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1.
Arch Biochem Biophys ; 380(2): 367-72, 2000 Aug 15.
Article in English | MEDLINE | ID: mdl-10933893

ABSTRACT

The contribution of the sn-glycerol-3-phosphate (G-3-P) shuttle in the control of energy metabolism is well established. It is also known that its activity may be modulated by hormones involved in thermogenesis, such as thyroid hormones or dehydroepiandrosterone and its metabolites, that act by inducing de novo synthesis of mitochondrial G-3-P dehydrogenase (mGPDH). However, little is known as to the factors that may influence the activity without enzyme induction. In the present study we investigated the possible role of the G-3-P shuttle in the thermogenic response to different hypothermic stresses. It was found that a decrease of body temperature causes the liver rapidly to enhance mGPDH activity and G-3-P-dependent respiration. The enhancement, which does not result from de novo synthesis of enzymes, has the potential of increasing heat production both by decreased ATP synthesis during the oxidation of G-3-P and by activation of the glycolytic pathway.


Subject(s)
Body Temperature Regulation/physiology , Glycerolphosphate Dehydrogenase/metabolism , Hypothermia/enzymology , Hypothermia/physiopathology , Mitochondria, Liver/enzymology , Adenosine Triphosphate/biosynthesis , Animals , Enzyme Activation , Female , Fluoroacetates/pharmacology , Glycerophosphates/metabolism , Glycolysis , Male , Mitochondria, Liver/drug effects , Rats , Rats, Sprague-Dawley
2.
FEBS Lett ; 469(2-3): 186-90, 2000 Mar 10.
Article in English | MEDLINE | ID: mdl-10713268

ABSTRACT

We have studied the role of changes in mitochondrial membrane potential (DeltaPsi) in two widely-used models of apoptosis, such as dexamethasone-treated rat thymocytes and U937 human cells treated with tumor necrosis factor-alpha and cycloheximide. To dissipate DeltaPsi, we used low concentrations of valinomycin, unable per se to induce apoptosis, and demonstrated that the decline in DeltaPsi exerts opposite effects in the two models. Indeed, in U937 cells, depolarization of mitochondria increased apoptosis, which decreased in rat thymocytes. This leads to the suggestion that disruption of DeltaPsi plays opposite roles depending on the experimental model. In U937 cells, the drop of DeltaPsi is a possible contributory cause for the apoptotic process; in rat thymocytes, it could be a limiting factor. We propose that these opposite effects could be due to the different ATP requirement of each apoptotic pathway.


Subject(s)
Apoptosis/physiology , Mitochondria/physiology , Adenosine Triphosphate/metabolism , Animals , Blotting, Western , Caspase 3 , Caspases/metabolism , Cells, Cultured , Cytochrome c Group/metabolism , Dexamethasone/pharmacology , Flow Cytometry , Humans , Ionophores/pharmacology , Membrane Potentials/physiology , Microscopy, Confocal , Rats , Rats, Sprague-Dawley , Thymus Gland/cytology , Tumor Necrosis Factor-alpha/pharmacology , U937 Cells , Valinomycin/pharmacology
3.
FEBS Lett ; 430(3): 409-13, 1998 Jul 03.
Article in English | MEDLINE | ID: mdl-9688582

ABSTRACT

The effect of the in vivo thyroid status on mitochondrial membrane potential (delta psi(m)) in isolated rat hepatocytes was studies by means of a cytofluorimetric technique and the delta psi(m)-specific probe JC-1. It is shown that the delta psi(m) level decreases in the order hypothyroid > euthyroid > hyperthyroid. Polarographic measurement of the hepatocyte respiratory rates revealed an opposite trend of values: the highest respiratory rate in hepatocytes from hyperthyroid animals, the lowest in those from hypothyroid ones. This means that mitochondrial energy coupling is highest in hypothyroid hepatocytes and lowest in hyperthyroid hepatocytes. 6-Ketocholestanol added to hepatocytes failed to counterbalance the uncoupling effect of thyroid hormones on delta psi(m) and respiration rate. Under the same conditions, 6-ketocholestanol appeared to be effective in recoupling of respiration uncoupled by low concentrations of the artificial protonophore FCCP. The mechanism and possible physiological functions of the thyroid hormone-induced decrease in mitochondrial energy coupling are discussed.


Subject(s)
Energy Metabolism/physiology , Liver/metabolism , Mitochondria, Liver/metabolism , Thyroid Hormones/physiology , Animals , Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone , Hyperthyroidism/chemically induced , Hyperthyroidism/metabolism , Hypothyroidism/chemically induced , Hypothyroidism/metabolism , Ketocholesterols/pharmacology , Male , Membrane Potentials , Mitochondria, Liver/physiology , Oxygen Consumption , Rats , Rats, Sprague-Dawley , Uncoupling Agents
4.
Biochemistry (Mosc) ; 63(2): 235-8, 1998 Feb.
Article in English | MEDLINE | ID: mdl-9526120

ABSTRACT

The present paper describes the possibility of determination of mitochondrial membrane potential (Deltapsi) in isolated hepatocytes making use of a Deltapsi-sensitive dye, i.e., the lipophilic cationic probe 5,5',6,6'-tetrachloro-1,1',3, 3'-tetraethylbenzimidazolcarbocyanine iodide (JC-1) and of cytofluorimetry. The validity of the method was proved by treating hepatocytes with FCCP (decrease of Deltapsi) and subsequent addition of 6-ketocholestanol (increase of Deltapsi). The results indicate that the proposed method may be used in laboratory practice.


Subject(s)
Flow Cytometry/methods , Liver/physiology , Mitochondria/physiology , Animals , Benzimidazoles/metabolism , Carbocyanines/metabolism , Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone/pharmacology , Fluorescent Dyes/metabolism , In Vitro Techniques , Intracellular Membranes/drug effects , Intracellular Membranes/physiology , Ketocholesterols/pharmacology , Liver/cytology , Liver/drug effects , Male , Membrane Potentials/drug effects , Mitochondria/drug effects , Oxygen Consumption/drug effects , Rats , Rats, Sprague-Dawley , Uncoupling Agents/pharmacology
5.
Arch Biochem Biophys ; 341(1): 122-8, 1997 May 01.
Article in English | MEDLINE | ID: mdl-9143361

ABSTRACT

Administered 3 beta-hydroxyandrost-5-ene-7,17-dione (7-oxo-DHEA) is more effective than 3 beta-hydroxyandrost-5-en-7-one (DHEA) as an inducer of liver mitochondrial sn-glycerol-3-phosphate dehydrogenase and cytosolic malic enzyme in rats. Like DHEA, the 7-oxo metabolite enhances liver catalase, fatty acylCoA oxidase, cytosolic sn-glycerol-3-phosphate dehydrogenase, mitochondrial substrate oxidation rate, and the reconstructed sn-glycerol 3-phosphate shuttle. The mitochondrial adenine nucleotide carrier is diminished by thyroidectomy and is restored to normal activity by administering 7-oxo-DHEA. The relationship between respiratory rate and proton motive force across the mitochondrial membrane was measured in the nonphosphorylating state. When treated with increasing concentrations of respiratory inhibitors liver mitochondria from rats treated with 7-oxo-DHEA or thyroid hormones show a more rapid decline of membrane potential than do normal liver mitochondria. Thus 7-oxo-DHEA induces an increased proton leak or slip as has been reported for the thyroid hormone by M.D. Brand [(1990) Biochem. Biophys. Acta 1018, 128-133]. This process may contribute to the enhanced thermogenesis caused by ergosteroids as well as by thyroid hormones.


Subject(s)
Dehydroepiandrosterone/analogs & derivatives , Membrane Potentials/drug effects , Mitochondria, Liver/metabolism , Animals , Cell Respiration/drug effects , Dehydroepiandrosterone/pharmacology , Glycerophosphates/metabolism , Hyperthyroidism , Hypothyroidism , Male , Mitochondria, Liver/drug effects , Mitochondria, Liver/enzymology , Mitochondrial ADP, ATP Translocases/metabolism , Phosphorylation , Protons , Rats , Rats, Sprague-Dawley , Thyroid Hormones/pharmacology , Thyroidectomy
6.
Biochem Mol Biol Int ; 41(3): 469-80, 1997 Mar.
Article in English | MEDLINE | ID: mdl-9090454

ABSTRACT

The specific involvement of cardiolipin in modulating and/or controlling the activity of a number of mitochondrial carriers, enzymes and receptors is well documented; however, comparatively less understood is its role for the integrated functions of intact mitochondria. The aim of the present research was to get a better insight into this problem by investigating the effect of in vitro addition of cardiolipin on the properties of isolated liver mitochondria. The results obtained show that cardiolipin induces extensive structural and functional perturbations at the level of the inner mitochondrial membrane. In fact, addition of cardiolipin to intact mitochondria causes a significant increase of proton leak associated with a parallel increase of respiratory rate in State 4. Concomitantly, a slight uncoupling of phosphorylation associated with a moderate increase in ATPase activity is observed. Furthermore, the pore-mediated membrane permeability to calcium is drastically modified, an effect that can be reversed by addition of cyclosporin.


Subject(s)
Cardiolipins/physiology , Mitochondria, Liver/physiology , Adenosine Triphosphatases/metabolism , Animals , Calcium/metabolism , Cell Respiration , Male , Membrane Potentials , Rats , Rats, Sprague-Dawley
8.
Biochem Mol Biol Int ; 33(6): 1063-71, 1994 Aug.
Article in English | MEDLINE | ID: mdl-7804131

ABSTRACT

It is well established that DHEA treatment is associated in the rat to an increase in fatty acids metabolism. This condition would require levels of L-carnitine much higher than those physiologically present in the liver. The possibility thus exist that during DHEA treatment the concentration of L-carnitine may become a limiting factor for fatty acids oxidation and therefore responsible of some of the effects observed after administration of the hormone. The present experiments were designed to test this hypothesis. The results show that the increase in the levels of peroxisomal enzymes induced in hepatocytes by DHEA, is greatly reduced by parallel administration of L-carnitine. Furthermore, L-carnitine administration counteracts the effect of DHEA on mitochondrial structure. On the contrary, carnitine has no significant effect on the reduction in weight gain observed upon short- or long-term treatment with DHEA.


Subject(s)
Carnitine/pharmacology , Dehydroepiandrosterone/pharmacology , Liver/drug effects , Mitochondria, Liver/drug effects , Animals , Body Weight , Catalase/metabolism , Glutathione/metabolism , Liver/metabolism , Male , Microbodies/enzymology , Microscopy, Electron , Mitochondria, Liver/metabolism , Mitochondria, Liver/ultrastructure , Organ Size , Rats , Rats, Sprague-Dawley , Time Factors
9.
Biokhimiia ; 59(6): 861-5, 1994 Jun.
Article in Russian | MEDLINE | ID: mdl-8075250

ABSTRACT

Oleate (10-60 microM) stimulates oxygen consumption in hepatocytes in the presence of oligomycin. This stimulation of respiration is partially suppressed by 20 microM carboxyatractylate but is insensitive to 0.5 microM cyclosporin A. The results obtained suggest that fatty acids can uncouple oxidative phosphorylation in hepatocytes and that the uncoupling mechanism is the same as that in isolated mitochondria in the presence of EGTA.


Subject(s)
Mitochondria, Liver/metabolism , Oleic Acids/pharmacology , Uncoupling Agents/metabolism , Animals , Atractyloside/analogs & derivatives , Atractyloside/pharmacology , Cyclosporine/pharmacology , Drug Synergism , Male , Mitochondria, Liver/drug effects , Oleic Acid , Oligomycins/pharmacology , Oxidative Phosphorylation , Oxygen/metabolism , Rats , Rats, Sprague-Dawley
10.
Biochem Mol Biol Int ; 32(6): 1147-55, 1994 Apr.
Article in English | MEDLINE | ID: mdl-8061632

ABSTRACT

Permeabilization of inner mitochondrial membrane by palmitic acid in the presence of Ca2+ (cyclosporin A-sensitive stimulation of respiration, decrease of delta psi and high amplitude swelling) is accompanied by activation of the external pathway of NADH oxidation in liver mitochondria. The "pore"-sealing agents (cyclosporin A, Mg2+ with ADP, and L-carnitine with ATP) are equally effective in preventing the induction of external pathway of NADH oxidation by Ca2+ with palmitate. However, activities of these agents are different in respect to recoupling of permeabilized mitochondria. Participation of cyclosporin A-sensitive "pore" in the fatty acid- and Ca(2+)-dependent induction of external pathway of NADH oxidation and in Ca(2+)-dependent uncoupling is discussed.


Subject(s)
Calcium/pharmacology , Cyclosporine/pharmacology , Mitochondria, Liver/metabolism , NAD/metabolism , Palmitic Acids/pharmacology , Adenosine Diphosphate/pharmacology , Adenosine Triphosphate/pharmacology , Animals , Carnitine/pharmacology , Intracellular Membranes/drug effects , Magnesium/pharmacology , Mitochondria, Liver/drug effects , Mitochondrial Swelling/drug effects , Oxidation-Reduction , Oxygen Consumption/drug effects , Palmitic Acid , Permeability/drug effects , Rats
11.
Biokhimiia ; 58(10): 1513-22, 1993 Oct.
Article in Russian | MEDLINE | ID: mdl-8268296

ABSTRACT

Pathways and mechanisms of oxidative phosphorylation uncoupling by long-chain fatty acids in liver and muscle mitochondria are considered. A conclusion is drawn that there exist at least three different pathways of uncoupling by fatty acids, namely: (i) a Ca(2+)-dependent cyclosporin A-sensitive pathway; (ii) uncoupling which is inhibited by carboxyatractylate or other inhibitors of the ADP/ATP-antiporter, (iii) uncoupling due to the low protonophoric activity of fatty acids.


Subject(s)
Fatty Acids/metabolism , Mitochondria, Liver/metabolism , Mitochondria/metabolism , Muscles/metabolism , Uncoupling Agents/pharmacology , Animals , Fatty Acids/antagonists & inhibitors , Mitochondrial ADP, ATP Translocases/metabolism , Oxidative Phosphorylation , Phospholipids/metabolism
12.
Biokhimiia ; 58(8): 1266-75, 1993 Aug.
Article in Russian | MEDLINE | ID: mdl-8399776

ABSTRACT

The ability of cyclosporin A, Mg2+ plus ADP and L-carnitine to enhance energy recoupling in liver mitochondria and to inhibit the induction of the external pathway of NADH oxidation during Ca(2+)-dependent oxidative phosphorylation uncoupling by palmitate has been studied. Cyclosporin A, Mg2+ plus ADP and L-carnitine plus ATP prevent with an equal efficiency the induction of the external pathway of NADH oxidation by palmitate and Ca2+ in mitochondria but differ drastically by their ability to increase the coupling in permeabilized mitochondria. The recoupling effect of cyclosporin is manifested after addition of Mg2+ plus ADP. The protective action of Mg2+ plus ADP is prevented by preincubation with carboxyatractylate. Oxidation of NADH via an external pathway results in delta psi generation, however, only in the presence of the recoupling factors. The role of the cyclosporin-sensitive pore in Ca(2+)-dependent damage of mitochondria as well as in the induction of the external pathway of NADH oxidation is discussed.


Subject(s)
Adenosine Diphosphate/pharmacology , Carnitine/pharmacology , Cyclosporine/pharmacology , Fatty Acids/pharmacology , Magnesium/pharmacology , Mitochondria, Liver/drug effects , Animals , Calcium/metabolism , Energy Metabolism , Mitochondria, Liver/metabolism , NAD/metabolism , Oxidation-Reduction , Rats
13.
Comp Biochem Physiol B ; 105(3-4): 643-7, 1993.
Article in English | MEDLINE | ID: mdl-8365116

ABSTRACT

1. An attempt to identify the cause of decrease of gain in body weight during dehydroepiandrosterone (DHEA) treatment was made comparing the effects of hormone treatment on chickens and rats. 2. Chickens treated with DHEA for 7-10 days do not change their weight gain with respect to controls although their mitochondrial respiration and peroxisomal catalase (index of peroxisomal mass) were increased. 3. Liver cytosolic malic enzyme and sn-glycerol-3-phosphate dehydrogenase were depressed in chickens treated with DHEA in comparison with activities in untreated controls. DHEA treatment did not increase the activity of mitochondrial sn-glycerol 3-phosphate dehydrogenase. 4. In contrast to rat liver cytosolic sn-glycerol-3-phosphate dehydrogenase this enzyme in chicken liver was inactive with NADPH.


Subject(s)
Chickens/metabolism , Dehydroepiandrosterone/pharmacology , Liver/drug effects , Rats, Sprague-Dawley/metabolism , Acyl-CoA Oxidase , Animals , Body Weight/drug effects , Catalase/metabolism , Glycerolphosphate Dehydrogenase/metabolism , Isocitrate Dehydrogenase/metabolism , Liver/enzymology , Malate Dehydrogenase/metabolism , Male , Microbodies/enzymology , Mitochondria, Liver/drug effects , Mitochondria, Liver/metabolism , NADP/metabolism , Oxidoreductases/metabolism , Rats
14.
J Bioenerg Biomembr ; 25(3): 313-21, 1993 Jun.
Article in English | MEDLINE | ID: mdl-8349575

ABSTRACT

Dehydroepiandrosterone (DHEA) treatment of rats decreases gain of body weight without affecting food intake; simultaneously, the activities of liver malic enzyme and cytosolic glycerol-3-P dehydrogenase are increased. In the present study experiments were conducted to test the possibility that DHEA enhances thermogenesis and decreases metabolic efficiency via transhydrogenation of cytosolic NADPH into mitochondrial FADH2 with a consequent loss of energy as heat. The following results provide evidence which supports the proposed hypothesis: (a) the activities of cytosolic enzymes involved in NADPH production (malic enzyme, cytosolic isocitrate dehydrogenase, and aconitase) are increased after DHEA treatment; (b) cytosolic glycerol-3-P dehydrogenase may use both NAD+ and NADP+ as coenzymes; (c) activities of both cytosolic and mitochondrial forms of glycerol-3-P dehydrogenase are increased by DHEA treatment; (d) cytosol obtained from DHEA-treated rats synthesizes more glycerol-3-P during incubation with fructose-1,6-P2 (used as source of dihydroxyacetone phosphate) and NADP+; the addition of citrate in vitro further increases this difference; (e) mitochondria prepared from DHEA-treated rats more rapidly consume glycerol-3-P added exogenously or formed endogenously in the cytosol in the presence of fructose-1,6-P2 and NADP+.


Subject(s)
Body Temperature Regulation/physiology , Dehydroepiandrosterone/pharmacology , Models, Biological , Oxidative Phosphorylation/drug effects , Animals , Body Temperature Regulation/drug effects , Body Weight/drug effects , Cells, Cultured , Citrates/metabolism , Citric Acid , Cytosol/enzymology , Dihydroxyacetone Phosphate/metabolism , Energy Metabolism/drug effects , Flavin-Adenine Dinucleotide/analogs & derivatives , Flavin-Adenine Dinucleotide/metabolism , Glycerolphosphate Dehydrogenase/metabolism , Glycerophosphates/metabolism , Glycolysis , Liver/cytology , Liver/metabolism , Malate Dehydrogenase/metabolism , Male , Mitochondria, Liver/drug effects , Mitochondria, Liver/metabolism , NADP/metabolism , Rats , Rats, Sprague-Dawley/metabolism
15.
Biokhimiia ; 58(4): 585-9, 1993 Apr.
Article in Russian | MEDLINE | ID: mdl-8507734

ABSTRACT

The effect of fatty acids and L-carnitine on Ca2+ retention in rat liver mitochondria have been studied. Ca(2+)-retention was estimated as a sum of consecutive Ca2+ additions which leaded to transient stimulation of respiration coupled with influx of Ca2+ L-carnitine increases the Ca(2+)-retention; such an effect requires ATP. The Ca(2+)-retention was increased in the presence of 50 microM ATP or ADP. In all cases carboxyatractylate prevented the increase in Ca(2+)-retention. Palmitate and FCCP added at concentrations producing similar stimulating effect on respiration inhibit Ca(2+)-retention to about the same degree. The effect of palmitate is strongly diminished by L-carnitine. Again, the L-carnitine effect requires ATP. The data obtained suggest that the protonophoric effect of fatty acid plays a crucial role in Ca(2+)-dependent damage of mitochondria.


Subject(s)
Calcium/metabolism , Carnitine/pharmacology , Fatty Acids/pharmacology , Mitochondria, Liver/drug effects , Adenosine Diphosphate/metabolism , Adenosine Triphosphate/metabolism , Animals , Atractyloside/analogs & derivatives , Atractyloside/pharmacology , Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone/pharmacology , Mitochondria, Liver/metabolism , Rats
16.
Biochim Biophys Acta ; 1117(1): 33-6, 1992 Jul 21.
Article in English | MEDLINE | ID: mdl-1627589

ABSTRACT

The physiological role of L-carnitine is to determine the transport of acyl-CoA through the mitochondrial membrane. However, some observations may also suggest a direct effect of the molecule per se on the physical properties of the membrane, most probably at the level of the binding site. This possibility has been investigated by studying the influence of adriamycin, a drug that binds to cardiolipin, on the effect of carnitine on isolated rat liver mitochondria. It has been found that adriamycin almost abolishes the activating effect of carnitine on state 2 respiration. The effect and its inhibition is seen by using either the L-form of carnitine or the D-form or both. Cardiolipin removes the effect of adriamycin and restores the activation by carnitine. It is proposed that some effects of carnitine on mitochondrial properties may be the result of interaction of carnitine with cardiolipin at the membrane level.


Subject(s)
Cardiolipins/metabolism , Carnitine/pharmacology , Mitochondria, Liver/metabolism , Animals , Binding Sites , Doxorubicin/pharmacology , Drug Interactions , Intracellular Membranes/drug effects , Intracellular Membranes/metabolism , Male , Mitochondria, Liver/drug effects , Oxygen Consumption/drug effects , Rats , Rats, Inbred Strains
17.
J Nutr ; 122(4): 967-76, 1992 Apr.
Article in English | MEDLINE | ID: mdl-1532421

ABSTRACT

The effects on the liver of feeding a diet containing 0.2% dehydroepiandrosterone were studied after short (7 d) and long (100 d) periods of treatment in rats. The short-term treatment caused hypertrophy of the hepatocytes that, at the ultrastructural level, seemed to be due to proliferation of peroxisomes and (to a minor extent) of mitochondria. The mitochondria seemed to have undergone transition from expanded to condensed configuration; accordingly, after isolation, their rate of coupled respiration was greater than that of control mitochondria. After long-term treatment, the structure of the hepatocytes reverted toward normal. In fact, at the ultrastructural level, the number and the size of peroxisomes was not significantly different from those of the controls, but degenerative phenomena were observed in the mitochondria. Attempts are made to explain the above ultrastructural and biochemical findings in view of the effects of dehydroepiandrosterone on the energy metabolism of liver.


Subject(s)
Dehydroepiandrosterone/toxicity , Liver/drug effects , Administration, Oral , Animals , Body Weight/drug effects , Dehydroepiandrosterone/administration & dosage , Dose-Response Relationship, Drug , Hepatomegaly/chemically induced , Liver/ultrastructure , Male , Microbodies/drug effects , Microbodies/ultrastructure , Organ Size/drug effects , Rats , Rats, Inbred Strains
18.
FEBS Lett ; 295(1-3): 51-4, 1991 Dec 16.
Article in English | MEDLINE | ID: mdl-1765167

ABSTRACT

The effect of ATP/ADP-antiporter inhibitors on palmitate-induced uncoupling was studied in heart muscle mitochondria and inside-out submitochondrial particles. In both systems palmitate is found to decrease the respiration-generated membrane potential. In mitochondria, this effect is specifically abolished by carboxyatractylate (CAtr) a non-penetrating inhibitor of antiporter. In submitochondrial particles, CAtr does not abolish the palmitate-induced potential decrease. At the same time, bongkrekic acid, a penetrating inhibitor of the antiporter, suppresses the palmitate effect on the potential both in mitochondria and particles. Palmitoyl-CoA which is known to inhibit the antiporter in mitochondria as well as in particles decreases the palmitate uncoupling efficiency in both these systems. These data are in agreement with the hypothesis that the ATP/ADP-antiporter is involved in the action of free fatty acids as natural uncouplers of oxidative phosphorylation.


Subject(s)
Mitochondria, Heart/metabolism , Palmitic Acids/pharmacology , Submitochondrial Particles/metabolism , Uncoupling Agents/pharmacology , Animals , Atractyloside/analogs & derivatives , Atractyloside/pharmacology , Bongkrekic Acid/pharmacology , Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone/pharmacology , Kinetics , Mitochondria, Heart/drug effects , Mitochondrial ADP, ATP Translocases/antagonists & inhibitors , Oxygen Consumption/drug effects , Palmitic Acid , Rabbits , Sodium Dodecyl Sulfate/pharmacology , Submitochondrial Particles/drug effects
19.
FEBS Lett ; 289(2): 187-9, 1991 Sep 09.
Article in English | MEDLINE | ID: mdl-1915847

ABSTRACT

It is shown that L-carnitine strongly increases the ability of rat liver mitochondria to respond to the train of Ca2+ additions by a transient stimulation of the State-4 respiration rate. Such an effect requires ATP and the L-carnitine efficiency strongly decreases when ATP is omitted. Oleate influences the mitochondria in a fashion opposite to that of L-carnitine. The oleate effect is strongly diminished by L-carnitine. Again, the L-carnitine effect requires ATP, and D-carnitine fails to substitute for L-carnitine. It is suggested that L-carnitine removes, in an ATP-dependent manner, endogenous or added fatty acids, which are involved in oxidative damage of Ca(2+)-loaded mitochondria.


Subject(s)
Calcium Chloride/pharmacology , Carnitine/pharmacology , Mitochondria, Liver/metabolism , Oxygen Consumption/drug effects , Adenosine Triphosphate/metabolism , Adenosine Triphosphate/pharmacology , Animals , Kinetics , Male , Mitochondria, Liver/drug effects , Rats , Rats, Inbred Strains
20.
J Submicrosc Cytol ; 14(3): 461-70, 1982 Jul.
Article in English | MEDLINE | ID: mdl-7175983

ABSTRACT

The possible functional significance of the close relation between structural and metabolic steady-states of isolated rat liver mitochondria, has been investigated by analysing the metabolic consequences of a primary block of the structural modifications. The structural changes have been blocked by means of factors acting primarily on the structure and the block was evaluated by electron microscope and angular light scattering measurements. Evidence has been obtained that: (a) the phosphorylative capacity of isolated mitochondria is not modified by conditions that completely abolish the structural changes; therefore, the configurational changes do not constitute as such a mechano-chemical mechanism for energy conservation and transformation. (b) The block of the structural changes is closely associated with the impairment of respiratory control: in fact there appears to be a close relation between the capacity of mitochondria to vary their structure and the ability to vary the respiratory rate, both being a function of ADP concentration.


Subject(s)
Mitochondria, Liver/ultrastructure , Oxygen Consumption , Adenosine Diphosphate/metabolism , Animals , Male , Mitochondria, Liver/metabolism , Osmolar Concentration , Oxidative Phosphorylation , Rats , Rats, Inbred Strains
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