Cells undergo metabolic reprogramming to adapt to changes in nutrient availability, cellular activity, and transitions in cell states. The balance between glycolysis and mitochondrial respiration is crucial for energy...Cells undergo metabolic reprogramming to adapt to changes in nutrient availability, cellular activity, and transitions in cell states. The balance between glycolysis and mitochondrial respiration is crucial for energy production, and metabolic reprogramming stipulates a shift in such balance to optimize both bioenergetic efficiency and anabolic requirements. Failure in switching bioenergetic dependence can lead to maladaptation and pathogenesis. While cellular degradation is known to recycle precursor molecules for anabolism, its potential role in regulating energy production remains less explored. The bioenergetic switch between glycolysis and mitochondrial respiration involves transcription factors and organelle homeostasis, which are both regulated by the cellular degradation pathways. A growing body of studies has demonstrated that both stem cells and differentiated cells exhibit bioenergetic switch upon perturbations of autophagic activity or endolysosomal processes. Here, we highlighted the current understanding of the interplay between degradation processes, specifically autophagy and endolysosomes, transcription factors, endolysosomal signaling, and mitochondrial homeostasis in shaping cellular bioenergetics. This review aims to summarize the relationship between degradation processes and bioenergetics, providing a foundation for future research to unveil deeper mechanistic insights into bioenergetic regulation.展开更多
Background: The active use of stem and progenitor cells in the therapy of various diseases requires thedevelopment of approaches for targeted modification of their properties. One such approach is the induction of a p...Background: The active use of stem and progenitor cells in the therapy of various diseases requires thedevelopment of approaches for targeted modification of their properties. One such approach is the induction of a prooranti-inflammatory phenotype. Methods: In this study, we investigated the effect of a pro-inflammatoryenvironment in vitro on multipotent mesenchymal stromal cells (MSC) by incubation with lipopolysaccharide (LPS).iCELLigence real-time cell analysis system was used for monitoring cell culture growth. Cell energy metabolism wasassessed using the Seahorse XFp Analyzer. For the rat stroke experiment, we used a photoinduced thrombosis (PT)model;after 24 h of surgery, vehicle or MSC or LPS-treated MSC was injected i.v. With magnetic resonance imaging(MRI) we evaluated the volume of ischemic brain injury. For the effect of MSC on neurological deficit after PT weused three methods: limb placement test, cylinder test, and beam-walking test. Results: LPS exposure led to asignificant increase in cell growth rate and to changes in their energy metabolism: glycolytic activity increasedsignificantly in the MSC, and non-glycolytic acidification also increased, while basic respiratory parameters weremaintained. With MRI we didn’t reveal changes in the volume of brain damage between all rat groups. Neurologicaldeficit was less only with using untreated MSC injection. Conclusion: Using LPS-treated MSC in the therapy ofischemic stroke in rats, we did not observe an increase in the neuroprotective properties of the cells, but instead notedsome decrease in their therapeutic efficacy. We attribute these changes to the formation of a pro-inflammatoryphenotype in MSC.展开更多
Microbiologically influenced corrosion （MIC） is a major cause of corrosion damages, facility failures, and financial losses, making MIC an important research topic. Due to complex microbiological activities and a la...Microbiologically influenced corrosion （MIC） is a major cause of corrosion damages, facility failures, and financial losses, making MIC an important research topic. Due to complex microbiological activities and a lack of deep understanding of the interactions between biofilms and metal surfaces, MIC occurrences and mechanisms are difficult to predict and interpret. Many theories and mechanisms have been pro- posed to explain MIC. In this review, the mechanisms of MIC are discussed using hioenergetics, microbial respiration types, and biofilm extracellular electron transfer （EET）. Two main MIC types, namely EET-MIC and metabolite MIC （M-ME）, are discussed. This brief review provides a state of the art insight into MIC mechanisms and it helps the diagnosis and prediction of occurrences of MIC under anaerobic conditions in the oil and gas industry.展开更多
Alzheimer’s disease （AD） is an increasingly pressing worldwide public-health, social, political and economic concern. Despite significant investment in multiple traditional therapeutic strategies that have achieved...Alzheimer’s disease （AD） is an increasingly pressing worldwide public-health, social, political and economic concern. Despite significant investment in multiple traditional therapeutic strategies that have achieved success in preclinical models addressing the pathological hallmarks of the disease, these efforts have not translated into any effective disease-modifying therapies. This could be because interventions are being tested too late in the disease process. While existing therapies provide symptomatic and clinical benefit, they do not fully address the molecular abnormalities that occur in AD neurons. The pathophysiology of AD is complex; mitochondrial bioenergetic deficits and brain hypometabolism coupled with increased mitochondrial oxidative stress are antecedent and potentially play a causal role in the disease pathogenesis. Dysfunctional mitochondria accumulate from the combination of impaired mitophagy, which can also induce injurious inflammatory responses, and inadequate neuronal mitochondrial biogenesis. Altering the metabolic capacity of the brain by modulating/potentiating its mitochondrial bioenergetics may be a strategy for disease prevention and treatment. We present insights into the mechanisms of mitochondrial dysfunction in AD brain as well as an overview of emerging treatments with the potential to prevent, delay or reverse the neurodegenerative process by targeting mitochondria.展开更多
BACKGROUND The pancreatic islet microcirculation adapts its metabolism to cope with limited oxygen availability and nutrient delivery.In diabetes,the balance between oxygen delivery and consumption is impaired.Insulin...BACKGROUND The pancreatic islet microcirculation adapts its metabolism to cope with limited oxygen availability and nutrient delivery.In diabetes,the balance between oxygen delivery and consumption is impaired.Insulin has been proven to exert complex actions promoting the maintenance of homeostasis of the pancreas under glucotoxicity.AIM To test the hypothesis that insulin administration can improve the integrated pancreatic microcirculatory oxygen profile and bioenergetics.METHODS The pancreatic microcirculatory partial oxygen pressure(PO_(2)),relative hemoglobin(rHb)and hemoglobin oxygen saturation(SO_(2))were evaluated in nondiabetic,type 1 diabetes mellitus(T1DM),and insulin-treated mice.A threedimensional framework was generated to visualize the microcirculatory oxygen profile.Ultrastructural changes in the microvasculature were examined using transmission electron microscopy.An Extracellular Flux Analyzer was used to detect the real-time changes in bioenergetics by measuring the oxygen consumption rate and extracellular acidification rate in islet microvascular endothelial cells(IMECs).RESULTS Significantly lower PO_(2),rHb,and SO_(2) values were observed in T1DM mice than in nondiabetic controls.Insulin administration ameliorated the streptozotocin-induced decreases in these microcirculatory oxygen parameters and improved the mitochondrial ultrastructural abnormalities in IMECs.Bioenergetic profiling revealed that the IMECs did not have spare respiratory capacity.Insulin-treated IMECs exhibited significantly greater basal respiration than glucotoxicity-exposed IMECs(P<0.05).An energy map revealed increased energetic metabolism in insulin-treated IMECs,with significantly increased ATP production,non-mitochondrial respiration,and oxidative metabolism(all P<0.05).Significant negative correlations were revealed between microcirculatory SO_(2) and bioenergetic parameters.CONCLUSION Glucotoxicity deteriorates the integrated pancreatic microcirculatory oxygen profile and bioenergetics,but this deterioration can be reversed by insulin administration.展开更多
<strong>Background:</strong> Urban air pollution contributes to lung and cardiovascular system dysfunction, making it a major concern for human health. Its impact on skin integrity, associated with increas...<strong>Background:</strong> Urban air pollution contributes to lung and cardiovascular system dysfunction, making it a major concern for human health. Its impact on skin integrity, associated with increased occurrence of atopic dermatitis, is now recognized, but its cellular mechanisms remain poorly understood. <strong>Objective:</strong> In the present study we aimed at establishing the impact of urban pollutant on mitochondrial dynamics and bioenergetics using the HaCaT cell model. We also sought to establish the protective effect of ECH-5195 (red <em>Panax ginseng</em> extract), standardized in ginsenosides, in reversing pollution-induced mitochondrial defects. <strong>Methods:</strong> Urban pollution exposure was mimicked by 1 h exposure of HaCaT cells with standardized atmospheric particulate matter containing PAHs, nitro-PAHs, PCB congeners, and chlorinated pesticides with a mean particulate diameter of 5.85 μm (SRM1648). <strong>Results:</strong> The presence of urban pollutant in the cultures increased the prevalence of hyperfission by 1.41-fold (p = 0.023) and fission by 1.35 fold (p = 0.006) in the reticular mitochondrial network. ECH-5195 reduced both pollution-induced hyperfission by 0.54-fold (p = 0.004) and fission by 0.68-fold (p = 0.0006) normalizing the mitochondrial reticular network. Pollution exposure was associated with a significant reduction of basal OCR and increased lactate production, pushing the cell to rely on glycolysis for ATP production. When ECH-5195 was used, OCR was significantly increased, and the glycolytic contribution to ATP production was reduced while both oxidative phosphorylation and mitochondrial respiration were increased demonstrating mitochondrial re-engagement in ATP production. <strong>Conclusions:</strong> Pollution exposure was disruptive for both the mitochondrial network dynamics and mitochondrial respiration. Ginsenosides in ECH-5195 efficiently protected both from pollution-induced defects.展开更多
Background:Adenosine triphosphatase inhibitory factor 1(IF1)is a key protein involved in energy metabolism.IF1 has been linked to various agerelated diseases,although its relationship with physical activity(PA)remains...Background:Adenosine triphosphatase inhibitory factor 1(IF1)is a key protein involved in energy metabolism.IF1 has been linked to various agerelated diseases,although its relationship with physical activity(PA)remains unclear.Additionally,the apolipoprotein A-I(apoA-I),a PA-modulated lipoprotein,could play a role in this relationship because it shares a binding site with IF1 on the cell-surface ATP synthase.We examined here the associations between chronic PA and plasma IF1 concentrations among older adults,and we investigated whether apoA-I mediated these associations.Methods:In the present work,1096 healthy adults(63.8%females)aged 70 years and over who were involved in the Multidomain Alzheimer Prevention Trial study were included.IF1 plasma concentrations(square root of ng/mL)were measured at the 1-year visit of the Multidomain Alzheimer Prevention Trial,while PA levels(square root of metabolic equivalent task min/week)were assessed using questionnaires administered each year from baseline to the 3-year visit.Multiple linear regressions were performed to investigate the associations between the first-year mean PA levels and IF1 concentrations.Mediation analyses were conducted to examine whether apoA-I mediated these associations.Mixedeffect linear regressions were carried out to investigate whether the 1-year visit IF1 concentrations predicted subsequent changes in PA.Results:Multiple linear regressions indicated that first-year mean PA levels were positively associated with IF1 concentrations(B=0.021;SE=0.010;p=0.043).Mediation analyses revealed that about 37.7%of this relationship was mediated by apoA-I(B_(ab)=0.008;SE=0.004;p=0.023).Longitudinal investigations demonstrated that higher concentrations of IF1 at the 1-year visit predicted a faster decline in PA levels over the subsequent 2 years(time×IF1:B=0.148;SE=0.066;p=0.025).Conclusion:This study demonstrates that regular PA is associated with plasma IF1 concentrations,and it suggests that apoA-I partly mediates this association.Additionally,this study finds that baseline concentrations of IF1 can predict future changes in PA.However,further research is needed to fully understand the mechanisms underlying these observations.展开更多
High glucose(HG)culture conditions in vitro and persistent exposure to hyperglycemia in diabetes patients are detrimental to stem cells,analogous to any other cell type in our body.It interferes with diverse signaling...High glucose(HG)culture conditions in vitro and persistent exposure to hyperglycemia in diabetes patients are detrimental to stem cells,analogous to any other cell type in our body.It interferes with diverse signaling pathways,i.e.mammalian target of rapamycin(mTOR)-phosphoinositide 3-kinase(PI3K)-Akt signaling,to impact physiological cellular functions,leading to low cell survival and higher cell apoptosis rates.While elucidating the underlying mechanism responsible for the apoptosis of adipose tissue-derived mesenchymal stem cells(MSCs),a recent study has shown that HG culture conditions dysregulate mTORPI3K-Akt signaling in addition to mitochondrial malfunctioning due to defective mitochondrial membrane potential(MtMP)that lowers ATP production.This organelle-level dysfunction energy-starves the cells and increases oxidative stress and ultrastructural abnormalities.Disruption of the mitochondrial electron transport chain produces an altered mitochondrial NAD+/NADH redox state as evidenced by a low NAD+/NADH ratio that primarily contributes to the reduced cell survival in HG.Some previous studies have also reported altered mitochondrial membrane polarity(causing hyperpolarization)and reduced mitochondrial cell mass,leading to perturbed mitochondrial homeostasis.The hostile microenvironment created by HG exposure creates structural and functional changes in the mitochondria,altering their bioenergetics and reducing their capacity to produce ATP.These are significant data,as MSCs are extensively studied for tissue regeneration and restoring their normal functioning in cell-based therapy.Therefore,MSCs from hyperglycemic donors should be cautiously used in clinical settings for cell-based therapy due to concerns of their poor sur-vival rates and increased rates of post engraftment proliferation.As hypergly-cemia alters the bioenergetics of donor MSCs,rectifying the loss of MtMP may be an excellent target for future research to restore the normal functioning of MSCs in hyperglycemic patients.展开更多
Nonalcoholic fatty liver disease(NAFLD) is today considered the most common form of chronic liver disease, affecting a high proportion of the population worldwide. NAFLD encompasses a large spectrum of liver damage, r...Nonalcoholic fatty liver disease(NAFLD) is today considered the most common form of chronic liver disease, affecting a high proportion of the population worldwide. NAFLD encompasses a large spectrum of liver damage, ranging from simple steatosis to steatohepatitis, advanced fibrosis and cirrhosis. Obesity, hyperglycemia, type 2 diabetes and hypertriglyceridemia are the most important risk factors. The pathogenesis of NAFLD and its progression to fibrosis and chronic liver disease is still unknown. Accumulating evidence indicates that mitochondrial dysfunction plays a key role in the physiopathology of NAFLD, although the mechanisms underlying this dysfunction are still unclear. Oxidative stress is considered an important factor in producing lethal hepatocyte injury associated with NAFLD. Mitochondrial respiratory chain is the main subcellular source of reactive oxygen species(ROS), which may damage mitochondrial proteins, lipids and mitochondrial DNA. Cardiolipin, a phospholipid located at the level of the inner mitochondrial membrane, plays an important role in several reactions and processes involved in mitochondrial bioenergetics as well as in mitochondrial dependent steps of apoptosis. This phospholipid is particularly susceptible to ROS attack. Cardiolipin peroxidation has been associated with mitochondrial dysfunction in multiple tissues in several physiopathological conditions, including NAFLD. In this review, we focus on the potential roles played by oxidative stress and cardiolipin alterations in mitochondrial dysfunction associated with NAFLD.展开更多
Hydrogen exhibits the potential to treat Alzheimer's disease. Stereotactic injection has been previously used as an invasive method of administering active hydrogen, but this method has limitations in clinical pra...Hydrogen exhibits the potential to treat Alzheimer's disease. Stereotactic injection has been previously used as an invasive method of administering active hydrogen, but this method has limitations in clinical practice. In this study, triple transgenic(3×Tg) Alzheimer's disease mice were treated with hydrogen-rich water for 7 months. The results showed that hydrogen-rich water prevented synaptic loss and neuronal death, inhibited senile plaques, and reduced hyperphosphorylated tau and neurofibrillary tangles in 3×Tg Alzheimer's disease mice. In addition, hydrogen-rich water improved brain energy metabolism disorders and intestinal flora imbalances and reduced inflammatory reactions. These findings suggest that hydrogen-rich water is an effective hydrogen donor that can treat Alzheimer's disease. This study was approved by the Animal Ethics and Welfare Committee of Shenzhen University, China(approval No. AEWC-20140615-002) on June 15, 2014.展开更多
Mitochondria are essential cellular organelles critical for generating adenosine triphosphate for cellular homeostasis, as well as various mechanisms that can lead to both necrosis and apoptosis. The field of ＂mi- to...Mitochondria are essential cellular organelles critical for generating adenosine triphosphate for cellular homeostasis, as well as various mechanisms that can lead to both necrosis and apoptosis. The field of ＂mi- tochondrial medicine＂ is emerging in which injury/disease states are targeted therapeutically at the level of the mitochondrion, including specific antioxidants, bioenergetic substrate additions, and membrane uncoupling agents. Consequently, novel mitochondrial transplantation strategies represent a potentially multifactorial therapy leading to increased adenosine triphosphate production, decreased oxidative stress, mitochondrial DNA replacement, improved bioenergetics and tissue sparing. Herein, we describe briefly the history of mitochondrial transplantation and the various techniques used for both in vitro and in vivo delivery, the benefits associated with successful transference into both peripheral and central nervous system tissues, along with caveats and pitfalls that hinder the advancements of this novel therapeutic.展开更多
Changes in the global environment such as ocean acidification （OA） may interact with anthropogenic pollutants including trace metals threatening the integrity of marine ecosystems. We analyze recent studies on the i...Changes in the global environment such as ocean acidification （OA） may interact with anthropogenic pollutants including trace metals threatening the integrity of marine ecosystems. We analyze recent studies on the interactive effects of OA and trace metals on marine organisms with a focus on the physiological basis of these interactions. Our analysis shows that the responses to elevated CO2 and metals are strongly dependent on the species, developmental stage, metal biochemistry and the degree of environmental hypercapnia, and cannot be directly predicted from the CO2-induced changes in metal solubility and speciation. The key physiological functions affected by both the OA and trace metal exposures involve acid-base regulation, pro- tein turnover and mitochondrial bioenergetics, reflecting the sensitivity of the underlying molecular and cellular pathways to CO2 and metals. Physiological interactions between elevated CO2 and metals may impact the organisms＇ capacity to maintain ac- id-base homeostasis and reduce the amount of energy available for fitness-related functions such as growth, development and re- production thereby affecting survival and performance of estuarine populations. Environmental hypercapnia may also affect the marine food webs by altering predator-prey interactions and the trophic transfer of metals in the food chain. However, our under- standing of the degree to which these effects can impact the function and integrity of marine ecosystems is limited due the scar- city of the published research and its bias towards certain taxonomic groups. Future research priorities should include studies of metal x Pco2 interactions focusing on critical physiological functions （including acid-base, protein and energy homeostasis） in a greater range of ecologically and economically important marine species, as well as including the field populations naturally ex- posed （and potentially adapted） to different levels of metals and CO2 in their environments [Current Zoology 61 （4）： 653-668, 2015].展开更多
Cardiogenic shock is the leading cause of death among patients hospitalized with acute myocardial infarction （MI）. Understanding the mechanisms for acute pump failure is therefore important. The aim of this study is...Cardiogenic shock is the leading cause of death among patients hospitalized with acute myocardial infarction （MI）. Understanding the mechanisms for acute pump failure is therefore important. The aim of this study is to examine in an acute MI dog model whether mitochondrial bio-energetic function within non-ischemic wall regions are associated with pump failure. Anterior MI was produced in dogs via ligation of left anterior descending （LAD） coronary artery, that resulted in an infract size of about 30% of the left ventricular wall. Measurements ofhemodynamic status, mitochondrial function, free radical production and mitochondrial uncoupling protein 3 （UCP3） expression were determined over 24 h period. Hemodynamic measurements revealed a 〉 50% reduction in cardiac output at 24 h post infarction when compared to baseline. Biopsy samples were obtained from the posterior non-ischemic wall during acute infarction. ADP/O ratios for isolated mitochondria from non-ischemic myocardium at 6 h and 24 h were decreased when compared to the ADP/O ratios within the same samples with and without palmitic acid （PA）. GTP inhibition of （PA）-stimulated state 4 respiration in isolated mitochondria from the non-ischemic wall increased by 7% and 33% at 6 h and 24 h post-infarction respectively when compared to sham and pre-infarction samples. This would suggest that the mitochondria are uncoupled and this is supported by an associated increase in UCP3 expression observed on western blots from these same biopsy samples. Blood samples from the coronary sinus measured by electron paramagnetic resonance （EPR） methods showed an increase in reactive oxygen species （ROS） over baseline at 6 h and 24 h post-infarction. In conclusion, mitochondrial bio-energetic ADP/O ratios as a result of acute infarction are abnormal within the non-ischemic wall. Mitochondria appear to be energetically uncoupled and this is associated with declining pump function. Free radical production may be associated with the induction of uncoupling proteins in the mitochondria.展开更多
The interest of this conference is agricultural, environmental, bioenergetics, and sanitary. In that context, domestic, agricultural and industrial environments produce organic waste, which needs to be collected, sele...The interest of this conference is agricultural, environmental, bioenergetics, and sanitary. In that context, domestic, agricultural and industrial environments produce organic waste, which needs to be collected, selected, stored and recycled properly in order to avoid environmental pollution and promote agriculture. The green Industry proposed involves the conversion of natural, non-toxic organic waste in order to efficiently produce organic fertilizers for agriculture. These types of fertilizers from biological origin are suitable because they are not toxic for human and the environment. Enzymatic reactions described in this presentation concern mainly the hydrolysis of proteins, sugars and lipids, the acidification of intermediate products from hydrolysis, the formation of acetate, and the production of methane. In other words, this review is timely as it discusses for the chemical behavior or the reactivity of different functional groups to better understand the enzymatic catalysis in the transformations of residual proteins, carbohydrates, and lipids to generate biomethane and fertilizers. In the same perspective, this review is to enrich the documentation related to organic reactions catalyzed by enzymes, which occur in the anaerobic degradation of residual organic substances, with emphasis on the structures of organic compounds and reaction mechanisms. This will allow understanding the displacement of the electrons of a reactive entity rich in electrons to another reactive entity that is poor in electrons to form new bonds in products.展开更多
The heart requires continuous ATP availability that is generated in the mitochondria.Althoughstudies using the cell culture and perfiused organ models have been carried out to investigate thebiochemistry in the mitoch...The heart requires continuous ATP availability that is generated in the mitochondria.Althoughstudies using the cell culture and perfiused organ models have been carried out to investigate thebiochemistry in the mitochondria in response to a change in substrate supply,mitochondrialbioenergetics of heart under normal feed or fasting conditions has not been studied at the tissuelevel with a sub-millimeter spatial resolution either in vivo or er vivo.Oxidation of many food-derived metabolites to generate ATP in the mitochondria is realized through the NADH/NAD+couple acting as a central electron carrier.We employed the Chance redox scanner thelow-temperat ure fluorescence scanner to image the three-dimensional(3D)spatial distribution of themitochondrial redox states in heart tissues of rats under normai feeding or an overnight star-vation for 14.5 h.Multiple consecutive sections of each heart were imaged to map three redoxindices,i.e,NADH,oxidized favoproteins Fp,including flavin adenine dinucleotide(FAD)andthe redox ratio NADH/Fp.The imaging results revealed the micro-heterogeneity and the spatial distribution of these redox indices.The quantitative analysis showed that in the fasted hearts thestandard deviation of both NADH and Fp,ie.,SD NADH and SDFp,significantly decreasedwith a p value of 0.032 and 0.045,respectively,indicating that the hearts become relatively morehomogeneous after fasting.The fasted hearts contained 28.6%less NADH(p=0.038).No sig.nificant change in Fp was foumnd(p=0.4).The NADH/Fp ratio decreased with a marginalP value(0.076).The decreased NADH im the fasted hearts is consistent with the cardiac celsreliance of fatty acids consumption for energy metabolism when glucose becomes scarce.Theexperimental o bservation of N ADH decrease induced by dietary restriction in the heart at tissuelevel has not been reported to our best knowledge.The Chance redox scanner demonstrated thefeasibility of 3D imaging of the mitochondrial redox st ate in the heart and provides a usefil toolto study heart metabolism and fiunction under normal,dietary-change and pathological con-ditions at tisue level. We would like to thank Dr.Joseph Baur for thehelpful discussion and Dr.Hui Qiao for animalpreparation and organ harvesting.展开更多
Several authors have addressed the importance of mitochondrial function in inflammatory syn-dromes,as it may play a role in the genesis of tissue injury.Sepsis and exposition to environmental particles are examples of...Several authors have addressed the importance of mitochondrial function in inflammatory syn-dromes,as it may play a role in the genesis of tissue injury.Sepsis and exposition to environmental particles are examples of inflammatory conditions.Sepsis occurs with an exacerbated inflammatory response that damages tissue mitochondria and impairs bioenergetic processes.One of the current hypotheses for the molecular mech-anisms underlying the complex condition of sepsis is that enhanced NO production and oxidative stress lead to mitochondrial dysfunction,bioenergetic derangement and organ failure.The mechanism of particulate mat-terhealth effects are believed to involve inflammation and oxidative stress.Components in particles that elicit inflammation have been poorly investigated,although recent research points out to the contribution of composi-tional elements and particle size.Oxygen metabolism and mitochondrial function appear to be important areas of study in inflammatory conditions for clarifying molecular mechanisms involved.展开更多
The experimental results showed that the duration of microbial retting processing of kenaf fibers by using aerobic microbe was four times shorter than that by using anaerobic microbe. The residual gum percentage,break...The experimental results showed that the duration of microbial retting processing of kenaf fibers by using aerobic microbe was four times shorter than that by using anaerobic microbe. The residual gum percentage,breaking strength, breaking elongation and linear density of aerobic retted kenaf bundle fibers did not show significantly difference with that of anaerobic retted kenaf bundle fibers by ANOVA-Tukey's studentized test at a = 5% except for the softness. The bioenergetic principle and the calculation of the amount of ATP produced during the decomposition processing of kenaf gums were used to explain why the retting duration in the case of using aerobic microbes was much shorter than that of using anaerobic microbes.展开更多
Normal cardiac function is accomplished through a continuous energy supply provided by mitochondria.Heart mitochondria are the major source of reactive oxygen and nitrogen species:superoxide anion(O_(2)^(-))and nitric...Normal cardiac function is accomplished through a continuous energy supply provided by mitochondria.Heart mitochondria are the major source of reactive oxygen and nitrogen species:superoxide anion(O_(2)^(-))and nitric oxide(NO).NO production by mitochondrial NOS(mtNOS)is modified by metabolic state and shows an exponential dependence on Δψ.The interaction between mtNOS and complexes I and IV might be a mechanism involved in the regulation of mitochondrial NO production.NO exerts a high affinity,reversible and physiological inhibition of cytochrome c oxidase activity.A second effect of NO on the respiratory chain is accomplished through its interaction with ubiquinol-cytochrome c oxidoreductase.The ability of mtNOS to regulate mitochondrial O_(2) uptake and O_(2)^(-)and H_(2)O_(2) productions through the interaction of NO with the respiratory chain is named mtNOS functional activity.Together,heart mtNOS allows NO to optimize the balance between cardiac energy production and utilization,and to regulate the steady-state concentrations of other oxygen and nitrogen species.展开更多
Living organisms are high ordered and organized systems accumulating and successively using low entropy energy to support all the processes needed for life. This low level of entropy is a required condition in order t...Living organisms are high ordered and organized systems accumulating and successively using low entropy energy to support all the processes needed for life. This low level of entropy is a required condition in order to make possible the use of endogenous energy for producing, for example, mechanical work. The commonly accepted picture of condensed matter physics, exclusively considering the perturbative coupling between QED Zero-Point-Field also known as “Quantum Vacuum” and the matter system, is unable to thoroughly explain the true origin of this low entropy energy reservoir and its dynamics. Recent researches instead suggested that energy and mass of every particle or body could be actually considered as arising from Quantum Vacuum dynamics which, in turn, can exhibit, under suitable conditions always occurring in the case of living systems, a coherent behavior characterized by a strong phase correlation between matter and an electromagnetic field trapped inside this ensemble. In this paper the preliminary model of Quantum Vacuum already proposed by author is reformulated in terms of QED coherence in condensed matter showing it is able to explain the origin of internal energy stock of living organisms. Within this theoretical framework, an interpretation of some important experimental results about biophotons emission by living systems under the influence of external stimuli is also proposed, suggesting their origin could also arise from Quantum Vacuum dynamics. This model, as shown, opens very interesting and exciting scenarios of further developments in the understanding of the birth and dynamics of life.展开更多
The degradation rate of Volatile Fatty Acids (VFAs) produced predominantly in the acidogenesis stage is a key process parameter to be optimised to ensure a successful Anaerobic digestion (AD). Thermodynamically, the o...The degradation rate of Volatile Fatty Acids (VFAs) produced predominantly in the acidogenesis stage is a key process parameter to be optimised to ensure a successful Anaerobic digestion (AD). Thermodynamically, the oxidation of the VFAs are energetically unfavourable, and as such external energy source apart from the energy derived from the hydrolysis of Adenosine Triphosphate (ATP) is needed for the initial activation of the VFAs, initial growth of the methanogens in AD process and improved degradation rate of the VFAs. Thus, this research investigated the influence of polyphosphate hydrolysis on the degradation rate of the VFAs at high concentration. Sodium-propionate, Sodium-butyrate and Sodium-acetate salts were added at the start of experiments in order to increase the concentration of the VFAs. The polyphosphate salts used were;Na-hexametaphosphate, Na-tripolyphosphate and potassium pyrophosphate. The control experiment was polyphosphate free and three process parameters (degradation rate, cumulative biogas production and specific methane content) of anaerobic digestion were investigated. The experiments were carried out at a mesophilic temperature of 37.5°C for 41 days. The results of the investigation showed that the treated reactors with the polyphosphate salt solution in low concentration performed better than the reactors with high concentration of the polyphosphate salts solution. All the treated reactors with poly-P salts performed better than reactor Nr-9 (control experiment), but reactor Nr-1 was outstanding with an improved degradation rate of 47%, cumulative biogas production of 21% and specific methane content of 23%.展开更多
文摘Cells undergo metabolic reprogramming to adapt to changes in nutrient availability, cellular activity, and transitions in cell states. The balance between glycolysis and mitochondrial respiration is crucial for energy production, and metabolic reprogramming stipulates a shift in such balance to optimize both bioenergetic efficiency and anabolic requirements. Failure in switching bioenergetic dependence can lead to maladaptation and pathogenesis. While cellular degradation is known to recycle precursor molecules for anabolism, its potential role in regulating energy production remains less explored. The bioenergetic switch between glycolysis and mitochondrial respiration involves transcription factors and organelle homeostasis, which are both regulated by the cellular degradation pathways. A growing body of studies has demonstrated that both stem cells and differentiated cells exhibit bioenergetic switch upon perturbations of autophagic activity or endolysosomal processes. Here, we highlighted the current understanding of the interplay between degradation processes, specifically autophagy and endolysosomes, transcription factors, endolysosomal signaling, and mitochondrial homeostasis in shaping cellular bioenergetics. This review aims to summarize the relationship between degradation processes and bioenergetics, providing a foundation for future research to unveil deeper mechanistic insights into bioenergetic regulation.
基金supported by Russian science foundation(grant 21-75-30009).
文摘Background: The active use of stem and progenitor cells in the therapy of various diseases requires thedevelopment of approaches for targeted modification of their properties. One such approach is the induction of a prooranti-inflammatory phenotype. Methods: In this study, we investigated the effect of a pro-inflammatoryenvironment in vitro on multipotent mesenchymal stromal cells (MSC) by incubation with lipopolysaccharide (LPS).iCELLigence real-time cell analysis system was used for monitoring cell culture growth. Cell energy metabolism wasassessed using the Seahorse XFp Analyzer. For the rat stroke experiment, we used a photoinduced thrombosis (PT)model;after 24 h of surgery, vehicle or MSC or LPS-treated MSC was injected i.v. With magnetic resonance imaging(MRI) we evaluated the volume of ischemic brain injury. For the effect of MSC on neurological deficit after PT weused three methods: limb placement test, cylinder test, and beam-walking test. Results: LPS exposure led to asignificant increase in cell growth rate and to changes in their energy metabolism: glycolytic activity increasedsignificantly in the MSC, and non-glycolytic acidification also increased, while basic respiratory parameters weremaintained. With MRI we didn’t reveal changes in the volume of brain damage between all rat groups. Neurologicaldeficit was less only with using untreated MSC injection. Conclusion: Using LPS-treated MSC in the therapy ofischemic stroke in rats, we did not observe an increase in the neuroprotective properties of the cells, but instead notedsome decrease in their therapeutic efficacy. We attribute these changes to the formation of a pro-inflammatoryphenotype in MSC.
基金supported by Science Foundation of China University of Petroleum,Beijing(Nos.2462017YJRC038 and 2462018BJC005)supported by the National Natural Science Foundation of China(Grant U1660118)+1 种基金the National Basic Research Program of China(973 Program,No.2014CB643300)the National Environmental Corrosion Platform(NECP)
文摘Microbiologically influenced corrosion （MIC） is a major cause of corrosion damages, facility failures, and financial losses, making MIC an important research topic. Due to complex microbiological activities and a lack of deep understanding of the interactions between biofilms and metal surfaces, MIC occurrences and mechanisms are difficult to predict and interpret. Many theories and mechanisms have been pro- posed to explain MIC. In this review, the mechanisms of MIC are discussed using hioenergetics, microbial respiration types, and biofilm extracellular electron transfer （EET）. Two main MIC types, namely EET-MIC and metabolite MIC （M-ME）, are discussed. This brief review provides a state of the art insight into MIC mechanisms and it helps the diagnosis and prediction of occurrences of MIC under anaerobic conditions in the oil and gas industry.
文摘Alzheimer’s disease （AD） is an increasingly pressing worldwide public-health, social, political and economic concern. Despite significant investment in multiple traditional therapeutic strategies that have achieved success in preclinical models addressing the pathological hallmarks of the disease, these efforts have not translated into any effective disease-modifying therapies. This could be because interventions are being tested too late in the disease process. While existing therapies provide symptomatic and clinical benefit, they do not fully address the molecular abnormalities that occur in AD neurons. The pathophysiology of AD is complex; mitochondrial bioenergetic deficits and brain hypometabolism coupled with increased mitochondrial oxidative stress are antecedent and potentially play a causal role in the disease pathogenesis. Dysfunctional mitochondria accumulate from the combination of impaired mitophagy, which can also induce injurious inflammatory responses, and inadequate neuronal mitochondrial biogenesis. Altering the metabolic capacity of the brain by modulating/potentiating its mitochondrial bioenergetics may be a strategy for disease prevention and treatment. We present insights into the mechanisms of mitochondrial dysfunction in AD brain as well as an overview of emerging treatments with the potential to prevent, delay or reverse the neurodegenerative process by targeting mitochondria.
基金Supported by the Beijing Municipal Natural Science Foundation,No.7212068the National Natural Science Foundation of China,No.81900747.
文摘BACKGROUND The pancreatic islet microcirculation adapts its metabolism to cope with limited oxygen availability and nutrient delivery.In diabetes,the balance between oxygen delivery and consumption is impaired.Insulin has been proven to exert complex actions promoting the maintenance of homeostasis of the pancreas under glucotoxicity.AIM To test the hypothesis that insulin administration can improve the integrated pancreatic microcirculatory oxygen profile and bioenergetics.METHODS The pancreatic microcirculatory partial oxygen pressure(PO_(2)),relative hemoglobin(rHb)and hemoglobin oxygen saturation(SO_(2))were evaluated in nondiabetic,type 1 diabetes mellitus(T1DM),and insulin-treated mice.A threedimensional framework was generated to visualize the microcirculatory oxygen profile.Ultrastructural changes in the microvasculature were examined using transmission electron microscopy.An Extracellular Flux Analyzer was used to detect the real-time changes in bioenergetics by measuring the oxygen consumption rate and extracellular acidification rate in islet microvascular endothelial cells(IMECs).RESULTS Significantly lower PO_(2),rHb,and SO_(2) values were observed in T1DM mice than in nondiabetic controls.Insulin administration ameliorated the streptozotocin-induced decreases in these microcirculatory oxygen parameters and improved the mitochondrial ultrastructural abnormalities in IMECs.Bioenergetic profiling revealed that the IMECs did not have spare respiratory capacity.Insulin-treated IMECs exhibited significantly greater basal respiration than glucotoxicity-exposed IMECs(P<0.05).An energy map revealed increased energetic metabolism in insulin-treated IMECs,with significantly increased ATP production,non-mitochondrial respiration,and oxidative metabolism(all P<0.05).Significant negative correlations were revealed between microcirculatory SO_(2) and bioenergetic parameters.CONCLUSION Glucotoxicity deteriorates the integrated pancreatic microcirculatory oxygen profile and bioenergetics,but this deterioration can be reversed by insulin administration.
文摘<strong>Background:</strong> Urban air pollution contributes to lung and cardiovascular system dysfunction, making it a major concern for human health. Its impact on skin integrity, associated with increased occurrence of atopic dermatitis, is now recognized, but its cellular mechanisms remain poorly understood. <strong>Objective:</strong> In the present study we aimed at establishing the impact of urban pollutant on mitochondrial dynamics and bioenergetics using the HaCaT cell model. We also sought to establish the protective effect of ECH-5195 (red <em>Panax ginseng</em> extract), standardized in ginsenosides, in reversing pollution-induced mitochondrial defects. <strong>Methods:</strong> Urban pollution exposure was mimicked by 1 h exposure of HaCaT cells with standardized atmospheric particulate matter containing PAHs, nitro-PAHs, PCB congeners, and chlorinated pesticides with a mean particulate diameter of 5.85 μm (SRM1648). <strong>Results:</strong> The presence of urban pollutant in the cultures increased the prevalence of hyperfission by 1.41-fold (p = 0.023) and fission by 1.35 fold (p = 0.006) in the reticular mitochondrial network. ECH-5195 reduced both pollution-induced hyperfission by 0.54-fold (p = 0.004) and fission by 0.68-fold (p = 0.0006) normalizing the mitochondrial reticular network. Pollution exposure was associated with a significant reduction of basal OCR and increased lactate production, pushing the cell to rely on glycolysis for ATP production. When ECH-5195 was used, OCR was significantly increased, and the glycolytic contribution to ATP production was reduced while both oxidative phosphorylation and mitochondrial respiration were increased demonstrating mitochondrial re-engagement in ATP production. <strong>Conclusions:</strong> Pollution exposure was disruptive for both the mitochondrial network dynamics and mitochondrial respiration. Ginsenosides in ECH-5195 efficiently protected both from pollution-induced defects.
基金supported by grants from the Region Occitanie/Pyrénées-Méditerranée(Grant No.1901175)the European Regional Development Fund(ERDF)(Grant No.MP0022856)+4 种基金This study received funding from la Fédération Française de Cardiologie”(FFC,Dotation Recherche),Alzheimer Prevention in Occitania and Catalonia(APOC Chair of Excellence-Inspire Program)Saint Louis University.The MAPT study was supported by grants from the Gérontopôle of Toulouse,the French Ministry of Health(PHRC 2008,2009)Pierre Fabre Research Institute(manufacturer of the omega-3 supplement)ExonHit Therapeutics SA,and Avid Radiopharmaceuticals,Inc.The promotion of this study was supported by the University Hospital Center of ToulouseThe data-sharing activity was supported by the Association Monegasque pour la Recherche sur la Maladie d'Alzheimer(AMPA)and the INSERM-University of Toulouse III UMR 1295(CERPOP)Research Unit.
文摘Background:Adenosine triphosphatase inhibitory factor 1(IF1)is a key protein involved in energy metabolism.IF1 has been linked to various agerelated diseases,although its relationship with physical activity(PA)remains unclear.Additionally,the apolipoprotein A-I(apoA-I),a PA-modulated lipoprotein,could play a role in this relationship because it shares a binding site with IF1 on the cell-surface ATP synthase.We examined here the associations between chronic PA and plasma IF1 concentrations among older adults,and we investigated whether apoA-I mediated these associations.Methods:In the present work,1096 healthy adults(63.8%females)aged 70 years and over who were involved in the Multidomain Alzheimer Prevention Trial study were included.IF1 plasma concentrations(square root of ng/mL)were measured at the 1-year visit of the Multidomain Alzheimer Prevention Trial,while PA levels(square root of metabolic equivalent task min/week)were assessed using questionnaires administered each year from baseline to the 3-year visit.Multiple linear regressions were performed to investigate the associations between the first-year mean PA levels and IF1 concentrations.Mediation analyses were conducted to examine whether apoA-I mediated these associations.Mixedeffect linear regressions were carried out to investigate whether the 1-year visit IF1 concentrations predicted subsequent changes in PA.Results:Multiple linear regressions indicated that first-year mean PA levels were positively associated with IF1 concentrations(B=0.021;SE=0.010;p=0.043).Mediation analyses revealed that about 37.7%of this relationship was mediated by apoA-I(B_(ab)=0.008;SE=0.004;p=0.023).Longitudinal investigations demonstrated that higher concentrations of IF1 at the 1-year visit predicted a faster decline in PA levels over the subsequent 2 years(time×IF1:B=0.148;SE=0.066;p=0.025).Conclusion:This study demonstrates that regular PA is associated with plasma IF1 concentrations,and it suggests that apoA-I partly mediates this association.Additionally,this study finds that baseline concentrations of IF1 can predict future changes in PA.However,further research is needed to fully understand the mechanisms underlying these observations.
文摘High glucose(HG)culture conditions in vitro and persistent exposure to hyperglycemia in diabetes patients are detrimental to stem cells,analogous to any other cell type in our body.It interferes with diverse signaling pathways,i.e.mammalian target of rapamycin(mTOR)-phosphoinositide 3-kinase(PI3K)-Akt signaling,to impact physiological cellular functions,leading to low cell survival and higher cell apoptosis rates.While elucidating the underlying mechanism responsible for the apoptosis of adipose tissue-derived mesenchymal stem cells(MSCs),a recent study has shown that HG culture conditions dysregulate mTORPI3K-Akt signaling in addition to mitochondrial malfunctioning due to defective mitochondrial membrane potential(MtMP)that lowers ATP production.This organelle-level dysfunction energy-starves the cells and increases oxidative stress and ultrastructural abnormalities.Disruption of the mitochondrial electron transport chain produces an altered mitochondrial NAD+/NADH redox state as evidenced by a low NAD+/NADH ratio that primarily contributes to the reduced cell survival in HG.Some previous studies have also reported altered mitochondrial membrane polarity(causing hyperpolarization)and reduced mitochondrial cell mass,leading to perturbed mitochondrial homeostasis.The hostile microenvironment created by HG exposure creates structural and functional changes in the mitochondria,altering their bioenergetics and reducing their capacity to produce ATP.These are significant data,as MSCs are extensively studied for tissue regeneration and restoring their normal functioning in cell-based therapy.Therefore,MSCs from hyperglycemic donors should be cautiously used in clinical settings for cell-based therapy due to concerns of their poor sur-vival rates and increased rates of post engraftment proliferation.As hypergly-cemia alters the bioenergetics of donor MSCs,rectifying the loss of MtMP may be an excellent target for future research to restore the normal functioning of MSCs in hyperglycemic patients.
文摘Nonalcoholic fatty liver disease(NAFLD) is today considered the most common form of chronic liver disease, affecting a high proportion of the population worldwide. NAFLD encompasses a large spectrum of liver damage, ranging from simple steatosis to steatohepatitis, advanced fibrosis and cirrhosis. Obesity, hyperglycemia, type 2 diabetes and hypertriglyceridemia are the most important risk factors. The pathogenesis of NAFLD and its progression to fibrosis and chronic liver disease is still unknown. Accumulating evidence indicates that mitochondrial dysfunction plays a key role in the physiopathology of NAFLD, although the mechanisms underlying this dysfunction are still unclear. Oxidative stress is considered an important factor in producing lethal hepatocyte injury associated with NAFLD. Mitochondrial respiratory chain is the main subcellular source of reactive oxygen species(ROS), which may damage mitochondrial proteins, lipids and mitochondrial DNA. Cardiolipin, a phospholipid located at the level of the inner mitochondrial membrane, plays an important role in several reactions and processes involved in mitochondrial bioenergetics as well as in mitochondrial dependent steps of apoptosis. This phospholipid is particularly susceptible to ROS attack. Cardiolipin peroxidation has been associated with mitochondrial dysfunction in multiple tissues in several physiopathological conditions, including NAFLD. In this review, we focus on the potential roles played by oxidative stress and cardiolipin alterations in mitochondrial dysfunction associated with NAFLD.
基金supported by the National Natural Science Foundation of China,No.21771126(to XBD)the Shenzhen Bureau of Science,Technology and Information of China,No.JCYJ20180305124000597(to XBD)。
文摘Hydrogen exhibits the potential to treat Alzheimer's disease. Stereotactic injection has been previously used as an invasive method of administering active hydrogen, but this method has limitations in clinical practice. In this study, triple transgenic(3×Tg) Alzheimer's disease mice were treated with hydrogen-rich water for 7 months. The results showed that hydrogen-rich water prevented synaptic loss and neuronal death, inhibited senile plaques, and reduced hyperphosphorylated tau and neurofibrillary tangles in 3×Tg Alzheimer's disease mice. In addition, hydrogen-rich water improved brain energy metabolism disorders and intestinal flora imbalances and reduced inflammatory reactions. These findings suggest that hydrogen-rich water is an effective hydrogen donor that can treat Alzheimer's disease. This study was approved by the Animal Ethics and Welfare Committee of Shenzhen University, China(approval No. AEWC-20140615-002) on June 15, 2014.
基金funded by NIH R21NS096670(AGR)University of Kentucky Spinal Cord and Brain Injury Research Center Chair Endowment(AGR),NIH/NINDS 2P30NS051220
文摘Mitochondria are essential cellular organelles critical for generating adenosine triphosphate for cellular homeostasis, as well as various mechanisms that can lead to both necrosis and apoptosis. The field of ＂mi- tochondrial medicine＂ is emerging in which injury/disease states are targeted therapeutically at the level of the mitochondrion, including specific antioxidants, bioenergetic substrate additions, and membrane uncoupling agents. Consequently, novel mitochondrial transplantation strategies represent a potentially multifactorial therapy leading to increased adenosine triphosphate production, decreased oxidative stress, mitochondrial DNA replacement, improved bioenergetics and tissue sparing. Herein, we describe briefly the history of mitochondrial transplantation and the various techniques used for both in vitro and in vivo delivery, the benefits associated with successful transference into both peripheral and central nervous system tissues, along with caveats and pitfalls that hinder the advancements of this novel therapeutic.
基金This work was in part supported by funds provided by the National Science Foundation award I0S-095107 and UNC Charlotte＇s Faculty Research Grant to I.M.S.
文摘Changes in the global environment such as ocean acidification （OA） may interact with anthropogenic pollutants including trace metals threatening the integrity of marine ecosystems. We analyze recent studies on the interactive effects of OA and trace metals on marine organisms with a focus on the physiological basis of these interactions. Our analysis shows that the responses to elevated CO2 and metals are strongly dependent on the species, developmental stage, metal biochemistry and the degree of environmental hypercapnia, and cannot be directly predicted from the CO2-induced changes in metal solubility and speciation. The key physiological functions affected by both the OA and trace metal exposures involve acid-base regulation, pro- tein turnover and mitochondrial bioenergetics, reflecting the sensitivity of the underlying molecular and cellular pathways to CO2 and metals. Physiological interactions between elevated CO2 and metals may impact the organisms＇ capacity to maintain ac- id-base homeostasis and reduce the amount of energy available for fitness-related functions such as growth, development and re- production thereby affecting survival and performance of estuarine populations. Environmental hypercapnia may also affect the marine food webs by altering predator-prey interactions and the trophic transfer of metals in the food chain. However, our under- standing of the degree to which these effects can impact the function and integrity of marine ecosystems is limited due the scar- city of the published research and its bias towards certain taxonomic groups. Future research priorities should include studies of metal x Pco2 interactions focusing on critical physiological functions （including acid-base, protein and energy homeostasis） in a greater range of ecologically and economically important marine species, as well as including the field populations naturally ex- posed （and potentially adapted） to different levels of metals and CO2 in their environments [Current Zoology 61 （4）： 653-668, 2015].
文摘Cardiogenic shock is the leading cause of death among patients hospitalized with acute myocardial infarction （MI）. Understanding the mechanisms for acute pump failure is therefore important. The aim of this study is to examine in an acute MI dog model whether mitochondrial bio-energetic function within non-ischemic wall regions are associated with pump failure. Anterior MI was produced in dogs via ligation of left anterior descending （LAD） coronary artery, that resulted in an infract size of about 30% of the left ventricular wall. Measurements ofhemodynamic status, mitochondrial function, free radical production and mitochondrial uncoupling protein 3 （UCP3） expression were determined over 24 h period. Hemodynamic measurements revealed a 〉 50% reduction in cardiac output at 24 h post infarction when compared to baseline. Biopsy samples were obtained from the posterior non-ischemic wall during acute infarction. ADP/O ratios for isolated mitochondria from non-ischemic myocardium at 6 h and 24 h were decreased when compared to the ADP/O ratios within the same samples with and without palmitic acid （PA）. GTP inhibition of （PA）-stimulated state 4 respiration in isolated mitochondria from the non-ischemic wall increased by 7% and 33% at 6 h and 24 h post-infarction respectively when compared to sham and pre-infarction samples. This would suggest that the mitochondria are uncoupled and this is supported by an associated increase in UCP3 expression observed on western blots from these same biopsy samples. Blood samples from the coronary sinus measured by electron paramagnetic resonance （EPR） methods showed an increase in reactive oxygen species （ROS） over baseline at 6 h and 24 h post-infarction. In conclusion, mitochondrial bio-energetic ADP/O ratios as a result of acute infarction are abnormal within the non-ischemic wall. Mitochondria appear to be energetically uncoupled and this is associated with declining pump function. Free radical production may be associated with the induction of uncoupling proteins in the mitochondria.
文摘The interest of this conference is agricultural, environmental, bioenergetics, and sanitary. In that context, domestic, agricultural and industrial environments produce organic waste, which needs to be collected, selected, stored and recycled properly in order to avoid environmental pollution and promote agriculture. The green Industry proposed involves the conversion of natural, non-toxic organic waste in order to efficiently produce organic fertilizers for agriculture. These types of fertilizers from biological origin are suitable because they are not toxic for human and the environment. Enzymatic reactions described in this presentation concern mainly the hydrolysis of proteins, sugars and lipids, the acidification of intermediate products from hydrolysis, the formation of acetate, and the production of methane. In other words, this review is timely as it discusses for the chemical behavior or the reactivity of different functional groups to better understand the enzymatic catalysis in the transformations of residual proteins, carbohydrates, and lipids to generate biomethane and fertilizers. In the same perspective, this review is to enrich the documentation related to organic reactions catalyzed by enzymes, which occur in the anaerobic degradation of residual organic substances, with emphasis on the structures of organic compounds and reaction mechanisms. This will allow understanding the displacement of the electrons of a reactive entity rich in electrons to another reactive entity that is poor in electrons to form new bonds in products.
基金supported by the Center of Magnetic Resonance and Optical Imaging(CMROn)--an NIH supported research resource P41RR02305(R.Reddy)。
文摘The heart requires continuous ATP availability that is generated in the mitochondria.Althoughstudies using the cell culture and perfiused organ models have been carried out to investigate thebiochemistry in the mitochondria in response to a change in substrate supply,mitochondrialbioenergetics of heart under normal feed or fasting conditions has not been studied at the tissuelevel with a sub-millimeter spatial resolution either in vivo or er vivo.Oxidation of many food-derived metabolites to generate ATP in the mitochondria is realized through the NADH/NAD+couple acting as a central electron carrier.We employed the Chance redox scanner thelow-temperat ure fluorescence scanner to image the three-dimensional(3D)spatial distribution of themitochondrial redox states in heart tissues of rats under normai feeding or an overnight star-vation for 14.5 h.Multiple consecutive sections of each heart were imaged to map three redoxindices,i.e,NADH,oxidized favoproteins Fp,including flavin adenine dinucleotide(FAD)andthe redox ratio NADH/Fp.The imaging results revealed the micro-heterogeneity and the spatial distribution of these redox indices.The quantitative analysis showed that in the fasted hearts thestandard deviation of both NADH and Fp,ie.,SD NADH and SDFp,significantly decreasedwith a p value of 0.032 and 0.045,respectively,indicating that the hearts become relatively morehomogeneous after fasting.The fasted hearts contained 28.6%less NADH(p=0.038).No sig.nificant change in Fp was foumnd(p=0.4).The NADH/Fp ratio decreased with a marginalP value(0.076).The decreased NADH im the fasted hearts is consistent with the cardiac celsreliance of fatty acids consumption for energy metabolism when glucose becomes scarce.Theexperimental o bservation of N ADH decrease induced by dietary restriction in the heart at tissuelevel has not been reported to our best knowledge.The Chance redox scanner demonstrated thefeasibility of 3D imaging of the mitochondrial redox st ate in the heart and provides a usefil toolto study heart metabolism and fiunction under normal,dietary-change and pathological con-ditions at tisue level. We would like to thank Dr.Joseph Baur for thehelpful discussion and Dr.Hui Qiao for animalpreparation and organ harvesting.
文摘Several authors have addressed the importance of mitochondrial function in inflammatory syn-dromes,as it may play a role in the genesis of tissue injury.Sepsis and exposition to environmental particles are examples of inflammatory conditions.Sepsis occurs with an exacerbated inflammatory response that damages tissue mitochondria and impairs bioenergetic processes.One of the current hypotheses for the molecular mech-anisms underlying the complex condition of sepsis is that enhanced NO production and oxidative stress lead to mitochondrial dysfunction,bioenergetic derangement and organ failure.The mechanism of particulate mat-terhealth effects are believed to involve inflammation and oxidative stress.Components in particles that elicit inflammation have been poorly investigated,although recent research points out to the contribution of composi-tional elements and particle size.Oxygen metabolism and mitochondrial function appear to be important areas of study in inflammatory conditions for clarifying molecular mechanisms involved.
文摘The experimental results showed that the duration of microbial retting processing of kenaf fibers by using aerobic microbe was four times shorter than that by using anaerobic microbe. The residual gum percentage,breaking strength, breaking elongation and linear density of aerobic retted kenaf bundle fibers did not show significantly difference with that of anaerobic retted kenaf bundle fibers by ANOVA-Tukey's studentized test at a = 5% except for the softness. The bioenergetic principle and the calculation of the amount of ATP produced during the decomposition processing of kenaf gums were used to explain why the retting duration in the case of using aerobic microbes was much shorter than that of using anaerobic microbes.
基金supported by research grants from the University of Buenos Aires(UBACYT 200-201-101-00140 and 200-201-301-00731)Agencia Nacional de Promoción Científica y Tecnológica(PICT 2012-0964)Consejo Nacional de Investigaciones Científicas y Técnicas(PIP 112-201-101-00444).
文摘Normal cardiac function is accomplished through a continuous energy supply provided by mitochondria.Heart mitochondria are the major source of reactive oxygen and nitrogen species:superoxide anion(O_(2)^(-))and nitric oxide(NO).NO production by mitochondrial NOS(mtNOS)is modified by metabolic state and shows an exponential dependence on Δψ.The interaction between mtNOS and complexes I and IV might be a mechanism involved in the regulation of mitochondrial NO production.NO exerts a high affinity,reversible and physiological inhibition of cytochrome c oxidase activity.A second effect of NO on the respiratory chain is accomplished through its interaction with ubiquinol-cytochrome c oxidoreductase.The ability of mtNOS to regulate mitochondrial O_(2) uptake and O_(2)^(-)and H_(2)O_(2) productions through the interaction of NO with the respiratory chain is named mtNOS functional activity.Together,heart mtNOS allows NO to optimize the balance between cardiac energy production and utilization,and to regulate the steady-state concentrations of other oxygen and nitrogen species.
文摘Living organisms are high ordered and organized systems accumulating and successively using low entropy energy to support all the processes needed for life. This low level of entropy is a required condition in order to make possible the use of endogenous energy for producing, for example, mechanical work. The commonly accepted picture of condensed matter physics, exclusively considering the perturbative coupling between QED Zero-Point-Field also known as “Quantum Vacuum” and the matter system, is unable to thoroughly explain the true origin of this low entropy energy reservoir and its dynamics. Recent researches instead suggested that energy and mass of every particle or body could be actually considered as arising from Quantum Vacuum dynamics which, in turn, can exhibit, under suitable conditions always occurring in the case of living systems, a coherent behavior characterized by a strong phase correlation between matter and an electromagnetic field trapped inside this ensemble. In this paper the preliminary model of Quantum Vacuum already proposed by author is reformulated in terms of QED coherence in condensed matter showing it is able to explain the origin of internal energy stock of living organisms. Within this theoretical framework, an interpretation of some important experimental results about biophotons emission by living systems under the influence of external stimuli is also proposed, suggesting their origin could also arise from Quantum Vacuum dynamics. This model, as shown, opens very interesting and exciting scenarios of further developments in the understanding of the birth and dynamics of life.
文摘The degradation rate of Volatile Fatty Acids (VFAs) produced predominantly in the acidogenesis stage is a key process parameter to be optimised to ensure a successful Anaerobic digestion (AD). Thermodynamically, the oxidation of the VFAs are energetically unfavourable, and as such external energy source apart from the energy derived from the hydrolysis of Adenosine Triphosphate (ATP) is needed for the initial activation of the VFAs, initial growth of the methanogens in AD process and improved degradation rate of the VFAs. Thus, this research investigated the influence of polyphosphate hydrolysis on the degradation rate of the VFAs at high concentration. Sodium-propionate, Sodium-butyrate and Sodium-acetate salts were added at the start of experiments in order to increase the concentration of the VFAs. The polyphosphate salts used were;Na-hexametaphosphate, Na-tripolyphosphate and potassium pyrophosphate. The control experiment was polyphosphate free and three process parameters (degradation rate, cumulative biogas production and specific methane content) of anaerobic digestion were investigated. The experiments were carried out at a mesophilic temperature of 37.5°C for 41 days. The results of the investigation showed that the treated reactors with the polyphosphate salt solution in low concentration performed better than the reactors with high concentration of the polyphosphate salts solution. All the treated reactors with poly-P salts performed better than reactor Nr-9 (control experiment), but reactor Nr-1 was outstanding with an improved degradation rate of 47%, cumulative biogas production of 21% and specific methane content of 23%.
