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At least 1,621 records · Page 90Linked to original sources
PubMed1985

Sensitivity of oligomycin-inhibited respiration of isolated rat liver mitochondria to perfluidone, a fluorinated arylalkylsulfonamide.

Oxygen electrode polarographic measurements of the rate of oxygen consumption by isolated rat liver mitochondria revealed that oligomycin inhibition of respiration was offset to different degrees by varying concentrations of perfluidone (1,1,1-trifluoro-N-(2 methyl-4-(phenylsulfonyl) methanesulfonamide). Using any of pyruvate-malate, succinate or ascorbate-TMPD (N,N,N',N'-tetramethyl-p-phenylenediamine) as substrate, this herbicidal and anti-inflammatory agent at 100 microM concentration caused a 5-fold stimulation of oligomycin-inhibited respiration. Higher concentrations of the herbicide (greater than or equal to 120 microM) gave lower stimulatory effects. Similar stimulatory effects were obtained with 1 microM FCCP (carbonylcyanide p-trifluoromethyoxyphenyl-hydrazone), a classical protonophore. Our results also show an enhanced oligomycin-sensitive ATPase action in intact mitochondria incubated with ATP and varying concentrations of perfluidone. Maximum enhancement effect (111.3%) was obtained at 120 microM perfluidone. FCCP (1 microM) stimulated this ATPase action by 130%. An initial inhibition of respiration by oligomycin is due to an interaction with the proton well of FOF1-ATP synthetase (Lardy, H.A. et al., Arch. Biochem. Biophys., 78 (1953) 587). Perfluidone probably increases the proton conductance of mitochondrial inner membrane in the same manner as FCCP and thus causes an increase in mitochondrial respiratory rate. As protons move into the matrix, delta mu H+, the proton electrochemical potential gradient becomes very small and the F0F1-ATP synthetase functions in the direction of hydrolysis of ATP rather than its shnthesis (Mitchell, P., Eur. J. Biochem., 95 (1979) 1). These findings therefore indicate that perfluidone acts in a way similar to FCCP, a classical uncoupler and protonophore.

Adenosine Triphosphatases↗
PubMed1995

Nitric oxide produced by activated astrocytes rapidly and reversibly inhibits cellular respiration.

Cultured astrocytes, activated to express the inducible form of nitric oxide synthase, produced up to 1 microM nitric oxide (NO) measured by a NO-selective electrode, while non-activated cells produced no detectable NO. The production of NO was associated with an inhibition of cellular respiration, measured simultaneously by an oxygen electrode. The inhibition of respiration was rapidly reversed by inhibiting the NO synthase or by binding the NO with haemoglobin. The respiratory inhibition had an NO, oxygen and substrate dependence consistent with NO-inhibition at cytochrome oxidase. This is the first demonstration that cells can reversibly inhibit mitochondrial respiration via NO production. This inhibition is large and potentially important in a range of pathophysiological conditions.

Animals↗
PubMed1987

The activating effects of bicarbonate on sperm motility and respiration at ejaculation.

Mature porcine sperm preserved in the cauda epididymis are quiescent. At ejaculation, they are mixed with the seminal vesicle fluid containing HCO3- and are rapidly activated. The role of HCO3- on the sperm activation process at ejaculation was studied in vitro. HCO3- quickly increased the motility, respiration rate and cAMP content of the porcine epididymal sperm. The extent of activation was proportional to the pCO2 in the medium. The activating effect of HCO3- on the motility was observed even in the absence of fructose as well as in the presence of KCN. 8-Bromoadenosine 3',5'-cyclic monophosphate and theophylline showed similar activating effects to that of HCO3-. However, HCO3(-)-free seminal plasma, Ca2+, amino acids, intermediates of the Krebs cycle, substrates of respiration and increases in the intracellular pH, extracellular pH or ionic strength of the medium had no effect. Fructose sustained the active state of the sperm and gradually increased both the motility and respiration rate when the dose of HCO3- was low. The anion channel blocker enhanced the activating effect of HCO3-. These results suggest that, upon ejaculation, HCO3- is a unique activator in vivo which makes the quiescent sperm motile via the HCO3(-)-adenylate cyclase-cAMP system, to which an endogenous HCO3- derived from metabolic CO2 may be related.

Animals↗
PubMed1991

In vivo regulation of mitochondrial respiration in cardiomyocytes: specific restrictions for intracellular diffusion of ADP.

Relative diffusivities of ADP and creatine in cardiomyocytes were studied. The isolated rat cardiomyocytes were lysed with saponin (40 micrograms/ml) to perforate or completely disrupt sarcolemma that was evidenced by leakage of 80-100% lactate dehydrogenase. In these cardiomyocytes mitochondria were used as 'enzymatic probes' to determine the average local concentration of substrates exerting acceptor control of respiration--ADP or creatine (the latter activates respiration via mitochondrial creatine kinase reaction)--when their concentrations in the surrounding medium were changed. The kinetic parameters for ADP and creatine in control of respiration of saponin-treated cardiomyocytes were compared with those determined in isolated mitochondria and skinned cardiac fibers. The apparent Km for creatine (at 0.2 mM ATP) was very close and in a range of 6.0-6.9 mM in all systems studied, showing the absence of diffusion difficulties for this substrate. On the contrary, the apparent Km for ADP increased from 18 +/- 1 microM for isolated mitochondria to 250 +/- 59 microM for cardiomyocytes with the lysed sarcolemma and to 264 +/- 57 microM for skinned fibers. This elevation of Km was not eliminated by inhibition of myokinase with diadenosine pentaphosphate. When 25 mM creatine was present, the apparent Km for ADP decreased to 36 +/- 6 microM. These data are taken to indicate specific restrictions of diffusion of ADP most probably due to its interaction with intermediate binding sites in cardiomyocytes. The important role of phosphocreatine-creatine kinase system of energy transport is to overcome the restrictions in regulation of energy fluxes due to decreased diffusivity of ADP.

Adenosine Diphosphate↗
PubMed1984

A comparison of mitochondrial respiration and membrane lipid composition in the rat and marmoset following dietary lipid supplementation.

Rats and marmosets were fed different lipid supplemented diets and the phospholipid fatty acid composition and the respiration rate of liver and heart mitochondria were determined. For both species, diets of differing lipid saturation had little effect on the ratio of saturated to unsaturated fatty acids in the mitochondrial membranes, however the omega 6/omega 3 unsaturated fatty acid ratio was significantly altered by diets of different lipid saturation. In comparison to animals fed low fat diets, mitochondrial respiration in the marmoset was reduced by high fat diets irrespective of the dietary level of lipid saturation. This effect of high fat diets on mitochondrial respiration was not observed for the rat.

Animals↗
PubMed1986

Comparative studies on mitochondrial respiration in four strains of rats (Rattus norvegicus).

Mitochondrial respiration and ATP synthesis were examined in young rats of the Sprague-Dawley, Wistar, BHE and Zucker strains. Both lean and obese Zucker rats were studied. Pyruvate-supported state 3 respiration was highest in mitochondria from Sprague-Dawley rats and least in mitochondria from obese Zucker rats. Succinate-supported state 3 respiration was highest in the Wistar group and least in the Sprague-Dawley rats. There appeared to be no relationship between oxygen consumption and the genetic tendency for hepatic hyperlipogenesis. ATP synthesis was greatest in the obese Zucker rats and least in the Sprague-Dawley rats. Differences in liver weights and mitochondrial yields may explain, in part, these observed strain differences in mitochondrial activity.

Animals↗
PubMed1986

Effects of urea, trimethylamine oxide, and osmolality on respiration and citrulline synthesis by isolated hepatic mitochondria from Squalus acanthias.

The effects of osmolality and of urea and trimethylamine oxide on citrulline synthesis and respiration by isolated hepatic mitochondria from Squalus acanthias (spiny dogfish) were determined. Optimal rates of citrulline synthesis and of respiration, as well as maximal respiratory control ratios, were obtained when the osmolality was about 300 mOsm when physiological concentrations of urea and trimethylamine oxide were present, analogous to mammalian mitochondria. Urea and trimethylamine oxide do not act as osmolytes and do not significantly affect these rates. When glutamate is not saturating, increasing concentrations of urea over the range of concentrations of physiological significance (e.g. 0.1-0.5 M) significantly inhibit citrulline synthesis, but not respiration. This response to urea concentration may reflect a specific homeostatic mechanism for maintaining physiological concentrations of urea.

Animals↗
PubMed1985

Respiration of mitochondria from the gonads of the sea urchin, Strongylocentrotus droebachiensis: the effects of petroleum fractions on oxygen consumption.

The respiration of mitochondria from gonads of Strongylocentrotus droebachiensis has been studied in the presence of 2-oxoglutarate, glutamate and succinate. The rate of oxygen consumption increased with temperature between 4 and 20 degrees C. Removal of gametes from ripe gonads was necessary to obtain good respiring mitochondria. Equilibration of respiration media with various petroleum fractions reduced the rate of oxygen consumption and the coupling of O2 consumption to ADP utilization. Lighter fractions (leaded gasolines, unleaded gasoline and related fractions) were more deleterious than medium fractions (kerosene and fuel oil). Heavy fraction (bunker C, vacuum bottoms and crude oil) were least deleterious. Tetraethyl lead contributed to the toxicity of the leaded fractions.

Acclimatization↗
PubMed1989

2,3,7,8, tetrachlorodibenzo-p-dioxin induces oxygen activation associated with cell respiration.

We have investigated the influence of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on bioenergetic functions of isolated heart-mitochondria. Electron transfer and energy conservation activities were found to be decreased in the presence of very low amounts of the polychlorinated biphenyl compound (1.5 nmol/mg mitochondrial protein). The effect was greatest when substrates for complex I were used. In this case coupling of oxidative phosphorylation to respiration was drastically diminished, essentially at the expense of state 3 respiration, and P/O values were found around 2 instead of 3. Succinate-related energy conservation remained practically unaffected in the presence of TCDD, suggesting an interference of the toxic compound at coupling site I. SOD plus catalase were found to protect energy-linked respiration from the effect of dioxin indicating the involvement of superoxide radicals and H2O2 in the development of the observed phenomena. The present contribution provides experimental evidence on the formation of these oxygen species in the presence of TCDD. Furthermore, the site of action of TCDD is demonstrated and discussed in relation to the oxygen radical formation observed.

Animals↗
PubMed2004

Inhibition of mitochondrial respiration by the anticancer agent 2-methoxyestradiol.

2-Methoxyestradiol (2ME2), a naturally occurring metabolite of estradiol, is known to have antiproliferative, antiangiogenic, and proapoptotic activity. Mechanistically, 2ME2 has been shown to downregulate hypoxia-inducible factor 1alpha (HIF1alpha) and to induce apoptosis in tumour cells by generating reactive oxygen species (ROS). In this study we report that 2ME2 inhibits mitochondrial respiration in both intact cells and submitochondrial particles, and that this effect is due to inhibition of complex I of the mitochondrial electron transport chain (ETC). The prevention by 2ME2 of hypoxia-induced stabilisation of HIF1alpha in HEK293 cells was found not to be due to an effect on HIF1alpha synthesis but rather to an effect on protein degradation. This is in agreement with our recent observation using other inhibitors of mitochondrial respiration which bring about rapid degradation of HIF1alpha in hypoxia due to increased availability of oxygen and reactivation of prolyl hydroxylases. The concentrations of 2ME2 that inhibited complex I also induced the generation of ROS. 2ME2 did not, however, cause generation of ROS in 143B rho(-) cells, which lack a functional mitochondrial ETC. We conclude that inhibition of mitochondrial respiration explains, at least in part, the effect of 2ME2 on hypoxia-dependent HIF1alpha stabilisation and cellular ROS production. Since these actions of 2ME2 occur at higher concentrations than those known to inhibit cell proliferation, it remains to be established whether they contribute to its therapeutic effect.

2-Methoxyestradiol↗
PubMed2006

Polyglutamine expansion inhibits respiration by increasing reactive oxygen species in isolated mitochondria.

Huntington's disease results from expansion of the polyglutamine (PolyQ) domain in the huntingtin protein. Although the cellular mechanism by which pathologic-length PolyQ protein causes neurodegeneration is unclear, mitochondria appear central in pathogenesis. We demonstrate in isolated mitochondria that pathologic-length PolyQ protein directly inhibits ADP-dependent (state 3) mitochondrial respiration. Inhibition of mitochondrial respiration by PolyQ protein is not due to reduction in the activities of electron transport chain complexes, mitochondrial ATP synthase, or the adenine nucleotide translocase. We show that pathologic-length PolyQ protein increases the production of reactive oxygen species in isolated mitochondria. Impairment of state 3 mitochondrial respiration by PolyQ protein is reversed by addition of the antioxidants N-acetyl-L-cysteine or cytochrome c. We propose a model in which pathologic-length PolyQ protein directly inhibits mitochondrial function by inducing oxidative stress.

Acetylcysteine↗
PubMed2005

Reduction of respiration rates by forming aggregations in diapausing adults of the shield bug, Parastrachia japonensis.

Parastrachia japonensis adults in diapause live mostly in aggregated conditions and can survive more than 1 year on only water. In this study, we demonstrated that diapausing adults had a high tendency to form clusters with no sexual bias. When 3-40 insects were enclosed in chambers of equal volume used to measure respiration, oxygen consumption was reduced to nearly half that when a single individual was enclosed. However, this reduction in metabolic rate was lost when the bugs were prevented from having physical contact with other individuals, partly lost by being enclosed with dead individuals, totally lost with the ones being washed with dietylether, and not influenced by humidity. No such effect of aggregation on respiration was found in adults in the reproductive stage, nor in two other diapausing bugs, Erthesina fullo and Plautia crossata, which hibernate in groups. From these results, we concluded that the reduction in oxygen consumption in P. japonensis was due mostly to physical contact with other individuals and partly to chemical cue that functioned to settle them down and resulted in a greatly reduced respiration rate. This trait is an effective strategy that allows diapausing adults to conserve energy and prolong survival.

Animals↗
PubMed2005

Leaf miner-induced changes in leaf transmittance cause variations in insect respiration rates.

Very little is known about alterations in microclimate when an herbivore feeds on host plant. Modifications of leaf transmittance properties induced by feeding activity of the leaf miner Phyllonorycter blancardella F. were measured using a spectrometer. Their effects on the herbivore's body temperature and respiration rate have been determined under controlled conditions and varying radiation level employing an infrared gas analyser. By feeding within leaf tissues, a miner induces the formation of feeding windows which transmit a large portion of incoming radiations within a mine. As a result, body temperature and respiration rate increase with radiation level when positioned below feeding windows. Therefore, the miner is not always protected from radiations despite living within plant tissues. The amount of CO(2) released by larvae below feeding windows at high radiation levels is about five-fold that recorded in the dark. By contrast, body temperature and respiration rate increase only slightly with radiation level when the insect is positioned below intact tissues through which radiation is only weakly transmitted. A mine offers its inhabitant a heterogeneous light environment that allows the insect larva to thermoregulate through behavioural modification. Our results highlight the importance of physical feedbacks induced by herbivory which alter significantly an insect's metabolism independently of its nutritional state.

Animals↗
PubMed1998

Selecting an adequate respiratory protective device: the choice between a respirator and breathing apparatus.

An adequate respiratory protective device should keep the concentration of the pollutant inside the facepiece below the appropriate occupational exposure limit. Filtering respirators will not provide adequate protection if the device fails in an atmosphere which is immediately dangerous to life or health (IDLH). It has therefore been suggested that in contaminant concentrations above an IDLH level it is more appropriate to select breathing apparatus with an emergency breathing facility. In this paper IDLH levels published by the US National Institute of Occupational Safety and Health have been compared with UK occupational exposure limits. For some substances there was a relatively small difference between the IDLH level and the short-term occupational exposure limit (STEL). The median ratio of the IDLH level to the STEL was 10 for gases and vapours and 50 for aerosols. For almost half the substances with UK occupational exposure limits there is no IDLH value. It is concluded that the published IDLH concentrations are, on their own, an insufficient basis for selecting breathing apparatus over a filtering respirator. It is equally important to consider the likelihood that a filtering device may fail catastrophically since this determines the risk from wearing a respirator in an IDLH atmosphere. More emphasis should be placed on the control of potentially high exposure levels by means other than respiratory protection.

Equipment Failure↗
PubMed1977

Studies on the pathogenesis of ischemic cell injury. VII. Proton gradient and respiration of renal tissue cubes, renal mitochondrial and submitochondrial particles following ischemic cell injury.

Electron transport in tissue cubes, isolated mitochondria and submitochondria particles were examined as a function of ischemic time. It was found that electron transport remains active in all systems beyond the 2 hour ischemic time interval. The NADH stimulated respiration, however, declined after 2 hours of ischemia in ASU (Ammonia-Sephadex-Urea) particles followed by respiration with matrix-located dehydrogenases tested by substrates such as glutamate, alpha-ketoglutarate and pyruvate plus malate. Succinate dependent respiration remains active at control levels. In contrast proton gradient reveals changes in two phases: Phase A is characterized by gradually increasing gradient without valinomycin and by a rapidly declining gradient with valinomycin in the medium. Phase B is characterized by a declining proton gradient with or without valinomycin. It is suggested that the alteration of the proton gradient between 1 and 2 hours ischemia is an important factor contributing to irreversible cell injury.

Animals↗
PubMed1997

Alteration in the control of mitochondrial respiration by outer mitochondrial membrane and creatine during heart preservation.

OBJECTIVE: This study aimed to evaluate the nature and extent of mitochondrial alterations during heart preservation. METHODS: Rat hearts, isolated after cardioplegia in situ, were preserved for 6 or 15 h at 4 degrees C either by immersion in cardioplegic solution or by low-flow perfusion (0.3 ml/min) with cardioplegic solution. The energy state of hearts at the end of preservation was determined by 31P-NMR spectroscopy and functional recovery was evaluated on reperfusion. Variables of mitochondrial respiration (maximal rate of respiration in the presence of ADP = delta Vmax, apparent Km for ADP, effect of creatine) were evaluated on skinned fibers and compared with those determined in controls and in hearts subjected to 1 hour of ischemia at 37 degrees C. RESULTS: Serious mitochondrial alterations were detected in fibers from 15 h immersed hearts: decrease of delta Vmax and of apparent Km for ADP, loss of the stimulatory effect of creatine, and disruption of the outer mitochondrial membrane. The extent of alternations was more accentuated in fibers from normothermic ischemic hearts, in which some damage of the inner mitochondrial membrane also occurred. In fibers from hearts preserved for 6 h, no significant changes in mitochondrial variables could be detected. When the hearts were preserved under low-flow perfusion for 15 h, only the stimulatory effect of creatine on respiration was significantly decreased. The extent of the loss of the stimulatory effect of creatine paralleled the accumulation of inorganic phosphate (Pi) during preservation and the decrease in left ventricular function on reperfusion. CONCLUSIONS: Alterations related to the outer membrane and the intermembrane space are among the earliest signs of damage to mitochondrial function during heart preservation. These alterations could be attributed to the swelling of mitochondria under the effect of Pi. The determination of mitochondrial parameters in biopsy samples could allow a simple and rapid evaluation of energy-producing and transfer capacities of the myocardium.

Adenosine Diphosphate↗
PubMed1997

Impairment of respiration and oxidative phosphorylation by redox cyclers 2-nitrosofluorene and menadione.

The present study was designed to investigate the effects of 2-nitrosofluorene (NOF), a metabolite of carcinogenic 2-acetylaminofluorene, on mitochondrial respiration and oxidative phosphorylation. NOF reacts with the NADH:ubiquinone oxidoreductase (complex I) and consumes oxygen in a rotenone-insensitive manner. Unlike menadione, which is able to bypass the rotenone-block and to restore ATP-formation, NOF-induced electron flow was almost completely uncoupled. In normal respiration both redox-cyclers decreased the respiratory control and P/O ratios at low concentrations (2-20 nmol/mg) in NADH-dependent oxidation. With succinate as substrate, only NOF was significantly active. In contrast to NOF, the hydroxamic acid N-hydroxy-2-acetylaminofluorene (N-OH-AAF) impaired mitochondrial energy conversion only at much higher concentrations (80 nmol/mg). At concentrations > 10 nmol/mg, NOF inhibited electron flow through the respiratory chain in NADH- and succinate-dependent oxidation, as determined by dinitrophenolate-uncoupled respiration. The small protective effect of L-cysteine indicates that covalent binding of the nitroso-compound to SH-groups may not explain sufficiently the inhibitory effect of NOF. The results support the notion that redox cyclers impair oxidative phosphorylation by establishing alternative pathways for electron transport in the respiratory chain.

2,4-Dinitrophenol↗
PubMed2001

Regulation of apoptosis by respiration: cytochrome c release by respiratory substrates.

Cytochrome c release from mitochondria is essential for apoptosis. Using human myelogenous leukemia ML-1a, its respiration-deficient and reconstituted cells, we demonstrated that respiratory function is essential for tumor necrosis factor-induced cytochrome c release. In a cell free system using mitochondrial fraction from ML-1a, initiation of respiration by substrates for complexes I, II, and III but not IV released cytochrome c, suggesting that reduction of coenzyme Q or complex III is essential for cytochrome c release. In the same system, disruption of mitochondrial outer membrane was neither enough nor the cause for cytochrome c release by succinate. These observations define an early pathway in which a change in respiration releases cytochrome c.

Apoptosis↗