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Energy Charge (energy + charge)

Distribution by Scientific Domains

Medical Sciences	50%
Life Sciences	25%
Earth and Environmental Science	25%

Selected Abstracts

Microbial biomass and activity under oxic and anoxic conditions as affected by nitrate additions

JOURNAL OF PLANT NUTRITION AND SOIL SCIENCE, Issue 1 2006
Jens Dyckmans
Abstract Soil microbial activity, biomass, and community structure were examined during the transition from oxic to anoxic conditions after the addition of glucose and with or without nitrate addition. In two sets of treatments, samples were incubated for up to 35 d in closed ampoules either aerobically until oxygen was depleted or anoxically throughout the experiment. Heat-flow rate was monitored to indicate microbial activity. Microbial biomass and community structure were measured by adenylate and phospholipid fatty acid (PFLA) content, and adenylate energy charge (AEC) was used to monitor the physiological status of the microbial biomass. Microbial activity was highest under oxic conditions and abruptly decreased under anoxic conditions. Activity peaks were observed after about 9 d of anoxic conditions probably triggered by increased nutrient availability from dying microbial biomass, but these peaks were smaller after initial oxic incubation or nitrate addition. Microbial biomass was unchanged under oxic conditions but decreased under anoxic conditions. Most surviving microbes switched into dormancy. Changes in the microbial-population structure were small and occurred only after 9 d of anoxic incubation. The results show that the nutrient status and the availability of electron acceptors such as nitrate were important factors ruling the direction and the extent of shifts in the microbial activity and community structures due to anoxic conditions. Mikrobielle Biomasse und Aktivität unter oxischen und anoxischen Bedingungen in Abhängigkeit von Nitratzugabe Untersucht wurden Aktivität, Menge und Zusammensetzung der mikrobiellen Biomasse im Übergang von oxischen zu anoxischen Bedingungen in Bodenproben nach Zugabe von Glucose sowie mit und ohne Nitratzugabe. Bodenproben wurden bis zu 35 Tage in geschlossenen Gefäßen entweder oxisch bis zum Verbrauch des Sauerstoffs oder von Beginn an anoxisch inkubiert. Dabei wurde der Wärmefluss als Indikator für die mikrobielle Aktivität gemessen. Menge und Zusammensetzung der mikrobiellen Biomasse wurden über die Gehalte an Adenylaten und Phospholipidfettsäuren bestimmt. Der ,Adenylate Energy Charge" (AEC) wurde genutzt, um den physiologischen Status der mikrobiellen Biomasse zu bestimmen. Die mikrobielle Aktivität war unter oxischen Bedingungen am höchsten und ging unter anoxischen Bedingungen drastisch zurück. Aktivitätspeaks wurden nach etwa 10 Tagen anoxischer Inkubation beobachtet und waren vermutlich verursacht durch ein erhöhtes Nährstoffangebot aus der abgestorbenen Biomasse. Diese Peaks waren geringer nach vorhergehender oxischer Inkubation bzw. nach Nitratzugabe. Die mikrobielle Biomasse war unter oxischen Bedingungen unverändert, nahm aber unter anoxischen Bedingungen ab, die meisten überlebenden Mikroben waren dabei dormant. Änderungen in der mikrobiellen Gesellschaft traten nur in geringem Umfang und erst nach 9 Tagen anoxischer Inkubation auf. Unsere Ergebnisse zeigen, dass das Nährstoffangebot und die Verfügbarkeit von Elektronenakzeptoren wie z.,B. Nitrat wichtige Steuergrößen für Richtung und Ausmaß von Veränderungen in der mikrobiellen Aktivität und Zusammensetzung unter anoxischen Bedingungen sind. [source]

Metabolic responses in ischemic myocardium after inhalation of carbon monoxide

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 8 2009
K. AHLSTRÖM
Background: To clarify the mechanisms of carbon monoxide (CO) tissue-protective effects, we studied energy metabolism in an animal model of acute coronary occlusion and pre-treatment with CO. Methods: In anesthetized pigs, a coronary snare and microdialysis probes were placed. CO (carboxyhemoglobin 5%) was inhaled for 200 min in test animals, followed by 40 min of coronary occlusion. Microdialysate was analyzed for lactate and glucose, and myocardial tissue samples were analyzed for adenosine tri-phosphate, adenosine di-phosphate, and adenosine mono-phosphate. Results: Lactate during coronary occlusion was approximately half as high in CO pre-treated animals and glucose levels decreased to a much lesser degree during ischemia. Energy charge was no different between groups. Conclusions: CO in the low-doses tested in this model results in a more favorable energy metabolic condition in that glycolysis is decreased in spite of maintained energy charge. Further work is warranted to clarify the possible mechanistic role of energy metabolism for CO protection. [source]

Anaerobic homolactate fermentation with Saccharomyces cerevisiae results in depletion of ATP and impaired metabolic activity

FEMS YEAST RESEARCH, Issue 3 2009
Derek A. Abbott
Abstract Conversion of glucose to lactic acid is stoichiometrically equivalent to ethanol formation with respect to ATP formation from substrate-level phosphorylation, redox equivalents and product yield. However, anaerobic growth cannot be sustained in homolactate fermenting Saccharomyces cerevisiae. ATP-dependent export of the lactate anion and/or proton, resulting in net zero ATP formation, is suspected as the underlying cause. In an effort to understand the mechanisms behind the decreased lactic acid production rate in anaerobic homolactate cultures of S. cerevisiae, aerobic carbon-limited chemostats were performed and subjected to anaerobic perturbations in the presence of high glucose concentrations. Intracellular measurements of adenosine phosphates confirmed ATP depletion and decreased energy charge immediately upon anaerobicity. Unexpectedly, readily available sources of carbon and energy, trehalose and glycogen, were not activated in homolactate strains as they were in reference strains that produce ethanol. Finally, the anticipated increase in maximal velocity (Vmax) of glycolytic enzymes was not observed in homolactate fermentation suggesting the absence of protein synthesis that may be attributed to decreased energy availability. Essentially, anaerobic homolactate fermentation results in energy depletion, which, in turn, hinders protein synthesis, central carbon metabolism and subsequent energy generation. [source]

Metabolic responses in ischemic myocardium after inhalation of carbon monoxide

Imbalance of plasma membrane ion leak and pump relationship as a new aetiological basis of certain disease states

JOURNAL OF INTERNAL MEDICINE, Issue 6 2003
G. Ronquist
Abstract. The basis for life is the ability of the cell to maintain ion gradients across biological membranes. Such gradients are created by specific membrane-bound ion pumps [adenosine triphosphatases (ATPases)]. According to physicochemical rules passive forces equilibrate (dissipate) ion gradients. The cholesterol/phospholipid ratio of the membrane and the degree of saturation of phospholipid fatty acids are important factors for membrane molecular order and herewith a determinant of the degree of non-specific membrane leakiness. Other operative principles, i.e. specific ion channels can be opened and closed according to mechanisms that are specific to the cell. Certain compounds called ionophores can be integrated in the plasma membrane and permit specific inorganic ions to pass. Irrespective of which mechanism ions leak across the plasma membrane the homeostasis may be kept by increasing ion pumping (ATPase activity) in an attempt to restore the physiological ion gradient. The energy source for this work seems to be glycolytically derived ATP formation. Thus an increase in ion pumping is reflected by increased ATP hydrolysis and rate of glycolysis. This can be measured as an accumulation of breakdown products of ATP and end-products of anaerobic glycolysis (lactate). In certain disease entities, the balance between ATP formation and ion pumping may be disordered resulting in a decrease in inter alia (i.a.) cellular energy charge, and an increase in lactate formation and catabolites of adenylates. Cardiac syndrome X is proposed to be due to an excessive leakage of potassium ions, leading to electrocardiographic (ECG) changes, abnormal Tl-scintigraphy of the heart and anginal pain (induced by adenosine). Cocksackie B3 infections, a common agent in myocarditis might also induce an ionophore-like effect. Moreover, Alzheimer's disease is characterized by the formation of extracellular amyloid deposits in the brain of patients. Perturbation of cellular membranes by the amyloid peptide during the development of Alzheimer's disease is one of several mechanisms proposed to account for the toxicity of this peptide on neuronal membranes. We have studied the effects of the peptide and fragments thereof on 45Ca2+ -uptake in human erythrocytes and the energetic consequences. Treatment of erythrocytes with the ,1,40 peptide, results in qualitatively similar nucleotide pattern and decrease of energy charge as the treatment with Ca2+ -ionophore A23187. Finally, in recent studies we have revealed and published in this journal that a rare condition, Tarui's disease or glycogenosis type VII, primarily associated with a defect M-subunit of phosphofructokinase, demonstrates as a cophenomenon an increased leak of Ca2+ into erythrocytes. [source]

Microbial biomass and activity under oxic and anoxic conditions as affected by nitrate additions

Ethanol Self-Administration and Alterations in the Livers of the Cynomolgus Monkey, Macaca fascicularis

ALCOHOLISM, Issue 1 2007
Priscilla Ivester
Background: Most of the studies of alcoholic liver disease use models in which animals undergo involuntary administration of high amounts of ethanol and consume diets that are often high in polyunsaturated fatty acids. The objectives of this study were (1) to evaluate whether cynomolgus monkeys (Macaca fascicularis) drinking ethanol voluntarily and consuming a diet with moderate amounts of lipid would demonstrate any indices of alcoholic liver disease past the fatty liver stage and (2) to determine whether these alterations were accompanied by oxidative stress. Methods: Six adult male and 6 adult female cynomolgus monkeys were allowed to consume ethanol voluntarily for 18 to 19 months. Additional monkeys were maintained on the same consumption protocol, but were not provided with ethanol. During the course of the study, liver biopsy samples were monitored for lipid deposition and inflammation, serum for levels of liver enzymes, and urine for concentrations of the isoprostane (IsoP) metabolite, 2,3-dinor-5,6-dihydro-15-F2t -IsoP, a biomarker for oxidative stress. Liver mitochondria were monitored for respiratory control and liver for concentrations of neutral lipids, adenine nucleotides, esterified F2 isoprostanes, oxidized proteins, 4-hydroxynonenal (HNE)-protein adducts, and protein levels of cytochrome P-450 2E1 and 3A4. Results: Ethanol consumption ranged from 0.9 to 4.05 g/kg/d over the period of the study. Serum levels of aspartate amino transferase were elevated in heavy-consuming animals compared with those in ethanol-naïve or moderate drinkers. Many of the ethanol consumers developed fatty liver and most showed loci of inflammation. Both hepatic energy charge and phosphorylation potential were decreased and NADH-linked respiration was slightly, but significantly depressed in coupled mitochondria as a result of heavy ethanol consumption. The urinary concentrations of 2,3-dinor-5,6-dihydro-15-F2t -IsoP increased as high as 33-fold over that observed in ethanol-abstinent animals. Liver cytochrome P-450 2E1 concentrations increased in ethanol consumers, but there were no ethanol-elicited increases in hepatic concentrations of the esterified F2 isoprostanes, oxidized proteins, or HNE-protein adducts. Conclusion: Our studies show that cynomolgus monkeys undergoing voluntary ethanol consumption for 1.5 years exhibit many of the features observed in the early stages of human alcoholic liver disease. Ethanol-elicited fatty liver, inflammation, and elevated serum aspartate amino transferase were evident with a diet that contained modest amounts of polyunsaturated lipids. The dramatic increases in urinary IsoP demonstrated that the animals were being subjected to significant oxidative stress that correlated with their level of ethanol consumption. [source]

The effects of pentoxifylline on liver regeneration after portal vein ligation in rats

LIVER INTERNATIONAL, Issue 2 2007
Uzer Kucuktulu
Abstract Aim: To determine the effects of pentoxifylline, a methyl xanthine derivative on hepatic cell production of uninterferred lobe after portal vein branch ligation. Methods: Sixty-six rats were randomly allocated into 9 groups with 8 rats in PVL groups and 6 rats in sham operation groups. The portal branches of the median and the lateral liver lobes, corresponding to approximately 70% of the liver voluma were ligated in the PVL groups. The control group received 0.9% NaCl solution. The rats in the treatment groups received pentoxypilline at the dose of 50 mg/kg/dy. After 1,2,4 days of portal vein ligation in both PVL and PVNL lobes the levels of adenine nucleotides were determined and flowcytometric analysis of cell cycles were performed. Results: On the first day of portal branch ligation energy charge was significantly lower, in pentoxifylline treated group comparing to pentoxfylline untreated group, both in PVL and PVNL lobes (P<0.05). Proliferative indexes were 0.38 and 0.29 in pentoxifylline treated and pentoxifylline untreated PVNL lobes respectively (P<0.05). Conclusion: Pentoxifylline treatment resulted in an increase of percentage of calls entering mitosis phase on the first day after PVL, somehow accelerating the regenaration process. [source]

Oxidative stress due to anesthesia and surgical trauma: Importance of early enteral nutrition

MOLECULAR NUTRITION & FOOD RESEARCH (FORMERLY NAHRUNG/FOOD), Issue 6 2009
Katerina Kotzampassi
Abstract Anesthesia and surgical trauma are considered major oxidative and nitrosative stress effectors resulting in the development of SIRS. In this study we evaluated the usefulness of early enteral nutrition after surgical trauma. Sixty male Wistar rats were subjected to midline laparotomy and feeding-gastrostomy. Twenty of these rats served as controls after recovering from the operation stress. The remaining rats received, through gastrostomy, enteral nutrition or placebo-feeding for 24 h. Oxidative stress markers and CC chemokine production were evaluated in rat serum and liver tissue. The operation itself was found to increase nitric oxide (NO) and malondialdehyde (MDA) and to decrease superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), as well as liver tissue energy charge (EC) in relation to controls. The rats receiving enteral feeding exhibited statistically significantly lower levels of NO and MDA, and higher levels of SOD, GSH-Px, and liver EC, in relation to placebo feeding rats. The operation significantly increased the chemokines monocyte chemoattractant protein (MCP)-1 and regulated upon activation, normal T-cell expressed, and secreted (RANTES) in rat serum, while enteral nutrition caused a further significant increase in chemokine levels in serum. mRNA chemokine expression in liver was increased in a similar pattern. These findings indicate that early enteral feeding might play an important role after surgery ameliorating oxidative stress, affecting positively the hepatic EC and regulating, via chemokine production, cell trafficking, and healing process. [source]

Altered metabolic fluxes result from shifts in metabolite levels in sucrose phosphorylase-expressing potato tubers

PLANT CELL & ENVIRONMENT, Issue 10 2002
A. R. Fernie
Abstract As reported in a previous paper (Plant, Cell and Environment 24, 357,365, 2001), introduction of sucrose phosphorylase into the cytosol of potato results in increased respiration, an inhibition of starch accumulation and decreased tuber yield. Herein a more detailed investigation into the effect of sucrose phosphorylase expression on tuber metabolism, in order to understand why storage and growth are impaired is described. (1) Although the activity of the introduced sucrose phosphorylase was low and accounted for less than 10% of that of sucrose synthase its expression led to a decrease in the activities of enzymes of starch synthesis relative to enzymes of glycolysis and relative to total amylolytic activity. (2) Incubation of tuber discs in [14C]glucose revealed that the transformants display a two-fold increase of the unidirectional rate of sucrose breakdown. However this was largely compensated by a large stimulation of sucrose re-synthesis and therefore the net rate of sucrose breakdown was not greatly affected. Despite this fact major shifts in tuber metabolism, including depletion of sucrose to very low levels, higher rates of glycolysis, and larger pools of amino acids were observed in these lines. (3) Expression of sucrose phosphorylase led to a decrease of the cellular ATP/ADP ratio and energy charge in intact growing tubers. It was estimated that at least 30% of the ATP formed during respiration is consumed as a result of the large acceleration of the cycle of sucrose breakdown and re-synthesis in the transformants. Although the absolute rate of starch synthesis in short-term labelling experiments with discs rose, starch synthesis fell relative to other fluxes including respiration, and the overall starch content of the tubers was lower than in wild-type tubers. (4) External supply of amino acids to replace sucrose as an osmoticum led to a feed-back inhibition of glycolysis, but did not restore allocation to starch. (5) However, an external supply of the non-metabolizable sucrose analogue palatinose , but not sucrose itself , stimulated flux to starch in the transformants. (6) The results indicate that the impaired performance of sucrose phosphorylase-expressing tubers is attributable to decreased levels of sucrose and increased energy consumption during sucrose futile cycling, and imply that sucrose degradation via sucrose synthase is important to maintain a relatively large sucrose pool and to minimize the ATP consumption required for normal metabolic function in the wild type. [source]

Assessment of metabolic and immune changes in postspawning Pacific oyster Crassostrea gigas: identification of a critical period of vulnerability after spawning

AQUACULTURE RESEARCH, Issue 9 2010
Yan Li
Abstract This study investigates the vulnerable period in postspawning Pacific oysters (Crassostrea gigas) through physiological and immunological assessments. After spawning, the oyster condition index reduced by 50% and required 70 days to recover to the prespawning level. The mantle glycogen reduced quickly while the reduction in tissue protein occurred slowly. The mantle tissue also lost more protein than gills. The analysis of adenylate energy charge indicated that oysters were stressed in the first 8 days after spawning. As a result of spawning, haemocyte phagocytosis was reduced and remained at a low level for 3 days. In contrast, the reduction of haemolymph antimicrobial activity did not occur until 3 days after spawning and continued to decline until day 8. This immunesuppression was not directly correlated to the changes in haemocyte density. Our study suggests that the first 8 days after spawning are a critical period for oyster survival due to the loss of energy and low immunity. This study further improves our understanding of the coincidence between spawning and summer mortality in oyster aquaculture. [source]