but was resilient in the longer term. Community composition changed significantly during light reduction, and showed resilience in the oxic layer and lack of resilience in the anoxic layer. Alpha diversity and the amplitude of daily oxygen fluctuations within and among treatments were strongly correlated, suggesting that higher diversity could lead to less variable oxygen concentrations, or vice versa. Our experiment showed that light deprivation induces multifaceted responses of community function (oxygen respiration) and structure, hence focusing on a single stability component could potentially be misleading.

Role of hydrodynamics in shaping chemical habitats and modulating the responses of coastal benthic systems to ocean global change.

Marine coastal zones are highly productive, and dominated by engineer species (e.g. macrophytes, molluscs, corals) that modify the chemistry of their surrounding seawater via their metabolism, causing substantial fluctuations in oxygen, dissolved inorganic carbon, pH, and nutrients. The magnitude of these biologically driven chemical fluctuations is regulated by hydrodynamics, can exceed values predicted for the future open ocean, and creates chemical patchiness in subtidal areas at various spatial (µm to meters) and temporal (minutes to months) scales. Although the role of hydrodynamics is well explored for planktonic communities, its influence as a crucial driver of benthic organism and community functioning is poorly addressed, particularly in the context of ocean global change. Hydrodynamics can directly modulate organismal physiological activity or indirectly influence an organism's performance by modifying its habitat. This review addresses recent developments in (i) the influence of hydrodynamics on the biological activity of engineer species, (ii) the description of chemical habitats resulting from the interaction between hydrodynamics and biological activity, (iii) the role of these chemical habitat as refugia against ocean acidification and deoxygenation, and (iv) how species living in such chemical habitats may respond to ocean global change. Recommendations are provided to integrate the effect of hydrodynamics and environmental fluctuations in future research, to better predict the responses of coastal benthic ecosystems to ongoing ocean global change.

Early Mesoproterozoic Ca-carbonate precipitates record fluctuations in shallow marine oxygenation

Oxygenation, a key control on marine life, has a long and varied history. This is well seen in the early Mesoproterozoic. During this critical period, midway between the Great Oxidation (GOE) and Neoproterozoic Oxidation (NOE) events, low marine levels of pulsed oxygenation - likely driven by fluctuations in cyanobacterial productivity - alternated with episodic anoxia. However, since baseline oxygen levels were low, deciphering the scale and variability of redox evolution during this prolonged interval is challenging. This in turn has made it difficult to confidently identify key underlying controls on redox evolution. Combining sedimentological and geochemical methods, we studied shallow ∼1.57 Ga shelf carbonates with contrasting depositional fabrics. Carbonate I/(Ca + Mg) data indicate that (i) carbonate mud precipitated in a weakly oxygenated water column, whereas (ii) seafloor crystal fans formed in more poorly oxygenated seawater, containing Fe2+ and Mn2+. We infer that in (i) weakly oxygenated (hypoxic-oxic) conditions reflect increased planktic cyanobacterial productivity that, in the absence of carbonate precipitation inhibitors (Fe2+ and Mn2+), promoted water column carbonate mud (‘whiting’) precipitation. At the same time, aerobic degradation of settling organic matter lowered seafloor CaCO3 saturation. In contrast, in (ii) more poorly oxygenated seawaters containing Fe2+ and Mn2+ inhibited calcite precipitation but permitted aragonite which formed seafloor crystal fans. Together, these contrasting precipitates indicate relatively rapid pulsed redox fluctuations. These were relatively subtle, but sufficient to result in contrasting carbonate sediments, readily recognizable in the field. We hypothesize that cyanobacterial productivity, possibly linked to the availability of nutrients such as phosphate, was a key influence on water column redox cyclicity during the Mesoproterozoic.

Development of a pO2-Guided Fine Needle Tumor Biopsy Device.

Tumor biopsies are an important aspect of oncology providing a guide for medical treatment and evaluation of disease progression. Highly heterogenous tumors have complex regions of active cancer cells interdigitated with necrotic tissue and healthy noncancerous tissue. The reliable access to tumor tissue pathology is therefore challenging and usually requires multiple needle insertions with accompanying patient discomfort and risk of infection. Oxygen levels provide a means of detecting and evaluating tumor tissue with levels reduced by 2-fold to 22-fold, depending on the type of organ. However, if the biopsy needle is placed in an area of normal tissue, there is always a chance that no diagnostic cells will be acquired for meaningful pathology and molecular analysis. While not the case in all tumors, there are cases where the in vivo oxygen levels differ with tumor cells having a value of pO2 lying between the anoxic necrotic tissue and normoxic normal tissue. The level of oxygen in tumor cells can also vary with time as related to complex biochemical pathways. The efficacy of radiation therapy is also sensitive to oxygen levels in tumors. Lower levels of oxygen present greater resistance to treatment. To address these concerns, a pO2-guided biopsy needle (OGBN) was developed to determine oxygen levels and fluctuations in highly resolved regions of tumors, in order to aide in determining the optimal region for cell sampling help in determining medical treatment options.

Rapid fluctuations in brain oxygenation during glucose-drinking behavior in trained rats.

Proper inflow of oxygen into brain tissue is essential for maintaining normal neural functions. Although oxygen levels in the brain's extracellular space depend upon a balance between its delivery from arterial blood and its metabolic consumption, the use of high-speed electrochemical detection revealed rapid increases in brain oxygen levels elicited by various salient sensory stimuli. These stimuli also increase intrabrain heat production, an index of metabolic neural activation, but these changes are slower and more prolonged than changes in oxygen levels. Therefore, under physiological conditions, the oxygen inflow into brain tissue exceeds its loss due to consumption, thus preventing any metabolic deficit. Here, we used oxygen sensors coupled with amperometry to examine the pattern of real-time oxygen fluctuations in the nucleus accumbens during glucose-drinking behavior in trained rats. Following the exposure to a glucose-containing cup, oxygen levels rapidly increased, peaked when the rat initiated drinking, and relatively decreased during consumption. Similar oxygen changes but more episodic drinking occurred when Stevia, a calorie-free sweet substance, was substituted for glucose. When water was substituted for glucose, rats tested the water but refused to consume all of it. Although the basic pattern of oxygen changes during this water test was similar to that with glucose drinking, the increases were larger. Finally, oxygen increases were significantly larger when rats were exposed to concealed glucose and made multiple unsuccessful attempts to obtain and consume it. Based on these data, we discuss the mechanisms underlying behavior-related brain oxygen fluctuations and their functional significance.NEW & NOTEWORTHY Oxygen sensors coupled with high-speed amperometry were used to examine brain oxygen fluctuations during glucose-drinking behavior in trained rats. Oxygen levels rapidly increased following presentation of a glucose-contained cup, peaking at the initiation of glucose drinking, and relatively decreasing during drinking. Oxygen increases were larger when rats were exposed to concealed glucose and made multiple attempts to obtain it. We discuss the mechanisms underlying behavior-related brain oxygen fluctuations and their functional significance.

Try or Die: Dynamics of Plant Respiration and How to Survive Low Oxygen Conditions.

Fluctuations in oxygen (O2) availability occur as a result of flooding, which is periodically encountered by terrestrial plants. Plant respiration and mitochondrial energy generation rely on O2 availability. Therefore, decreased O2 concentrations severely affect mitochondrial function. Low O2 concentrations (hypoxia) induce cellular stress due to decreased ATP production, depletion of energy reserves and accumulation of metabolic intermediates. In addition, the transition from low to high O2 in combination with light changes—as experienced during re-oxygenation—leads to the excess formation of reactive oxygen species (ROS). In this review, we will update our current knowledge about the mechanisms enabling plants to adapt to low-O2 environments, and how to survive re-oxygenation. New insights into the role of mitochondrial retrograde signaling, chromatin modification, as well as moonlighting proteins and mitochondrial alternative electron transport pathways (and their contribution to low O2 tolerance and survival of re-oxygenation), are presented.

New Insights on the Diurnal Mechanism of Calcification in the Stony Coral, Stylophora pistillata

Scleractinian corals are evolutionary-successful calcifying marine organisms, which utilize an endo-symbiotic relationship with photosynthetic dinoflagellate algae that supply energy products to their coral hosts. This energy further supports a higher calcification rate during the day in a process known as light enhanced calcification. Although this process has been studied for decades, the mechanisms behind it are still unknown. However, photosynthesis and respiration also cause daily fluctuations in oxygen and pH levels, resulting in the coral facing highly variable conditions. Here we correlated gene expression patterns with the physiological differences along the diel cycle to provide new insights on the daily dynamic processes, including circadian rhythm, calcification, symbiosis, cellular arrangement, metabolism, and energy budget. During daytime, when solar radiation levels are highest, we observed increased calcification rate combined with an extensive up-regulation of genes associated with reactive oxygen species, redox, metabolism, ion transporters, skeletal organic matrix, and mineral formation. During the night, we observed a vast shift toward up-regulation of genes associated with cilia movement, tissue development, cellular movement, antioxidants, protein synthesis, and skeletal organic matrix formation. Our results suggest that light enhanced calcification is related to several processes that occur across the diel cycle; during nighttime, tissue might elevate away from the skeleton, extending the calcifying space area to enable the formation of a new organic framework template. During daytime, the combination of synthesis of acid-rich proteins and a greater flux of ions to the sites of calcification facilitate the conditions for extensive mineral growth.

Tissue- and substrate-dependent mitochondrial responses to acute hypoxia–reoxygenation stress in a marine bivalve (Crassostrea gigas )

Hypoxia is a major stressor for aquatic organisms, yet intertidal organisms such as the oyster Crassostrea gigas are adapted to frequent oxygen fluctuations by metabolically adjusting to shifts in oxygen and substrate availability during hypoxia-reoxygenation (H/R). We investigated the effects of acute H/R stress (15 min at ∼0% O2 and 10 min reoxygenation) on isolated mitochondria from the gill and the digestive gland of C. gigas respiring on different substrates (pyruvate, glutamate, succinate, palmitate and their mixtures). Gill mitochondria showed better capacity for amino acid and fatty acid oxidation compared with mitochondria from the digestive gland. Mitochondrial responses to H/R stress strongly depended on the substrate and the activity state of mitochondria. In mitochondria oxidizing NADH-linked substrates, exposure to H/R stress suppressed oxygen consumption and generation of reactive oxygen species (ROS) in the resting state, whereas in the ADP-stimulated state, ROS production increased despite little change in respiration. As a result, electron leak (measured as H2O2 to O2 ratio) increased after H/R stress in the ADP-stimulated mitochondria with NADH-linked substrates. In contrast, H/R exposure stimulated succinate-driven respiration without an increase in electron leak. Reverse electron transport (RET) did not significantly contribute to succinate-driven ROS production in oyster mitochondria except for a slight increase in the OXPHOS state during post-hypoxic recovery. A decrease in NADH-driven respiration and ROS production, enhanced capacity for succinate oxidation and resistance to RET might assist in post-hypoxic recovery of oysters mitigating oxidative stress and supporting rapid ATP re-synthesis during oxygen fluctuations, as is commonly observed in estuaries and intertidal zones.

Submerged macrophytes regulate diurnal nitrous oxide emissions from a shallow eutrophic lake: A case study of Lake Wuliangsuhai in the temperate arid region of China

Submerged macrophytes can increase oxygen concentrations of water and promote diel oxygen fluctuations, and this phenomenon is hypothesized to play a vital role in regulating nitrous oxide (N2O) emissions from eutrophic lakes. However, the effects of submerged macrophytes on N2O emissions in shallow eutrophic lakes remain poorly investigated. In this study, Lake Wuliangsuhai, a typical shallow eutrophic lake, was investigated to study the role of submerged macrophytes in regulating N2O emissions. We measured the N2O fluxes and related parameters through continual 72-h in situ diel monitoring in two sampling sections that covered dense submerged macrophyte areas and open water. In this study, the dissolved oxygen (DO) concentration of the water in the submerged macrophyte area exhibited significant diurnal variations, with significantly higher water oxygen concentrations than the open water area during the daytime. The N2O fluxes of Lake Wuliangsuhai ranged from 0.01 to 0.24 μmol m−2 h−1, with an average value of 0.11 μmol m−2 h−1. Moreover, significant diel variations in the N2O flux and net N2O production were observed in the submerged macrophyte areas, where the maximum N2O flux occurred at midday. The molar ratios of NH4+-N to oxygen (N/O ratio) of the water were responsible for the diel variations in the N2O production in the lake. However, the high oxygen concentration of the water was the major regulator of the N2O flux of Lake Wuliangsuhai. Therefore, submerged macrophyte restoration is significant not only for water quality improvement in shallow eutrophic lakes but also for N2O emission mitigation by increasing the DO concentration of the water.

Mitochondrial capacity and reactive oxygen species production during hypoxia and reoxygenation in the ocean quahog, Arctica islandica.

Oxygen fluctuations are common in marine waters, and hypoxia-reoxygenation (H-R) stress can negatively affect mitochondrial metabolism. The long-lived ocean quahog, Arctica islandica, is known for its hypoxia tolerance associated with metabolic rate depression, yet the mechanisms that sustain mitochondrial function during oxygen fluctuations are not well understood. We used top-down metabolic control analysis (MCA) to determine aerobic capacity and control over oxygen flux in the mitochondria of quahogs exposed to short-term hypoxia (24 h <0.01% O2) and subsequent reoxygenation (1.5 h 21% O2) compared with normoxic control animals (21% O2). We demonstrated that flux capacity of the substrate oxidation and proton leak subsystems were not affected by hypoxia, while the capacity of the phosphorylation subsystem was enhanced during hypoxia associated with a depolarization of the mitochondrial membrane. Reoxygenation decreased the oxygen flux capacity of all three mitochondrial subsystems. Control over oxidative phosphorylation (OXPHOS) respiration was mostly exerted by substrate oxidation regardless of H-R stress, whereas control by the proton leak subsystem of LEAK respiration increased during hypoxia and returned to normoxic levels during reoxygenation. During hypoxia, reactive oxygen species (ROS) efflux was elevated in the LEAK state, whereas it was suppressed in the OXPHOS state. Mitochondrial ROS efflux returned to normoxic control levels during reoxygenation. Thus, mitochondria of A. islandica appear robust to hypoxia by maintaining stable substrate oxidation and upregulating phosphorylation capacity, but remain sensitive to reoxygenation. This mitochondrial phenotype might reflect adaptation of A. islandica to environments with unpredictable oxygen fluctuations and its behavioural preference for low oxygen levels.

Soil oxygen depletion and corresponding nitrous oxide production at hot moments in an agricultural soil

Hot moments of nitrous oxide (N2O) emissions induced by interactions between weather and management make a major contribution to annual N2O budgets in agricultural soils. The causes of N2O production during hot moments are not well understood under field conditions, but emerging evidence suggests that short-term fluctuations in soil oxygen (O2) concentration can be critically important. We conducted high time-resolution field observations of O2 and N2O concentrations during hot moments in a dryland agricultural soil in Northern China. Three typical management and weather events, including irrigation (Irr.), fertilization coupled with irrigation (Fer.+Irr.) or with extreme precipitation (Fer.+Pre.), were observed. Soil O2 and N2O concentrations were measured hourly for 24 h immediately following events and measured daily for at least one week before and after the events. Soil moisture, temperature, and mineral N were simultaneously measured. Soil O2 concentrations decreased rapidly within 4 h following irrigation in both the Irr. and Fer.+Irr. events. In the Fer.+Pre. event, soil O2 depletion did not occur immediately following fertilization but began following subsequent continuous rainfall. The soil O2 concentration dropped to as low as 0.2% (with the highest soil N2O concentration of up to 180 ppmv) following the Fer.+Pre. event, but only fell to 11.7% and 13.6% after the Fer.+Irr. and Irr. events, which were associated with soil N2O concentrations of 27 ppmv and 3 ppmv, respectively. During the hot moments of all three events, soil N2O concentrations were negatively correlated with soil O2 concentrations (r = −0.5, P < 0.01), showing a quadratic increase as soil O2 concentrations declined. Our results provide new understanding of the rapid short response of N2O production to O2 dynamics driven by changes in soil environmental factors during hot moments. Such understanding helps improve soil management to avoid transitory O2 depletion and reduce the risk of N2O production.

Transcriptional response of key metabolic and stress response genes of a nuculanid bivalve, Lembulus bicuspidatus from an oxygen minimum zone exposed to hypoxia-reoxygenation.

Benthic animals inhabiting the edges of marine oxygen minimum zones (OMZ) are exposed to unpredictable large fluctuations of oxygen levels. Sessile organisms including bivalves must depend on physiological adaptations to withstand these conditions. However, as habitats are rather inaccessible, physiological adaptations of the OMZ margin inhabitants to oxygen fluctuations are not well understood. We therefore investigated the transcriptional responses of selected key genes involved in energy metabolism and stress protection in a dominant benthic species of the northern edge of the Namibian OMZ, the nuculanid clam Lembulus bicuspidatus,. We exposed clams to normoxia (~5.8ml O2 l-1), severe hypoxia (36h at ~0.01ml O2 l-1) and post-hypoxic recovery (24h of normoxia following 36h of severe hypoxia). Using newly identified gene sequences, we determined the transcriptional responses to hypoxia and reoxygenation of the mitochondrial aerobic energy metabolism (pyruvate dehydrogenase E1 complex, cytochrome c oxidase, citrate synthase, and adenine nucleotide translocator), anaerobic glycolysis (hexokinase (HK), phosphoenolpyruvate carboxykinase (PEPCK), phosphofructokinase, and aldolase), mitochondrial antioxidants (glutaredoxin, peroxiredoxin, and uncoupling protein UCP2) and stress protection mechanisms (a molecular chaperone HSP70 and a mitochondrial quality control protein MIEAP) in the gills and the labial palps of L. bicuspidatus. Exposure to severe hypoxia transcriptionally stimulated anaerobic glycolysis (including HK and PEPCK), antioxidant protection (UCP2), and quality control mechanisms (HSP70 and MIEAP) in the gills of L. bicuspidatus. Unlike UCP2, mRNA levels of the thiol-dependent mitochondrial antioxidants were not affected by hypoxia-reoxygenation stress. Transcript levels of marker genes for aerobic energy metabolism were not responsive to oxygen fluctuations in L. bicuspidatus. Our findings highlight the probable importance of anaerobic succinate production (via PEPCK) and mitochondrial and proteome quality control mechanisms in responses to oxygen fluctuations of the OMZ bivalve L.bicuspidatus. The reaction of L.bicuspidatus to oxygen fluctuations implies parallels to that of other hypoxia-tolerant bivalves, such as intertidal species.

Hsp90 and its mitochondrial homologue TRAP-1 independently regulate hypoxia adaptations in Caenorhabditis elegans

Mitochondrial adaptations to various environmental cues contribute to cellular and organismal adaptations across multiple model organisms. Due to increased complexity, a direct connection between mitochondrial integrity and oxygen fluctuations, and survival fitness was not demonstrated. Here, using C. elegans as a model system, we studied the role of HIF-1, Hsp90, and TRAP-1 in mitochondrial adaptations during chemical hypoxia. We show that Hsp90mt (Hsp90 mutant) but not HIF-1mt (HIF-1 mutant) affects hypoxia adaptation in nematodes. TRAP-1KD (TRAP-1 knockdown) interfered with the survival and fecundity of worms. Compared to Hsp90mt, TRAP-1KD has induced a significant decrease in mitochondrial integrity and oxygen consumption rate. The complex I inhibitor rotenone did not affect ATP levels in Hsp90mt worms. However, ATP levels were decreased in TRAP-1KD worms under similar conditions. The glucose restriction has reduced, and glucose supplementation has increased the survival rate in Hsp90mt worms. Neither glucose restriction nor glucose supplementation has significantly affected the survival of TRAP-1KD worms in response to hypoxia. However, TRAP-1 inhibition using a nanocarrier drug has dramatically reduced the survival rate in response to hypoxia. Our results suggest that Hsp90 and TRAP-1 independently regulate hypoxia adaptations and metabolic plasticity in C. elegans. Considering the emerging roles of TRAP-1 in altered energy metabolism and cellular adaptations, our findings gain importance.