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PubMed1978

Proton electrochemical gradient and rate of controlled respiration in mitochondria.

The correlation between deltamuH, the proton electrochemical potential difference, and the rate of controlled respiration is analyzed. deltamuH (the proton concentration gradient) is measured on the distribution of [3H]acetate, and deltapsi (the membrane potential) on the distribution of 86Rb+, 45Ca2+ and [3H]triphenylmethylphosphonium used either alone or simultaneously. The effects of the addition of ADP + hexokinase (state-3 ADP) and of carbonylcyanide trifluoromethoxyphenylhydrazone (state-3 uncoupler) on respiration and deltamuH are not equivalent: the uncoupler depresses deltamuH more than ADP at equivalent respiratory rates. The effects of the additions of nigericin-valinomycin and of ionophore A23187 (state-3 cation transport) and of carbonylcyanide trifluoromethoxy-phenylhydrazone (state 3-uncoupler) on respiration and deltamuH are also not equivalent: the uncoupler depresses deltamuH more than A23187 and nigericin + valinomycin at equivalent respiratory rate. A23187 is very efficient in stimulating respiration with negligible deltamuH changes.

Adenosine Diphosphate↗
PubMed1979

The respiration of brain mitochondria and its regulation by monovalent cation transport.

The Na+ and K+ permeability properties of rat brain mitochondria were determined to explain the influences of these cations upon respiration. A new procedure for isolating exceptionally intact mitochondria with minimal contamination by synaptosomes was developed for this purpose. Respiration was uncoupled by Na+ and less so by K+. Uncoupling was maximal in the presence of EDTA plus Pi and was decreased by Mg2+. Maximal uncoupler-stimulated respiration rates were inhibited by Na+ but largely unaffected by K+. The inhibition by Na+ was relatively insensitive to Mg2+. Membrane Na+ and K+ conductances as well as neutral exchanges (Na+/H+ and K+/H+ antiport activities) were determined by swelling measurements and correlated with metabolic effects of the cations. Cation conductance, i.e. electrophoretic Na+ or K+ permeation, was increased by EDTA (Na+ greater than K+) and decreased by Mg2+. Magnesium preferentially suppressed Na+ conductance so as to reverse the cation selectivity (K+ greater than Na+). Neutral cation/H+ exchange rates (Na+ greater than K+) were not influenced by chelator or Mg2+. The extent of cation-dependent uncoupling of respiration correlated best with the inner membrane conductance of the ion according to an empirical relationship derived with the model K+ conductor valinomycin. The metabolic influences of Na+ and K+ can be explained in terms of coupled flow of these ions with protons and their effect upon the H+ electrochemical gradient although alternative possibilities are discussed. These in vitro studies are compared to previous observations in situ to assess their physiological significance.

Animals↗
PubMed1983

Control of mitochondrial respiration. The contribution of the adenine nucleotide translocator depends on the ATP- and ADP-consuming enzymes.

The consequence of the complexity of the metabolic network on the amount of control strength of adenine nucleotide translocator was investigated with isolated rat liver mitochondria. Two experimental systems were compared: (i) mitochondria in the presence of yeast hexokinase (hexokinase system) and (ii) the same system plus additional pyruvate kinase (pyruvate kinase system). In both systems the control strength was analysed for the adenine nucleotide translocator by inhibitor titration studies with carboxyatractyloside and for the hexokinase or pyruvate kinase by changing their relative activities. Experimental results were compared with computer simulation of these systems and that of a third one, where the extramitochondrial ATP/ADP ratio was held constant by perifusion (perifusion system). The results demonstrate quite different flux-dependent control strength of the translocator in the three systems. In the hexokinase system the control strength of the translocator on mitochondrial respiration was zero up to respiration rates of about 60 nmol O2/mg protein per min. For higher rates, the control strength increased until the maximum value (0.45) was reached in the fully active state. Here, the same value was also found in the pyruvate kinase system. In all other states of respiration the translocator exerts a higher control strength in the pyruvate kinase system than in the hexokinase system. This different behaviour was attributed to the various changes in the adenine nucleotide pattern caused by partial inhibition of the translocator in the hexokinase and pyruvate kinase system. The data clearly show that the sharing of control strength depends not only on the respiration rate but also on the complexity of the metabolic system.

Adenosine Diphosphate↗
PubMed1983

Phosphorylating efficiency of isolated rat liver mitochondria respiring under the conditions of steady-State 4.

A limited, but significant net formation of ATP was observed during the very first period of respiratory State 4. The synthesis appeared to depend on respiration, since it was completely inhibited by KCN or by 2,4-dinitrophenol. Accordingly, State 4 respiration was observed to be inhibited to a large extent by oligomycin. After the initial increase, the level of ATP remained unmodified under the conditions of steady-state 4. Also, the maintenance of the equilibrium level of ATP was very sensitive to KCN or 2,4-dinitrophenol. Under the very same conditions of State 4, the mitochondria exhibited a significant ATPase activity, which appeared to be competitively inhibited by ADP. Therefore, it might be concluded that the apparently constant level of ATP observed in State 4 results from a balanced equilibrium between a respiration-dependent synthesis and a continuous hydrolysis. A comparison between the amount of ATP hydrolysed in State 4 and the amount of oxygen consumed under the same conditions indicated that the phosphorylating efficiency of respiring mitochondria in State 4 is as high as in State 3.

2,4-Dinitrophenol↗
PubMed1984

Inhibitory action of hexavalent chromium (Cr(VI)) on the mitochondrial respiration and a possible coupling to the reduction of Cr(VI).

The reduction of hexavalent chromium (Cr(VI] in isolated liver mitochondria was studied under different redox conditions in the respiratory chain. With 25 microM Na2CrO4 the rates were 1.6 +/- 0.7, 13.9 +/- 0.6 and 12.7 +/- 0.7 nmole Cr(VI) reduced 15 min/mg protein with the electron transport chain oxidized, reduced and only complex 1 reduced respectively. Electrons from succinate, bypassing complex 1, were apparently unavailable for Cr(VI)-reduction. The kinetics of chromate reduction was studied with only complex 1 in a reduced state. A rapid and a slow phase were found, probably corresponding to different electron donors in the mitochondria. Blocking the free thiols with N-ethylmaleimide lead to less than 10% decrease in the rapid initial Cr(VI)-reduction and to about 20% decrease during the whole incubation period (15 min). The amounts of free thiols were moderately decreased (15%) in chromate treated mitochondria during the slow reduction of Cr(VI) only. SH-groups may thus participate as reductants during the slow reduction phase. The respiration rate was inhibited about 50% by 25 microM Na2CrO4 when the mitochondria oxidized NAD-linked substrates. In contrast, succinate stimulated respiration was inhibited 50% by 3.6 mM Na2CrO4. The observed inhibition was Na2CrO4 in the micromolar range was therefore probably localized at complex 1 and may be coupled to the reduction of Cr(VI) at the same place. The respiration of isolated hepatocytes was also affected by Na2CrO4. Five micromolar chromate caused 5-10% inhibition. The inhibitory action of chromate on the mitochondrial respiration may thus constitute an important cytotoxic mechanism.

Animals↗
PubMed1989

Cerebral mitochondrial respiration in diabetic and chronically hypoglycemic rats.

The respiratory function of cerebral mitochondria harvested from genetically diabetic (BB/W) and streptozotocin-diabetic rats deprived of insulin for 3-4 weeks was found to be unchanged from control values. Furthermore, insulin-deprived BB/W rats subjected to 30 min of insulin-induced hypoglycemic coma demonstrated a normal mitochondrial respiration following a 60 min period of glucose restitution, a finding consistent with earlier results in non-diabetic rats. However, in rats exposed to 1 week of moderate hypoglycemia (plasma glucose = 3.0 mumol.ml-1), both state 3 respiration and the respiratory control ratio (RCR) were reduced from control. In fact, when the chronic hypoglycemia was imposed following a 3-4 week period of diabetic hyperglycemia, the state 3 rate and RCR were found to be reduced to a greater degree than in chronically hypoglycemic, non-diabetic, previously normoglycemic rats. Finally, when 1 week of moderate hypoglycemia preceded a 30 min period of insulin-induced hypoglycemic coma, a disturbed pattern of mitochondrial respiration (i.e. increased state 4, decreased RCR) was found at 60 min of recovery following coma. These results indicate that chronic increases in glucose (and insulin deprivation) have no effect on cerebral mitochondrial respiratory function, whereas prolonged, albeit moderate, reductions in cerebral glucose supply result in perturbations in mitochondrial respiration. These results demonstrate the importance of an adequate glucose supply for normal mitochondrial activity.

Animals↗
PubMed1985

Mechanism of the stimulation of respiration by fatty acids in rat liver.

The mechanism of stimulation of hepatic respiration by fatty acids was studied in isolated rat hepatocytes. Stimulation of respiration by fatty acids varied from about 35% to about 105% depending on chain length. The stimulatory effect of octanoate (1 mM) or oleate (0.5 mM) was prevented by oligomycin (2 micrograms/ml). With carboxyatractyloside (100 microM) and ouabain (2 mM) the stimulation of respiration was partially inhibited (by 50-70 and 50-60%, respectively). From these results it can be concluded that the increased rate of respiration after addition of fatty acids is coupled to ATP synthesis. A large part (50-60%) of this ATP is utilized by the (Na+ + K+)-ATPase.

2,4-Dinitrophenol↗
PubMed1990

Essential role of ferrous iron in cyanide-resistant respiration in Hansenula anomala.

Antimycin A-dependent induction of cyanide-resistant respiration in Hansenula anomala was completely blocked by o-phenanthroline, alpha,alpha'-dipyridyl, or 8-hydroxyquinoline. Pulse-labeling of the cells with [35S]methionine in the presence of both antimycin A and o-phenanthroline indicated that the 36-kDa protein previously reported to be involved in cyanide-resistant respiration [(1989) J. Biochem. 105, 864-866] was formed in mitochondria even under these conditions. The addition of Fe2+, but not Fe3+, ions to these cells in the presence of cycloheximide resulted in the rapid expression of cyanide-resistant respiration activity. These results suggest that in the presence of both antimycin A and o-phenanthroline an inactive form of the 36-kDa protein was formed and Fe2+ ions converted it to the active form. It is also likely that Fe2+ ions are involved in the reaction mechanism of cyanide-resistant respiration.

2,2'-Dipyridyl↗
PubMed1993

Inhibition of uncoupled respiration in tumor cells. A possible role of mitochondrial Ca2+ efflux.

Uncouplers CCCP (2-4 microM) or DNP (200-400 microM) when added to EL-4 thymoma or Ehrlich carcinoma ascites cells initially stimulated endogenous respiration about 2-fold but then inhibited it to a first-order rate 20-25% of controls. This inhibition was accelerated by intracellular acidification or by A23187, a Ca2+/H(+)-antiporter (i.e. when mitochondrial Ca2+ efflux was stimulated) whereas Ruthenium red, an inhibitor of uniporter-driven Ca2+ efflux, significantly slowed down the effect of uncouplers. The respiratory inhibition was associated with NAD(P)H oxidation and was partially reversed by exogenous substrates (glutamine or glucose). In the permeabilized cells, endogenous and glutamine-supported respiration was inhibited by EGTA, while succinate-supported respiration was Ca2+ independent. It is suggested that mitochondrial Ca2+ is necessary for NADH-dependent respiration of tumor cells, and uncouplers inhibit it by activation of mitochondrial Ca2+ efflux.

2,4-Dinitrophenol↗
PubMed1995

Nitric oxide regulates mitochondrial respiration and cell functions by inhibiting cytochrome oxidase.

Nitric oxide (NO) reversibly inhibits mitochondrial respiration by competing with oxygen at cytochrome oxidase. Concentrations of NO measured in a range of biological systems are similar to those shown to inhibit cytochrome oxidase and mitochondrial respiration. Inhibition of NO synthesis results in a stimulation of respiration in a number of systems. It is proposed that NO exerts some of its main physiological and pathological effects on cell functions by inhibiting cytochrome oxidase. Further NO may be a physiological regulator of the affinity of mitochondrial respiration for oxygen, enabling mitochondria to act as sensors of oxygen over the physiological range.

Animals↗
PubMed1985

Magnitude of ouabain-sensitive respiration of lamb hepatocytes (Ovis aries).

In lamb hepatocyte preparations with viabilities greater than 90%, ouabain-sensitive respiration accounted for approximately 50% of the total cellular O2 consumption. Lamb hepatocyte preparations with viability of less than 50% exhibited lower (P less than 0.05) total and ouabain-sensitive respiration. The decrease in ouabain-sensitive respiration in these preparations entirely accounted for the drop in total respiration.

Age Factors↗
PubMedDate not supplied

Effect of local anesthetics on cellular respiration and thymidine transport in hepatocytes from young and old rats.

The effect of local anesthetics (procaine, nicotinoyl-procaine, tetracaine, and dibucaine) on thymidine uptake and cellular respiration was investigated in hepatocytes from 3- and 24-month-old rats. All local anesthetics inhibited the "high-affinity" as well as the "low-affinity" thymidine transport system in a non-competitive manner immediately upon addition. Nicotinoyl-procaine, tetracaine, and dibucaine showed a similar inhibition profile with an inhibition of 10--15% at 50 mumol/l, or of more than 60% at 1 mmol/l. The less-lipophilic procaine showed a distinctly lower inhibition (10% at 1 mmol/l). The inhibitory effect was reversible and not dependent on Ca2+. All local anesthetics exerted identical effects in hepatocytes from young and old rats. Nicotinoyl-procaine and tetracaine inhibited cellular respiration in young and old rats up to a maximum of 50%. Procaine did not reduce O2 consumption below 1 mmol/l. This inhibition appeared also immediately upon addition, was not reversible, and not dependent on Ca2+. It is concluded that local anesthetics impair quite different biological processes like thymidine transport and cellular respiration in hepatocytes from young and old animals even at concentrations below 100 mumol/l. The magnitude of inhibition was correlated to the lipid solubility of the local anesthetics. The mechanism seemed to be different to the anesthetic action and it is supposed that it is a direct hydrophobic interaction with membrane proteins. Thus the local anesthetic-induced increase in membrane fluidity could not improve the age-dependent impairment of thymidine transport. The reduction of respiration is considered to be due to reduced O2 diffusion. This inhibition is in striking contrast to previously observed stimulatory effects which in part lead to the use of local anesthetics in geriatrics.

Aging↗
PubMed1981

Respiration of Leishmania mexicana amastigotes and promastigotes.

Promastigotes of Leishmania mexicana mexicana recently derived from amastigotes by transformation in vitro respired at a rate (17 nmol O2/min per 10(8) parasites) 4-5 times higher than that of amastigotes, but when the difference in cell protein content between the two preparations was taken into account the rates were not significantly different (32 nmol O2/min per mg protein). The respiration of both amastigotes and promastigotes was sensitive to cyanide, azide, antimycin A, 2-n-heptyl-4-hydroxyquinoline-N-oxide and high concentrations of amytal, but insensitive to rotenone and salicyl-hydroxamic acid, indicating that the two developmental forms possess a similar cytochrome-containing respiratory chain. D-Glucose and non-esterified fatty acids stimulated promastigote respiration and amastigote transformation to promastigotes in vitro; possibly these substances are important exogenous energy substrates for both forms of the parasites. Amino acids (incuding L-proline) and proteins did not appear to be used as energy substrates. The respiration rate of promastigotes was found to rise significantly upon continued sub-culture in vitro; at the same time cell size and protein content increased.

Amino Acids↗
PubMed1995

Effect of PQQ glucose dehydrogenase overexpression in Escherichia coli on sugar-dependent respiration.

Pyrroloquinoline quinone glucose dehydrogenase (PQQGDH) was overexpressed in Escherichia coli, and its impact on sugar-dependent respiration was investigated. Sugar-dependent respiration patterns under PQQGDH overexpression can be devided into two types. The first type involves D-glucose and D-mannose, which are utilized by the phosphotransferase system (PTS) and are also the substrates of PQQGDH. As a result of PQQGDH overexpression, the apparent Km value of sugar-dependent respiration shifted to higher concentration compared with E. coli parental cells. The second type included D-xylose and D-galactose, which are the substrates of PQQGDH, but not the PTS sugars. PQQGDH overexpressing cells showed much higher respiration than parental cells. These results suggested that PQQGDH overexpression may alter sugar utilization preferences in E. coli, suggesting further possible applications in metabolic engineering for carbon source utilization.

Electrodes↗
PubMed1994

Effect of heavy metals and mineral nutrients on forest litter respiration rate.

Two hypotheses were tested: (1) heavy metals such as Zn, Pb and Cd can suppress the respiration rate of forest litter at low-moderate pollution levels, and (2) mineral nutrients such as K, Ca and Mg can counteract the toxicity of heavy metals when applied onto the polluted litter. In a completely randomised design, three doses of heavy metals were used: Cd-10, 50, 250; Pb-100, 500, 2500; Zn-200, 1000, 5000 microg/g dwt litter, respectively. For Ca, Mg and K, the doses corresponded to 100, 500 and 2500 microg/g. A significant decrease in cumulated CO2 evolution after 4 weeks of incubation was found for the litter samples treated with medium doses of Zn, Cd/Ca, Cd/Mg, Pb/Ca, Pb/Mg, Pb/K, Zn/Mg, Zn/Ca, Zn/K and for all the highest-dose treatments. The largest drop in respiration rate in both the medium and the highest doses was caused by additions of Zn either alone or in combination with K, Ca or Mg. The additions of mineral nutrients were found to decrease the litter respiration rate below the value measured for the respective heavy metal alone in the case of Cd/Ca, Cd/Mg, Pb/Ca, Pb/Mg and Pb/K in the medium-dose treatments, and for Cd/Ca, Cd/Mg, Cd/K, Pb/Ca and Pb/Mg in the highest-dose treatments. In all other cases, additions of the mineral nutrients did not influence the respiration rate significantly when compared to the effect of the respective heavy metal.

Journal Article↗
PubMed1985

Effects of succinylacetone on growth and respiration of L1210 leukemia cells.

4,6-Dioxoheptanoic acid (succinylacetone, SA), a potent inhibitor of heme biosynthesis, suppressed growth and decreased respiration of L1210 leukemia cells in vitro. Growth of cells incubated in the presence of 2--4 mM SA for the first 2 days declined, and after 3 days virtually ceased. L1210 cells in the logarithmic growth phase exhibited active respiration (40 +/- 9.3 nanoatoms oxygen/min X 10(7) cells at 37 degrees C) which was inhibited by and released by uncouplers of oxidative phosphorylation. These and other inhibitors of mitochondrial function clearly demonstrate a mitochondrial basis for the cellular respiration in both control and SA-treated cells. L1210 cells in the stationary phase exhibited a marked decrease in oxygen consumption compared to cells in logarithmic growth. At the concentrations used in this study, SA was not immediately toxic to L1210 cells, but inhibited growth at 2 days without lowering levels of cellular heme. Thus, it appears unlikely that inhibition of growth of L1210 cells by SA can be ascribed either to heme depletion or to impairment of respiration.

Animals↗
PubMed1988

Inhibition of mitochondrial respiration by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in mouse brain in vivo.

This is the first report on in vivo effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) on mitochondrial respiration in mouse brain. C57/BL mice, injected with 40 mg/kg of MPTP subcutaneously, were sacrificed by cervical dislocation 5-6 h after the injection. Mitochondrial suspensions were prepared from whole brains. Mitochondrial respiration was studied polarographically. The state 3 respiration, i.e., the active respiration in the presence of tricarboxylic acid (TCA) cycle substrates and ADP with coupled phosphorylation of ADP to ATP, was significantly inhibited in mice treated with MPTP. This inhibition was prevented by pretreatment of mice with pargyline. Activity of mitochondrial NADH-ubiquinone oxidoreductase was also inhibited in mice treated with MPTP.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1981

Influence of growth hormone and thyroxine on thermotropic effects of respiration and 1-anilino-8-naphthalene sulfonate fluorescence and on lipid composition of cardiac membranes.

The effects of hypophysectomy and subsequent administration of growth hormone and/or L-thyroxine on thermotropic properties of State 3 respiration (ADP-induced), cholesterol, phospholipid and fatty acid composition of phospholipid fraction were examined in myocardial mitochondria of rats. Temperature-dependence of 1-anilino-8-naphthalene sulfonate fluorescence was determined in vesicles prepared from lipids of heart mitochondria. Transition temperature obtained from the Arrhenius plots of respiration occurred at 21 and 24 degrees C for heart mitochondria of normal and hypophysectomized rats, respectively. Most notably, after hypophysectomy the rate of respiration was lower below 24 degrees C, but was progressively higher above that temperature when compared to normal rats. The energy of activation was 148 and 36% larger below and above the transition temperature, respectively. Growth hormone restored almost completely the energy of activation and respiratory rates to normal levels. Administration of L-thyroxine, with or without growth hormone, did not significantly change the rate of respiration but decreased the transition temperature to 17.7-17.9 degrees C. Lipid and phospholipid content, as well as percent distribution of phospholipids and their fatty acid composition were not statistically different among the different groups of rats. Only cholesterol content was increased after hypophysectomy. Administration of growth hormone and thyroxine did not significantly change the total unsaturation index of fatty acids, but growth hormone increased the content of arachidonic acid (20 : 4) by 70% but decreased the docosahexaenoic acid (22 : 6) three times which may have a beneficial effect on mitochondrial membranes. These and other results suggest that hormones exert different effects on subcellular organelles in different tissues, like heart and liver.

Anilino Naphthalenesulfonates↗