Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “RESPIRATION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,585 records · Page 88Linked to original sources

Intraspecific litter diversity and nitrogen deposition affect nutrient dynamics and soil respiration.

Anthropogenic forces are concurrently reducing biodiversity and altering terrestrial nutrient cycles. As natural populations decline, genetic diversity within single species also declines. The consequences of intraspecific genetic loss for ecosystem functions are poorly understood, and interactions among intraspecific diversity, nitrogen deposition, and nutrient cycling are unknown. We present results from an experiment that simulated both a decline in biodiversity and an increase in nitrogen deposition. In soil microcosms, we tested effects of variation in intraspecific litter diversity and nitrogen deposition on soil respiration and nitrogen leaching. Increases in intraspecific litter diversity increased soil respiration overall, with the greatest increases in respiration occurring under high nitrogen deposition. Nitrogen deposition increased the amount of inorganic nitrogen leached, while the amount of dissolved organic nitrogen leached was correlated with initial litter chemistry (lignin concentration) and remained independent of litter diversity and nitrogen deposition treatments. Our results demonstrate the potential for losses in genetic diversity to interact with other global environmental changes to influence terrestrial nutrient cycles.

Ecosystem↗

Phenophases alter the soil respiration-temperature relationship in an oak-dominated forest.

Soil respiration (SR) represents a major component of forest ecosystem respiration and is influenced seasonally by environmental factors such as temperature, soil moisture, root respiration, and litter fall. Changes in these environmental factors correspond with shifts in plant phenology. In this study, we examined the relationship between canopy phenophases (pre-growth, growth, pre-dormancy, and dormancy) and SR sensitivity to changes in soil temperature (T(S)). SR was measured 53 times over 550 days within an oak forest in northwest Ohio, USA. Annual estimates of SR were calculated with a Q(10) model based on T(S) on a phenological (PT), or annual timescale (AT), or T(S) and soil volumetric water content (VWC) on a phenological (PTM) or annual (ATM) timescale. We found significant (p<0.01) difference in apparent Q(10) from year 2004 (1.23) and year 2005 (2.76) during the growth phenophase. Accounting for moisture-sensitivity increased model performance compared to temperature-only models: the error was -17% for the ATM model and -6% for the PTM model. The annual models consistently underestimated SR in summer and overestimated it in winter. These biases were reduced by delineating SR by tree phenophases and accounting for variation in soil moisture. Even though the bias of annual models in winter SR was small in absolute scale, the relative error was about 91%, and may thus have significant implications for regional and continental C balance estimates.

Models, Theoretical↗

Effects of various tetrahydroisoquinoline derivatives on mitochondrial respiration and the electron transfer complexes.

We report effect of various tetrahydroisoquinoline derivatives on mitochondrial respiration and the electron transfer complexes. Generally these compounds were potent inhibitors of NADH-linked mitochondrial state 3 respiration and complex I. Presence of a phenyl group at the C1 position or oxidation of N-methylated isoquinones into N-methylisoquinolinium ion augmented the potency to inhibit mitochondrial respiration and complex I. Many of these compounds have been identified in human brains. In view of the mitochondrial and oxidative stress hypothesis, our results suggest involvement of these neurotoxins as potential causes of mitochondrial failure in Parkinson's disease.

Animals↗

A membrane-bound nitrate reductase encoded by the narGHJI operon is responsible for anaerobic respiration in Halomonas maura.

The halophilic bacterium Halomonas maura is capable of anaerobic respiration on nitrates. By insertional mutagenesis with the minitransposon Tn-5 we obtained the mutant Tc62, which was incapable of anaerobic respiration on nitrates. An analysis of the regions adjacent to the transposon allowed us to characterize the membrane-bound anaerobic-respiratory nitrate reductase narGHJI gene cluster in H. maura. We identified consensus sequences for fumarate and nitrate reductase regulator (FNR)-like protein-binding sites in the promoter regions of the nar genes and consensus sequences corresponding to the NarL binding sites upstream of the nar genes. RT-PCR analysis showed that the narGHJI operon was expressed in response to anaerobic conditions when nitrate was available as electron acceptor. This membrane-bound nitrate reductase is the only enzyme responsible for anaerobic respiration on nitrate in H. maura. In this article we discuss the possible relationship between this enzyme and a dissimilatory nitrate-reduction-to-ammonia process (DNRA) in H. maura and its role in the colonization of the rhizosphere.

Anaerobiosis↗

Cytochrome C effect on respiration of heart mitochondria: influence of various factors.

The effect of exogenous cytochrome c on respiration rate of the rat and human heart mitochondria was assessed in situ, using permeabilized fibers. It was (i) much more pronounced in State 2 and 4 than in State 3 with all the respiratory substrates (pyruvate+malate, succinate, palmitoyl-CoA+carnitine and octanoyl-L-carnitine), (ii) different with different substrates, (iii) much higher after ischemia in both metabolic states, particularly in the case of succinate oxidation compared to pyruvate+malate, (iv) the highest in State 4 with succinate as a substrate. Similar results were obtained with the isolated rat and rabbit heart mitochondria. The differences in the degree of stimulation of mitochondrial respiration by cytochrome c and, thus, sensitivity of cytochrome c test in evaluation of the intactness/injury of outer mitochondrial membrane are probably determined by the differences in the cytochrome c role in the control of mitochondrial respiration in the above-described conditions.

Animals↗

Age and gender do not influence the ability to detect respiration by photoplethysmography.

OBJECTIVE: The non-invasive technique photoplethysmography (PPG) can detect changes in blood volume and perfusion in a tissue. Respiration causes variations in the peripheral circulation, making it possible to monitor breaths using an optical sensor attached to the skin. The respiratory-synchronous part of the PPG signal (PPGr) has been used to monitor respiration during anaesthesia, and in postoperative and neonatal care. Studies addressing possible differences in PPGr signal characteristics depending on gender or age are lacking. METHODS: We studied three groups of 16 healthy subjects each during normal breathing; young males, old males and young females, and calculated the concordance between PPGr, derived from a reflection mode PPG sensor on the forearm, and a reference CO(2 )signal. The concordance was quantified by using a squared coherence analysis. Time delay between the two signals was calculated. In this process, we compared three different methods for calculating time delay. RESULTS: Coherence values >or=0.92 were seen for all three groups without any significant differences depending on age or gender (p = 0.67). Comparison between the three different methods for calculating time delay showed a correlation r = 0.93. CONCLUSIONS: These results demonstrate clinically important information implying the possibility to register qualitative PPGr signals for respiration monitoring, regardless of age and gender.

Adult↗

Sequential neuromuscular changes in rhesus monkeys during the initial adaptation to oral respiration.

Experimental induction of oral respiration in primates altered the neuromuscular use of specific craniofacial muscles. Obstruction of the nasal passage in the rhesus monkey induced changes in the electromyographic discharge (EMG) of both mandibular and facial muscles during the first 6 months of adaptation. Eighteen craniofacial muscles were studied with regard to their type of neuromuscular pattern. The EMG discharge was analyzed in terms of whether it had a rhythmic discharge or a continuous recruitment of motor units. The results of the investigation revealed that certain muscles in the control monkey using nasal respiration could be rhythmically or continuously active, but no significant trend was apparent with either pattern over time. In contrast, a significant number of muscles became rhythmically active within the first month of adaptation to oral respiration in the experimental animals. The rhythmic pattern was evident in key muscles that actively depressed the mandible, protruded the tongue, altered the shape of the tongue, and raised the upper lip. Continuous activity was induced in the first month within the suprahyoid region and tongue but later, by the fifth month, in specific lip and elevator muscles. These results suggested that the neuromuscular system adapted immediately to nasal obstruction but would vary as to (1) which muscles would be important in the initial adaptation, (2) the mode of adaptation, and (3) the time when a particular pattern first began to be used.

Adaptation, Physiological↗

The effect of inorganic phosphate on creatine kinase in respiring rat heart mitochondria.

The ability of creatine to stimulate the respiration of rat heart mitochondria in vitro is reversibly affected by the concentration of inorganic phosphate. The rate of oxygen consumption due to post-ADP state-4 respiration in the presence of 20 mM creatine is reduced significantly when the potassium phosphate concentration is raised from 5 to 20 mM. State-3 respiration is reduced only by potassium phosphate concentrations higher than 20 mM. The rate of synthesis of creatine phosphate is also affected by phosphate concentration, and the apparent Km of the coupled reactions for ADP is significantly higher at 25 mM phosphate as compared to that at 5 mM phosphate. These observations are consistent with the hypothesis that inorganic phosphate acts as an effector molecule, regulating creatine phosphate synthesis by favoring the dissociation of mitochondrial creatine kinase from the mitochondrial membrane. Such regulation may be important in the case of cells undergoing partial or severe ischemia, where changes in phosphate concentration within this range have been reported.

Adenosine Diphosphate↗

Resting state respiration of mitochondria: reappraisal of the role of passive ion fluxes.

Rat liver mitochondria respiring under resting state conditions in the presence of oligomycin were rapidly blocked with cyanide and the dissipation of the membrane potential, measured with a tetraphenylphosphonium-sensitive electrode, was followed over time. The plot of the rate of membrane potential dissipation versus the actual value of the membrane potential was nonlinear and identical to the plot of resting state respiration (titrated with small amounts of a respiratory inhibitor) versus the membrane potential. The relationship between the respiratory chain activity and the proton-motive force in mitochondria oxidizing succinate with either oxygen or ferricyanide as electron acceptors was also found to be identical. These results are interpreted as an indication that the passive permeability of the inner mitochondrial membrane toward ions is far more significant in maintaining resting state respiration than is the molecular slippage of the pumps in the respiratory chain. These results also confirm the non-ohmic characteristics of the inner mitochondrial membrane.

Animals↗

Inhibition of mitochondrial respiration by neutral, monocationic, and dicationic bis-pyridines related to the dopaminergic neurotoxin 1-methyl-4-phenylpyridinium cation (MPP+).

The cytotoxic effect of the dopaminergic neurotoxin 1-methyl-4-phenylpyridinium (MPP+) is believed to be associated with a compromise in cellular energy arising as a consequence of its persistent inhibition of mitochondrial respiration. MPP+ is a rather weak inhibitor of electron transport, but it undergoes passive accumulation inside actively respiring mitochondria in response to the transmembrane electrochemical potential gradient. In order to test the prediction that dicationic analogs of MPP+ might be concentrated to a much greater extent and thereby exert especially potent inhibition of respiration on the intact organelle, we synthesized four differently spaced bis-pyridines, each in neutral, monocationic, and dicationic forms, and evaluated their inhibitory activities in intact mitochondria and in electron transport particles (ETP). Compared to the neutrals, the monocations and especially the dications exhibit reduced inhibition in ETP, but the inhibition in mitochondria is enhanced selectively for the cationic inhibitors presumably on account of their accumulation in the mitochondrial matrix. This enhancement is limited by the relatively poor ability of the cationic bis-pyridines to enter mitochondria, as judged from experiments which evaluated the rate of onset of inhibition (without preincubation), in the absence and presence of tetraphenylborate (TPB-). The dications appear to be transported less well than the monocations, and only the most lipophilic dication exhibited a substantially greater accumulation-dependent enhancement of inhibitory activity on mitochondria than did the corresponding monocation. The compounds studied here constitute a novel class of respiratory chain probes which may be useful for a variety of studies on mitochondria.

1-Methyl-4-phenylpyridinium↗

Inactivation and reactivation of mitochondrial respiration by charged detergents.

Respiration of submitochondrial preparations can be inhibited by the cationic detergent cetyl trimethyl ammonium bromide and the anionic detergent sodium dodecyl sulfate in the range of 0.3-2 mumol of detergent per mg of mitochondrial membrane protein depending on the substrate and detergent used. This inhibition can be rapidly reversed by neutralizing a given detergent by the detergent of the opposite charge. At higher levels of the inhibiting detergent, no such reactivation was observed. Spin labeling assays of membrane structure were used to correlate structural effects with the loss and recovery of respiratory functions. Because the detergents progressively disrupt membrane structure, mitochondrial were cross-linked with bifunctional imidoesters to an extent that osmotic properties and detergent lysis were gone, but respiration remained. Such fixed respiring mitochondria also show inhibition reactivation phenomena.

Binding, Competitive↗

Energy transduction in photosynthetic bacteria. X. Composition and function of the branched oxidase system in wild type and respiration deficient mutants of Rhodopseudomonas capsulata.

The respiratory chain of Rhodopseudomonas capsulata, strain St. Louis and of two respiration deficient mutants (M6 and M7) has been investigated by examining the redox and spectral characteristics of the cytochromes and their response to substrates and to specific respiratory inhibitors. Since the specific lesions of M6 and M7 have been localized on two different branches of the multiple oxidase system of the wild type strain, the capability for aerobic growth of these mutants can be considered as a proof of the physiological significance of both branched systems "in vivo". Using M6 and M7 mutants the response of the branched chain to respiratory inhibitors could be established. Cytochrome oxidase activity, a specific function of an high potential cytochrome b (E'0 = +413 mV) is sensitive to low concentrations of KCN (5-10(-5) M); CO is a specific inhibitor of an alternative oxidase, which is also inhibited by high concentrations of KCN (10(-3) M). Antimycin A inhibits preferentially the branch of the chain affected by low concentrations of cyanide. Redox titrations and spectral data indicate the presence in the membrane of three cytochromes of b type (E'0 = +413, +260, +47 vM) and two cytochromes of c type (E'0 = +342, +94 mV). A clear indication of the involvement in respiration of cytochrome b413, cytochrome c342 and cytochrome b47 has been obtained. Only 50% of the dithionite reducible cytochrome b can be reduced by respiratory substrates also in the presence of high concentrations of KCN or in anaerobiosis. The presence and function of quinones in the respiratory electron transport system has been clearly demonstrated. Quinones, which are reducible by NADH and succinate to about the same extent can be reoxidized through both branches of the respiratory chain, as shown by the response of their redox state to KCN. The possible site of the branching of the electron transport chain has been investigated comparing the per cent level of reduction of quinones and of cytochromes b and c as a function of KCN concentrations in membranes from wild type and M6 mutants cells. The site of the branching has been localized at the level of quinones-cytochrome b47. A tentative scheme of the respiratory chains operating in Rhodopseudomonas capsulata, St. Louis and in the two respiration deficient mutants, M6 and M7 is presented.

Anaerobiosis↗

Influence of different energy drains on the interrelationship between the rate of respiration, proton-motive force and adenine nucleotide patterns in isolated mitochondria.

The respiration of rat liver mitochondria was stimulated by three different ways of energy drain: (a) partial uncoupling (equivalent to direct collapse of the proton-motive force), (b) intramitochondrial utilization of ATP for citrulline synthesis, and (c) extramitochondrial utilization of ATP for glucose phosphorylation. At identical rates of respiration, the intramitochondrial ATP : ADP ratios were the same in all three systems. Furthermore, the proton-motive force was the same in partially uncoupled mitochondria and in the presence of hexokinase plus glucose up to a respiration rate amounting to about 60% of that of the fully active state. However, external ATP : ADP ratios were considerably different in various systems at comparable rates of oxygen uptake, being the lowest under conditions when ATP was being utilized externally. On this basis, it is concluded that the respiratory rate is controlled directly by the proton-motive force and the mitochondrial ATP-synthesizing system operates under near-equilibrium conditions with respect to the membrane energy state parameters. However, a disequilibrium exists at the step of the transport of ATP from mitochondria to the external (cytoplasmic) compartment.

Adenosine Diphosphate↗

An investigation on the effect of oligomycin on state-4 respiration in isolated rat-liver mitochondria.

The inhibitory action of oligomycin on State-4 respiration in rat-liver mitochondria has been investigated in detail with regard to the extent, mode and characteristics of the inhibition. The possibility that this effect may be due either to some damage of the mitochondrial preparation used or to the presence of heavy contaminations by microsomes has been excluded. It has been found that the concentration of specific binding sites is the same in State 4 as in State 3. The extent of the inhibition appears to be related to the ADP concentration, rather than to ATP/ADP ratios. The inhibition of this antibiotic on State-4 respiration does not depend on the experimental conditions used (i.e., choice of substrates or composition of the reaction medium). In agreement with these observations, it has been found that the membrane potential of State 4 is significantly increased when oligomycin is added. All these results provide further evidence to the conclusion that a large portion of State-4 respiration is linked to phosphorylation.

Adenosine Diphosphate↗

Control of state 3 respiration in liver mitochondria from rats subjected to chronic ethanol consumption.

Male Sprague-Dawley rats were pair-fed a liquid diet containing 36% of calories as ethanol for at least 31 days. Mitochondria were isolated from the livers and assayed for state 3, state 4 and uncoupled respiration at all three coupling sites. Assay conditions were established that maximized state 3 respiration with each substrate while maintaining a high respiratory control ratio. In mitochondria from ethanol-fed animals, state 3 respiratory rates were decreased at all three coupling sites. The decreased state 3 rate observed at site III was still significantly higher than the state 3 rates observed at site II in mitochondria from either ethanol-fed or control animals. Moreover, the maximal (FCCP-uncoupled) rates with succinate and alpha-ketoglutarate were the same in mitochondria from ethanol-fed and control animals, whereas with glutamate-malate as substrate it was lowered 23% by chronic ethanol consumption. To investigate the role of cytochrome oxidase in modulating the respiratory rate with site I and site II substrates, the effects of cyanide on state 3 and FCCP-uncoupled respiration were determined. When the mitochondria were uncoupled there was no decrease in the rate of succinate oxidation until the rates of ascorbate and succinate oxidation became equivalent. Conversely, parallel inhibition of ascorbate, succinate and glutamate-malate state 3 respiratory rates were observed at all concentrations (1-50 microM) of cyanide utilized. These observations suggest strongly that in coupled mitochondria ethanol-elicited decreases in cytochrome oxidase activity depress the state 3 respiratory rates with site I and II substrates.

Adenosine Triphosphate↗

Regulation of mitochondrial resting state respiration: slip, leak, heterogeneity?

The contribution of molecular slippage of proton pumps, of proton leak and of coupling heterogeneity of mitochondrial population to the well-known non-linear interrelationship between resting state respiration and the protonmotive force is discussed in view of the following experimental findings. (1) After blocking mitochondrial respiration with cyanide, the rate of dissipation of the membrane potential is non-linearly dependent on the actual membrane potential, similarly to the resting state respiration in mitochondria titrated with small amounts of an inhibitor. In contrast, delta pH dissipates proportionally to its actual value. (2) The rate of electron flow from succinate to ferricyanide depends upon the protonmotive force, similarly to the flow from succinate to oxygen. This strongly suggests that the H+/e- stoichiometry in complexes III and IV of the respiratory chain is constant. (3) Mitochondria 'in situ', in permeabilized Ehrlich ascites cells, exhibit the same non-linear flux/force relationship as isolated mitochondria. These results strongly suggest that the non-ohmic characteristics of the inner mitochondrial membrane, with respect to protons driven by the membrane potential but not by the concentration gradient, is the main factor responsible for the nonlinear flux/force relationship in resting state mitochondria.

Animals↗

On isolated hepatocytes mitochondrial swelling induced in hypoosmotic medium does not affect the respiration rate.

In isolated hepatocytes incubated in hypoosmotic media, a large increase in the mitochondrial volume is not directly involved in the activation of respiration. Moreover, results of the quantification of the various bioenergetic parameters are not in accordance with an activation of the respiratory chain as previously proposed (Halestrap, A.P. (1989) Biochim. Biophys. Acta, 973, 355-382), but point more to an inhibition of respiration. The same respiration rate is obtained in hypoosmolar incubation media in vitro and in situ for a higher overall thermodynamic driving force over the electron transport chain.

Adenosine Diphosphate↗

K+-dependent Na+ transport driven by respiration in Escherichia coli cells and membrane vesicles.

Respiration-driven Na+ transport from Escherichia coli cells and right-side-out membrane vesicles is strictly dependent on K+. Cells from an E. colic mutant deficient in three major K+ transport systems were incapable of accumulating K+ or expelling Na+ unless valinomycin was added. Membrane vesicles from an E. coli mutant from which the genes encoding the two known electrogenic Na+/nH+ antiporters nhaA and nhaB were deleted transported Na+ as well as did vesicles from wild-type cells. Quantitative analysis of Delta psi and Delta pH showed a high driving force for electrogenic Na+/nH+ antiport whether K+ was present or not, although Na+ transport occurred only in its presence. These results suggest that an Na+/nH+ antiporter is not responsible for the Na+ transport. Respiration-driven efflux of Na+ from vesicles was found to be accompanied by primary uphill efflux of K+. Also, no respiration-dependent efflux of K+ was observed in the absence of Na+. Such coupling between Na+ and K+ fluxes may be explained by the operation of an Na+, K+/H+ antiporter previously described in E. coli membrane vesicles (Verkhovskay, M.L., Verkhovsky, M.I. and Wikström, M. (1995) FEBS Lett. 363, 46-48). Active Na+ transport is abolished when delta mu H+ is eliminated by a protonophore, but at low concentrations the protonophore actually accelerated Na+ transport. Such an effect may be expected if the Na+, K+/H+ antiporter normally operates in tight conjunction with respiratory chain complexes, thus exhibiting some phenomenological properties of a primary redox-linked sodium pump.

Biological Transport↗