Respiratory Metabolism Research Articles

Respiratory muscle metabolic activity on PET/CT correlates with obstructive ventilatory defect severity and prognosis in patients undergoing lung cancer surgery.

Respiratory muscle activity is increased in patients with chronic respiratory disease. 18 F-FDG-PET/CT can assess respiratory muscle activity. We hypothesized that respiratory muscles metabolism was correlated to lung function impairment and was associated to prognosis in patients undergoing lung cancer surgery based on the research question whether respiratory muscle metabolism quantitatively correlates with the severity of lung function impairment in patients? Does respiratory muscle hypermetabolism have prognostic value? Patients undergoing 18 F-FDG-PET/CT and pulmonary function tests prior to lung cancer surgery were identified. Maximum Standardized Uptake Value (SUVm) were measured in each respiratory muscle group (sternocleidomastoid, scalene, intercostal, diaphragm), normalized against deltoid SUVm. Respiratory muscle hypermetabolism was defined as SUVm >90th centile in any respiratory muscle group. Clinical outcomes were collected from a prospective cohort. One hundred fifty-six patients were included, mostly male [110 (71%)], 53 (34%) with previous diagnosis of COPD. Respiratory muscle SUVm were: scalene: 1.84 [1.51-2.25], sternocleidomastoid 1.64 [1.34-1.95], intercostal 1.01 [0.84-1.16], diaphragm 1.79 [1.41-2.27]. Tracer uptake was inversely correlated to FEV1 for the scalene (r=-0.29, p < 0.001) and SCM (r=-0.17, p=0.03) respiratory muscle groups and positively correlated to TLC for the scalene (r=0.17, p=0.04). Respiratory muscle hypermetabolism was found in 45 patients (28.8%), who had a lower VO2 max (15.4 [14.2-17.5] vs. 17.2 mL/kg/min [15.2-21.1], p=0.07) and poorer overall survival when adjusting to FEV1% (p < 0.01). Our findings show respiratory muscle hypermetabolism is associated with lung function impairment and has prognostic significance. 18 F-FDG/PET-CT should be considered as a tool for assessing respiratory muscle activity and to identify high-risk patients.

Influence of temperature on respiratory metabolism during early development of Totoaba macdonaldi

Environmental temperature can act as a positive or negative modulator of the physiology and metabolism of poikilothermic organisms. As a general rule, larvae and juveniles are more sensitive to temperature stress than adults, which represents a key factor that partly determines their development and growth in aquaculture. Therefore, this study analyzed the effect of exposure to temperatures of 21, 24, and 27°C on the respiratory metabolism (RM) of Totoaba macdonaldi in different developmental stages. For this purpose, eggs, larvae with 4, 6, 8, 14, and 22 days post-hatch (dph), and juveniles of 25 dph were exposed to the experimental temperatures for 5 h. After the exposure time, oxygen consumption measurements were performed. The results clearly show that temperature (21 to 27°C) has the greatest effect on RM in eggs and larvae at 4 and 22 dph (3.1 ± 0.3 to 4.3 ± 0.3 μmol O2 h-1 egg-1, 2.9 ± 0.3 to 10.5 ± 1.2 μmol O2 h-1 larvae-1 and 102.0 ± 6.4 to 189.8 ± 15.3 μmol O2 h-1 larvae-1, respectively). This thermal sensitivity was not observed from 6, 8, and 14 dph larvae and juveniles at 25 dph, where morphological development was the main factor that influencing the RM. Therefore, this study shows that temperature affects RM in different development stages of totoaba, beginning in the egg stage and intensifying once the larvae hatch until 22 dph. Understanding how temperature affects energy expenditure by measuring RM is essential to establish culture conditions that allow better physiological performance and growth in the early life stages of T. macdonaldi.

Designing Single-Atom Active Sites on sp2 -Carbon Linked Covalent Organic Frameworks to Induce Bacterial Ferroptosis-Like for Robust Anti-Infection Therapy.

With the threat posed by drug-resistant pathogenic bacteria, developing non-antibiotic strategies for eradicating clinically prevalent superbugs remains challenging. Ferroptosis is a newly discovered form of regulated cell death that can overcome drug resistance. Emerging evidence shows the potential of triggering ferroptosis-like for antibacterial therapy, but the direct delivery of iron species is inefficient and may cause detrimental effects. Herein, an effective strategy to induce bacterial nonferrous ferroptosis-like by coordinating single-atom metal sites (e.g., Ir and Ru) into the sp2 -carbon-linked covalent organic framework (sp2 c-COF-Ir-ppy2 and sp2 c-COF-Ru-bpy2 ) is reported. Upon activating by light irradiation or hydrogen peroxide, the as-constructed Ir and Ru single-atom catalysts (SACs) can significantly expedite intracellular reactive oxygen species burst, enhance glutathione depletion-related glutathione peroxidase 4 deactivation, and disturb the nitrogen and respiratory metabolisms, leading to lipid peroxidation-driven ferroptotic damage. Both SAC inducers show potent antibacterial activity against Gram-positive bacteria, Gram-negative bacteria, clinically isolated methicillin-resistant Staphylococcus aureus (MRSA), and biofilms, as well as excellent biocompatibility and strong therapeutic and preventive potential in MRSA-infected wounds and abscesses. This delicate nonferrous ferroptosis-like strategy may open up new insights into the therapy of drug-resistant pathogen infection.

Myosin II regulatory light chain phosphorylation and formin availability modulate cytokinesis upon changes in carbohydrate metabolism.

Cytokinesis, the separation of daughter cells at the end of mitosis, relies in animal cells on a contractile actomyosin ring (CAR) composed of actin and class II myosins, whose activity is strongly influenced by regulatory light chain (RLC) phosphorylation. However, in simple eukaryotes such as the fission yeast Schizosaccharomyces pombe, RLC phosphorylation appears dispensable for regulating CAR dynamics. We found that redundant phosphorylation at Ser35 of the S. pombe RLC homolog Rlc1 by the p21-activated kinases Pak1 and Pak2, modulates myosin II Myo2 activity and becomes essential for cytokinesis and cell growth during respiration. Previously, we showed that the stress-activated protein kinase pathway (SAPK) MAPK Sty1 controls fission yeast CAR integrity by downregulating formin For3 levels (Gómez-Gil et al., 2020). Here, we report that the reduced availability of formin For3-nucleated actin filaments for the CAR is the main reason for the required control of myosin II contractile activity by RLC phosphorylation during respiration-induced oxidative stress. Thus, the restoration of For3 levels by antioxidants overrides the control of myosin II function regulated by RLC phosphorylation, allowing cytokinesis and cell proliferation during respiration. Therefore, fine-tuned interplay between myosin II function through Rlc1 phosphorylation and environmentally controlled actin filament availability is critical for a successful cytokinesis in response to a switch to a respiratory carbohydrate metabolism.

Taurine Stimulates AMP-Activated Protein Kinase and Modulates the Skeletal Muscle Functions in Rats via the Induction of Intracellular Calcium Influx

Taurine (2-aminoethanesulfonic acid) is a free amino acid abundantly found in mammalian tissues. Taurine plays a role in the maintenance of skeletal muscle functions and is associated with exercise capacity. However, the mechanism underlying taurine function in skeletal muscles has not yet been elucidated. In this study, to investigate the mechanism of taurine function in the skeletal muscles, the effects of short-term administration of a relatively low dose of taurine on the skeletal muscles of Sprague-Dawley rats and the underlying mechanism of taurine function in cultured L6 myotubes were investigated. The results obtained in this study in rats and L6 cells indicate that taurine modulates the skeletal muscle function by stimulating the expression of genes and proteins associated with mitochondrial and respiratory metabolism through the activation of AMP-activated protein kinase via the calcium signaling pathway.

Mitochondrial control of microglial phagocytosis by the translocator protein and hexokinase 2 in Alzheimer’s disease

Microglial phagocytosis is an energetically demanding process that plays a critical role in the removal of toxic protein aggregates in Alzheimer's disease (AD). Recent evidence indicates that a switch in energy production from mitochondrial respiration to glycolysis disrupts this important protective microglial function and may provide therapeutic targets for AD. Here, we demonstrate that the translocator protein (TSPO) and a member of its mitochondrial complex, hexokinase-2 (HK), play critical roles in microglial respiratory-glycolytic metabolism and phagocytosis. Pharmacological and genetic loss-of-function experiments showed that TSPO is critical for microglial respiratory metabolism and energy supply for phagocytosis, and its expression is enriched in phagocytic microglia of AD mice. Meanwhile, HK controlled glycolytic metabolism and phagocytosis via mitochondrial binding or displacement. In cultured microglia, TSPO deletion impaired mitochondrial respiration and increased mitochondrial recruitment of HK, inducing a switch to glycolysis and reducing phagocytosis. To determine the functional significance of mitochondrial HK recruitment, we developed an optogenetic tool for reversible control of HK localization. Displacement of mitochondrial HK inhibited glycolysis and improved phagocytosis in TSPO-knockout microglia. Mitochondrial HK recruitment also coordinated the inflammatory switch to glycolysis that occurs in response to lipopolysaccharide in normal microglia. Interestingly, cytosolic HK increased phagocytosis independent of its metabolic activity, indicating an immune signaling function. Alzheimer's beta amyloid drastically stimulated mitochondrial HK recruitment in cultured microglia, which may contribute to microglial dysfunction in AD. Thus, targeting mitochondrial HK may offer an immunotherapeutic approach to promote phagocytic microglial function in AD.

Tcf7l2 in hepatocytes regulates de novo lipogenesis in diet-induced non-alcoholic fatty liver disease in mice

Aims/hypothesisNon-alcoholic fatty liver disease (NAFLD) associated with type 2 diabetes may more easily progress towards severe forms of non-alcoholic steatohepatitis (NASH) and cirrhosis. Although the Wnt effector transcription factor 7-like 2 (TCF7L2) is closely associated with type 2 diabetes risk, the role of TCF7L2 in NAFLD development remains unclear. Here, we investigated how changes in TCF7L2 expression in the liver affects hepatic lipid metabolism based on the major risk factors of NAFLD development.MethodsTcf7l2 was selectively ablated in the liver of C57BL/6N mice by inducing the albumin (Alb) promoter to recombine Tcf7l2 alleles floxed at exon 5 (liver-specific Tcf7l2-knockout [KO] mice: Alb-Cre;Tcf7l2f/f). Alb-Cre;Tcf7l2f/f and their wild-type (Tcf7l2f/f) littermates were fed a high-fat diet (HFD) or a high-carbohydrate diet (HCD) for 22 weeks to reproduce NAFLD/NASH. Mice were refed a standard chow diet or an HCD to stimulate de novo lipogenesis (DNL) or fed an HFD to provide exogenous fatty acids. We analysed glucose and insulin sensitivity, metabolic respiration, mRNA expression profiles, hepatic triglyceride (TG), hepatic DNL, selected hepatic metabolites, selected plasma metabolites and liver histology.ResultsAlb-Cre;Tcf7l2f/f essentially exhibited increased lipogenic genes, but there were no changes in hepatic lipid content in mice fed a normal chow diet. However, following 22 weeks of diet-induced NAFLD/NASH conditions, liver steatosis was exacerbated owing to preferential metabolism of carbohydrate over fat. Indeed, hepatic Tcf7l2 deficiency enhanced liver lipid content in a manner that was dependent on the duration and amount of exposure to carbohydrates, owing to cell-autonomous increases in hepatic DNL. Mechanistically, TCF7L2 regulated the transcriptional activity of Mlxipl (also known as ChREBP) by modulating O-GlcNAcylation and protein content of carbohydrate response element binding protein (ChREBP), and targeted Srebf1 (also called SREBP1) via miRNA (miR)-33-5p in hepatocytes. Eventually, restoring TCF7L2 expression at the physiological level in the liver of Alb-Cre;Tcf7l2f/f mice alleviated liver steatosis without altering body composition under both acute and chronic HCD conditions.Conclusions/interpretationIn mice, loss of hepatic Tcf7l2 contributes to liver steatosis by inducing preferential metabolism of carbohydrates via DNL activation. Therefore, TCF7L2 could be a promising regulator of the NAFLD associated with high-carbohydrate diets and diabetes since TCF7L2 deficiency may lead to development of NAFLD by promoting utilisation of excess glucose pools through activating DNL.Data availabilityRNA-sequencing data have been deposited into the NCBI GEO under the accession number GSE162449 (www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE162449).Graphical abstract

Magnetic field delays the senescence of strawberries by maintaining energy state and regulating respiratory metabolism

Strawberries are prone to rapid quality deterioration after harvest. Research has confirmed that a magnetic field can improve fruit quality during postharvest storage. However, how the magnetic field impacts the postharvest physiology of strawberries is far from being explored. In this study, the magnetic field (MF, 4 mT, and 50 Hz) was employed during the storage of strawberries at 4 °C for 1, 3, 5, 7, 10, and 15 d, and conventional refrigeration (CR) was used as the control. The results showed that the MF maintained better fruit quality, as indicated by lower decay incidence, declined weight loss, and greater firmness retention. The decrease in soluble solids content and titratable acidity of strawberries caused by respiratory depletion was also alleviated by MF. Furthermore, an improvement in the adenosine triphosphate level, energy charge, activity of enzymes (H+-ATPase, Ca2+-ATPase, succinate dehydrogenase, and cytochrome oxidase) involved in the respiratory metabolism, as well as primary respiratory metabolites (D-glucose, succinic acid, fumaric acid, and citric acid) were observed for the strawberries of MF group. Accumulations of hydrogen peroxide, superoxide anion, and malondialdehyde were suppressed with the application of MF. Overall, the MF contributed to maintaining higher energy and membrane integrity and function, regulating the levels of energy metabolism enzymes, and mitigating reactive oxygen species accumulation, which might be a part of the mechanism involved in retarding the senescence and decay of harvested strawberries.

Sub-lethal effects of spinetoram application interacts with temperature in complex ways to influence respiratory metabolism, life history and macronutrient composition in false codling moth (Thaumatotibia leucotreta)

In many pests, insecticide efficacy is dependent on environmental conditions, including ambient temperature. However, it remains unknown if thermal history alters sub-lethal effects to potentially enhance or reduce pesticide resistance in the false codling moth (FCM), Thaumatotibia leucotreta. Here, using FCM, a pest of economic importance in South Africa infesting several commercial food crops, we report results of sub-lethal exposure to spinetoram, an insecticide that disrupts the nervous system. We investigate whether insecticide efficacy is temperature dependent or perhaps interacts with thermal history by testing the effect of a combination of a sub-lethal dose of spinetoram (4 mg/100 ml) and developmental temperature acclimation (22˚C and 28˚C, i.e., a few degrees above or below optimal development temperatures) on the metabolic rate, life history traits and body composition of FCM in the laboratory. A sub-lethal dose of spinetoram reduced metabolic rate of FCM pupae significantly, led to smaller pupal mass and decreased emergence rates. Additionally, males acclimated at 28 °C had a significantly higher emergence rate compared to males acclimated at 22 °C. Body water, body lipids and body protein reserves of adult FCM tended to be higher in the insecticide treatment compared to the control in the 22 °C acclimation group. In the 28 °C acclimation group, body water, lipids and proteins were lower in the insecticide treatment versus the control. Furthermore, sex influenced both emergence rate and body composition with the direction of change depending on insecticide and temperature treatments. Overall, a sub-lethal dose of spinetoram negatively affects body composition and life history traits but interacts with temperature in complex ways. Therefore, both lethal and sub-lethal effects of spinetoram on FCM, in combination with information on the thermal environment experienced by the pest, should be taken into consideration when pest control decisions are made.

CBL/CAP Is Essential for Mitochondria Respiration Complex I Assembly and Bioenergetics Efficiency in Muscle Cells.

CBL is rapidly phosphorylated upon insulin receptor activation. Mice whole body CBL depletion improved insulin sensitivity and glucose clearance; however, the precise mechanisms remain unknown. We depleted either CBL or its associated protein SORBS1/CAP independently in myocytes and assessed mitochondrial function and metabolism compared to control cells. CBL- and CAP-depleted cells showed increased mitochondrial mass with greater proton leak. Mitochondrial respiratory complex I activity and assembly into respirasomes were reduced. Proteome profiling revealed alterations in proteins involved in glycolysis and fatty acid degradation. Our findings demonstrate CBL/CAP pathway couples insulin signaling to efficient mitochondrial respiratory function and metabolism in muscle.

Comparing electrochemical and spectroscopic properties of three cytochrome nanowires from Geobacter sulfurreducens.

The model anaerobic bacterium, Geobacter sulfurreducens, produces filaments that mediate extracellular electron transfer as part of its respiratory metabolism in oxygen-free environments. The physical, biological, and chemical principles supporting conductivity in protein filaments such as those produced by Geobacter have considerable importance for our understanding of biogeochemical cycles, impacts of climate change, and advanced biomedical devices. We have recently discovered that G. sulfurreducens produces at least three such filaments, which structural studies revealed to be polymers of multiheme cytochromes, OmcS, OmcE, and OmcZ. All three filaments are composed of these cytochrome subunits with bis-histidine-coordinated hemes forming a chain along the fiber axis. Our work aims to understand the structure-property relationships in these conductive filaments, including those that directly support long-range electron transport. Our structural studies show that the arrangement of heme in OmcS and OmcE are nearly identical, despite lacking sequence homology. These two filaments also exhibit heme coordinated across the subunit-subunit interface by histidines from neighboring subunits. The structure of OmcZ is distinct in that it lacks this interfacial heme. One heme per subunit is offset from the axial chain and largely exposed to solvent. Moreover, all heme pairs in these filaments, and indeed most heme pairs within multiheme c-type cytochrome structures in the Protein Databank, cluster into common rotation angle and separation distance arrangement, suggesting conserved electron transfer motifs across domains of life. Spectroscopic comparison between OmcS, OmcE, and OmcZ filaments, and their disassembled monomers will be discussed. Additionally, an outline of the biophysical and electrochemical characterizations of cytochrome filaments and their monomeric subunits will be addressed. The new concepts that will be concluded from the investigation of conductive cytochrome filaments in Geobacter will lead to a better understanding of biological structures supporting long-range electronic conductivity.

Dimethyl fumarate ameliorates fungal keratitis by limiting fungal growth and inhibiting pyroptosis.

We aimed to investigate the therapeutic role of dimethyl fumarate (DMF) in fungal keratitis. Human corneal epithelial cells (HCECs) and mouse models of fungal keratitis were used in this study. The antifungal effect of DMF on Aspergillus fumigatus (A. fumigatus) was confirmed by examining the minimum inhibitory concentration (MIC), biofilm formation, conidial adherence and corneal fungal loads. Slit-lamp photography, haematoxylin and eosin staining and immunostaining were used to assess the severity of corneal impairment. RT-PCR, western blot, ELISA, immunohistochemistry and immunostaining were performed to examine the effects of DMF on the expression of the inflammatory mediators during fungal infection. In vitro, DMF limited A. fumigatus growth, biofilm formation, and conidial adherence and reduced the mRNA levels of AldA, GlkA, GAPDH, HxkA, PgkA, Sdh2, GelA and ChsF in A. fumigatus. In vivo, DMF effectively decreased corneal fungal loads. DMF attenuated corneal inflammatory impairment by suppressing inflammatory cell accumulation and downregulating cytokine expression. DMF notably downregulated the high expression of NLRP3, cleaved GSDMD, cleaved caspase-1, mature IL-1β and mature IL-18 induced by fungi. The production of Nrf2 and HO-1 could be further increased by DMF in infected HCECs. Nrf2 siRNA pretreatment counteracted DMF-mediated downregulation of the expression of the active forms of IL-18, IL-1β, caspase-1 and GSDMD. DMF limits fungal growth by suppressing biofilm formation, conidial adherence and respiratory metabolism. It also exerts an anti-inflammatory effect on fungal keratitis by inhibiting pyroptosis, which could be regulated by Nrf2. Our results suggest that DMF plays a therapeutic role in fungal keratitis.

Pressure treatment has a differential effect on cyanide- and ethanol-induced autofluorescence response in yeast.

Cellular processes associated with biological membranes and multimeric associations exhibit pressure sensitivity. In cellular respiration for example, pressure-regulated respiratory oxidases and cytochromes are found in piezophilic microbes, and pressure reduces oxygen consumption rates in eukaryotes. The presence of piezotolerant obligate aerobic yeasts in deep sea environments further justifies investigating pressure effects on cellular respiratory mechanisms. Ambient pressure analysis of UV-excited autofluorescence signals used for monitoring respiratory metabolism have identified multiple cellular NADH and NADPH conformations, significant because the distribution of conformational forms depends on metabolic conditions. Here, we use UV-excited autofluorescence spectroscopy with the spectral response quantified using phasor analysis to monitor cellular NADH and NADPH conformation in Saccharomyces cerevisiae (baker's yeast) suspensions after 30-minute pressure treatment at up to 11 kpsi (75.8 MPa). Specifically, we investigate the effects of pressure treatment on the autofluorescence response to the additions of cyanide and ethanol (both respiratory inhibitors at ambient pressure). The autofluorescence response to cyanide measured 30 min after pressure release shows a diminished response, while the response to ethanol shows no detectable difference when compared with the response prior to pressure treatment. Conditions for this study are similar to those previously reported to activate transcription factors in yeast due to pressure-induced stress tolerance, suggesting autofluorescence may be useful for assessing mitochondrial functional under induced stress-tolerance conditions.

Emergent Scaling of Dissolved Oxygen (DO) in Freshwater Streams Across Contiguous USA

AbstractDissolved oxygen (DO) indicates the overall stream water quality and ecosystem health. We investigated emergent scaling of DO with the dominant environmental drivers in freshwater (non‐coastal) streams across the contiguous United States. Available data of monthly to quarterly sampling frequencies during 1998–2015 were obtained for 86 U.S. streams. Data analytics indicated water temperature (Tw) and pH (a proxy of carbon dioxide) dominating the key environmental process components of DO concentrations in the freshwater streams. The “climatic” process component (comprising Tw and net radiation) had, respectively, ∼3 and ∼9 times stronger control on DO than the “biogeochemical” (total nitrogen, total phosphorus, pH, and specific conductivity) and “hydro‐atmospheric” exchange (stream flow and atmospheric pressure) components. The predominant climatic control on stream DO was linked to the high extent of vegetated land (on average ∼53%) and steep slope (∼10%) in the draining watersheds, despite the notable presence of agricultural land (∼35%). An emergent power law scaling relationship was then developed to acceptably predict DO (mg/l) based on Tw (K) and pH, with the approximate exponents of −15/2 and 1/2, respectively (Nash‐Sutcliffe Efficiency = 0.72–0.73). The scaling law demonstrated the underlying organizing principles such as the depletion of stream DO due to reduced dissolution and increased metabolic respiration with the increasing temperature and nutrients. The scaling law was persistent across the various U.S. streams, representing gradients in climate, hydrology, biogeochemistry, and land use/cover. The findings would help understand and manage water quality and ecosystem health in freshwater streams across the United States and beyond.

Effects of photobiomodulation as an adjunctive treatment in chronic obstructive pulmonary disease: a narrative review.

Chronic obstructive pulmonary disease (COPD) is a disease characterized by chronic airway inflammation and remodeling and lung parenchymal inflammation and destruction, which result in many pulmonary and extrapulmonary manifestations. The anti-inflammatory effect of photobiomodulation (PBM) has been reported in previous studies. This review was conducted to evaluate the direct effect of PBM on lung inflammation in COPD. The other effects of PBM on modulation of peripheral and respiratory muscle metabolism and angiogenesis in lung tissues were also discussed. The databases of PubMed, Cochrane Library, and Google Scholar were searched to find the relevant studies. Keywords included PBM and related terms, COPD-related signs, and lung inflammation. A total of 12 articles were selected and reviewed in this study. Based on the present review, PBM is helpful in reducing lung inflammation through decreasing the inflammatory cytokines and chemokines at multiple levels and increasing anti-inflammatory cytokines. In addition, PBM also improves both peripheral and respiratory muscle metabolism and promote angiogenesis. This review demonstrated that PBM is a promising adjunctive treatment modality for COPD management which merits further validation.

Long-term methamphetamine self-administration increases mesolimbic mitochondrial oxygen consumption and decreases striatal glutathione

Neurotoxic regimens of methamphetamine (METH) are known to increase reactive oxygen species (ROS), affect redox homeostasis, and lead to damage in dopamine neurons. Functional changes induced by long-term METH self-administration on mitochondrial respiratory metabolism and redox homeostasis are less known. To fill this gap, we implanted a jugular catheter into adult male mice and trained them to nose poke for METH infusions. After several weeks of METH exposure, we collected samples of the ventral striatum (vST) and the ventral midbrain (vMB). We used HPLC to determine the levels of the ROS scavenger glutathione in its reduced (GSH) and oxidized forms. Then, we used high-resolution respirometry to determine the oxygen consumption rate (OCR) of mitochondrial complexes. Finally, using in vivo electrophysiology, we assessed changes in dopamine neuron firing activity in the VTA. METH self-administration produced a decrease of the GSH pool in vST, correlating with lifetime METH intake. We observed increased mitochondrial respiration across the two mesolimbic regions. METH self-administration decreases firing rate and burst activity but increases the number of spontaneously active dopamine neurons per track. We conclude that METH self-administration progressively decreased the antioxidant pool in sites of higher dopamine release and produced an increase in mitochondrial metabolism in the mesolimbic areas, probably derived from the increased number of dopamine neurons actively firing. However, dopamine neuron firing activity is decreased by METH self-administration, reflecting a new basal level of dopamine neurotransmission.

Proteome adaptations of the organohalide-respiring Desulfitobacterium hafniense strain DCB-2 to various energy metabolisms.

Desulfitobacterium hafniense was isolated for its ability to use organohalogens as terminal electron acceptors via organohalide respiration (OHR). In contrast to obligate OHR bacteria, Desulfitobacterium spp. show a highly versatile energy metabolism with the capacity to use different electron donors and acceptors and to grow fermentatively. Desulfitobacterium genomes display numerous and apparently redundant members of redox enzyme families which confirm their metabolic potential. Nonetheless, the enzymes responsible for many metabolic traits are not yet identified. In the present work, we conducted an extended proteomic study by comparing the proteomes of Desulfitobacterium hafniense strain DCB-2 cultivated in combinations of electron donors and acceptors, triggering five alternative respiratory metabolisms that include OHR, as well as fermentation. Tandem Mass Tag labelling proteomics allowed us to identify and quantify almost 60% of the predicted proteome of strain DCB-2 (2,796 proteins) in all six growth conditions. Raw data are available via ProteomeXchange with identifier PXD030393. This dataset was analyzed in order to highlight the proteins that were significantly up-regulated in one or a subset of growth conditions and to identify possible key players in the different energy metabolisms. The addition of sodium sulfide as reducing agent in the medium - a very widespread practice in the cultivation of strictly anaerobic bacteria - triggered the expression of the dissimilatory sulfite reduction pathway in relatively less favorable conditions such as fermentative growth on pyruvate, respiration with H2 as electron donor and OHR conditions. The presence of H2, CO2 and acetate in the medium induced several metabolic pathways involved in carbon metabolism including the Wood-Ljungdahl pathway and two pathways related to the fermentation of butyrate that rely on electron-bifurcating enzymes. While the predicted fumarate reductase appears to be constitutively expressed, a new lactate dehydrogenase and lactate transporters were identified. Finally, the OHR metabolism with 3-chloro-4-hydroxyphenylacetate as electron acceptor strongly induced proteins encoded in several reductive dehalogenase gene clusters, as well as four new proteins related to corrinoid metabolism. We believe that this extended proteomic database represents a new landmark in understanding the metabolic versatility of Desulfitobacterium spp. and provides a solid basis for addressing future research questions.

Fine Tuning of ROS, Redox and Energy Regulatory Systems Associated with the Functions of Chloroplasts and Mitochondria in Plants under Heat Stress.

Heat stress severely affects plant growth and crop production. It is therefore urgent to uncover the mechanisms underlying heat stress responses of plants and establish the strategies to enhance heat tolerance of crops. The chloroplasts and mitochondria are known to be highly sensitive to heat stress. Heat stress negatively impacts on the electron transport chains, leading to increased production of reactive oxygen species (ROS) that can cause damages on the chloroplasts and mitochondria. Disruptions of photosynthetic and respiratory metabolisms under heat stress also trigger increase in ROS and alterations in redox status in the chloroplasts and mitochondria. However, ROS and altered redox status in these organelles also activate important mechanisms that maintain functions of these organelles under heat stress, which include HSP-dependent pathways, ROS scavenging systems and retrograde signaling. To discuss heat responses associated with energy regulating organelles, we should not neglect the energy regulatory hub involving TARGET OF RAPAMYCIN (TOR) and SNF-RELATED PROTEIN KINASE 1 (SnRK1). Although roles of TOR and SnRK1 in the regulation of heat responses are still unknown, contributions of these proteins to the regulation of the functions of energy producing organelles implicate the possible involvement of this energy regulatory hub in heat acclimation of plants.

Analysis of seed viability through respiration metabolism using CO2 sensors and internet of things (IoT) system

The respiration metabolism is an indicator of seed viability. The respiration process can be measured through the production of CO2 during the seed germination process. The respiration process can be measured through the production of CO2 during the seed germination process. This study aims to create a CO2 measuring device that can measure in real-time using a CO2 sensor and an IoT system. The study consisted of two experiments. The first experiment was to create a seed respiration measuring device using a CO2 sensor and an IoT system. The second experiment was to validate. The first experiment’s results were that a device can detect carbon dioxide levels automatically in the measurement range from 400 ppm to 5000 ppm. The device had online data storage through a database that can be monitored using the IoT system and is equipped with backup data storage using an SD card to avoid data loss in the cloud due to internet connection failure. The second experiment used a randomized complete block design. The treatment consisted of six levels of soybean seed viability (94.8%, 92.4%, 90.4%, 88.4%, 66.0%, 40.8% based on germination test). The results showed that the CO2 measurement could differentiate the viability of seeds.

Benzo(a)pyrene-induced mitochondrial respiration and glycolysis disturbance in human neuroblastoma cells.

Mammalian cells generate ATP through mitochondrial respiration and glycolysis. Mitochondria not only play a key role in cell energy metabolism but also in cell cycle regulation. As a neurotoxic pollutant, benzo(a)pyrene (BaP) can trigger neuronal oxidative damage and apoptosis. However, the features of BaP-induced energy metabolism disturbance in SH-SY5Y cells has rarely been addressed. This study aimed to measure oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) as indications of respiratory activities and glycolytic. SH-SY5Y cells were treated with BaP to establish a cytotoxicity model, and butylated hydroxy anisole (BHA) was used to alleviate the damages induced by BaP. Using the Seahorse Extracellular Flux analyzer (XFp), we found that BaP significantly reduced basal respiration, ATP-linked OCR in SH-SY5Y cells with dose- and time-dependent. BHA supplementation recovered the mitochondrial respiration, synchronously attenuated intracellular ROS generation and lipid peroxidation, and simultaneously reversed the abnormal changes in antioxidant biomarkers, then rescued BaP-induced cell apoptosis. But long-term exposure to BaP or exposure to a high dosage of BaP could decrease OCR associated with maximal respiratory, spare capacity, and glycolysis metabolism. At the same time, the damage to cells is also more severe with the rate of apoptosis and mitochondrial membrane potential (ΔΨm) loss rising sharply, which were not entirely reversed by BHA. This study provides energy metabolism-related, indicative biomarkers of cytotoxicity induced by BaP, which might provide information for early prevention and intervention.