scholarly journals Nutritional effects on mitochondrial bioenergetics. Alterations in oxidative phosphorylation by rat liver mitochondria

1984 ◽  
Vol 218 (1) ◽  
pp. 61-67 ◽  
Author(s):  
J Ferreira ◽  
L Gil
Keyword(s):  
Oxidative Phosphorylation ◽  
Respiratory Control ◽  
Atp Synthesis ◽  
Liver Mitochondria ◽  
Rat Liver Mitochondria ◽  
Mitochondrial Atpase ◽  
Protein Free Diet ◽  
Energy Dependent ◽  
Hydrolysis Of ◽  
Rate Controlling Step

Rats malnourished since birth and fed on a protein-free diet for 2 weeks showed a 23-27% decrease in the State-3 oxidation of glutamate, succinate and ascorbate + NNN′ N′-tetramethyl-p-phenylenediamine by liver mitochondria compared with control fed animals. ATP synthesis and the respiratory control index were diminished at the three coupling sites, but significant alterations were not observed in ADP/O ratios. Vmax. for NADH oxidation in electron-transport particles was 40% lower. Mitochondrial cytochromes b and c1 remained unchanged, but cytochrome c was increased by 26%. Cytochromes a + a3 were diminished by 22%. Vmax. for mitochondrial ATPase was 23% lower. These results suggest that the lower content of cytochrome a + a3 at the rate-controlling step of oxidative phosphorylation in malnourished rats might be mainly responsible for the decrease in substrate oxidations as well as ATP synthesis at the three coupling sites. The decreased synthesis and hydrolysis of ATP suggests that other energy-dependent mitochondrial processes could be decreased during malnutrition.

scholarly journals The maturation of the inner membrane of foetal rat liver mitochondria. An example of a positive-feedback mechanism

1975 ◽  
Vol 150 (3) ◽  
pp. 477-488 ◽  
Author(s):  
J K Pollak
Keyword(s):  
Oxidative Phosphorylation ◽  
Rat Liver ◽  
Mitochondrial Membrane ◽  
Respiratory Control ◽  
Liver Mitochondria ◽  
Neonatal Rat ◽  
Rat Liver Mitochondria ◽  
Inner Mitochondrial Membrane ◽  
Mature Adult ◽  
Foetal Rat

A new method was devised for the isolation of foetal and neonatal rat lvier mitochondria, giving higher yields than conventional methods. 2. During development from the perinatal period to the mature adult, the ratio of cytochrome oxidase/succinate-cytochrome c reductase changes. 3. The inner mitochondrial membrane of foetal liver mitochondria possesses virtually no osmotic activity; the permeability to sucrose decreases with increasing developmental age. 4. Foetal rat liver mitochondria possess only marginal respiratory control and do not maintain Ca2+-induced respiration; they also swell in respiratory-control medium in the absence of substrate. ATP enhances respiratory control and prevents swelling, adenylyl imidodiphosphate, ATP+atractyloside enhance the R.C.I. (respiratory control index), Ca2+-induced respiratory control and prevent swelling, whereas GTP and low concentrations of ADP have none of these actions. It is concluded that the effect of ATP depends on steric interaction with the inner mitochondrial membrane. 5. When 1-day pre-partum foetuses are obtained by Caesarean section and maintained in a Humidicrib for 90 min, mitochondrial maturation is ‘triggered’, so that their R.C.I. is enhanced and no ATP is required to support Ca2+-dependent respiratory control or to inhibit mitochondrial swelling. 6. It is concluded that foetal rat liver mitochondria in utero do not respire, although they are capable of oxidative phosphorylation in spite of their low R.C.I. The different environmental conditions which the neonatal rat encounters ex utero enable the hepatic mitochondria to produce ATP, which interacts with the inner mitochondrial membrane to enhance oxidative phosphorylation by an autocatalytic mechanism.

scholarly journals A permeability barrier in mitochondria in ‘high-energy states’ against positively charged disulphides

1968 ◽  
Vol 107 (5) ◽  
pp. 645-654 ◽  
Author(s):  
S. Skrede
Keyword(s):  
Oxidative Phosphorylation ◽  
Energy State ◽  
Respiratory Control ◽  
Liver Mitochondria ◽  
High Energy ◽  
Rat Liver Mitochondria ◽  
Permeability Barrier ◽  
Inner Mitochondrial Membrane ◽  
Energy States ◽  
State 1

1. In rat liver mitochondria in state 1 or 4 there is a permeability barrier against cystamine, probably in the inner membrane. 2. The permeability barrier was broken (a) when oxidative phosphorylation was uncoupled, (b) when the respiratory chain was inhibited or in anaerobiosis, or (c) when phosphate was added in the absence of exogenous substrate. Under these conditions increased amounts of [35S]cystamine residues were bound to matrix proteins. 3. It appears that the permeability barrier against cystamine in mitochondria reflects a ‘high-energy state’. A gradual increase in the permeability for cystamine strikingly coincided with the loss of respiratory control induced by increasing concentrations of different uncoupling agents. 4. Cystamine caused uncoupling of oxidative phosphorylation in state 2 or 5, but not in state 1, 3 or 4. The uncoupling effect of cystamine was dependent on the phosphorylation potential. ATP counteracted, whereas ADP potentiated, the uncoupling by cystamine. 5. The variable penetration of cystamine appears to depend on its positive charge, since a dication derivative, NNN′N′-tetramethylcystamine, has a similar pattern of penetration, whereas an uncharged derivative, NN′-diacetylcystamine, penetrates rapidly into mitochondria irrespective of their metabolic state. 6. It is suggested that a charge barrier is present in or across the inner mitochondrial membrane in ‘high-energy states’.

scholarly journals Deterioration of rat liver mitochondria under conditions of metabolite deprivation

1980 ◽  
Vol 188 (3) ◽  
pp. 817-822 ◽  
Author(s):  
J W Parce ◽  
P I Spach ◽  
C C Cunningham
Keyword(s):  
Atpase Activity ◽  
Sucrose Solution ◽  
Adenine Nucleotides ◽  
Respiratory Control ◽  
Liver Mitochondria ◽  
Phospholipid Metabolism ◽  
Rat Liver Mitochondria ◽  
Second Phase ◽  
Mitochondrial Atpase ◽  
Sequence Of Events

In a previous study [Parce, Cunningham & Waite (1978) Biochemistry 17, 1634-1639] changes in mitochondrial phospholipid metabolism and energy-linked functions were monitored as coupled mitochondria were aged in iso-osmotic sucrose solution at 18 degrees C. The sequence of events that occur in mitochondrial deterioration under the above conditions have been established more completely. Total adenine nucleotides are depleted early in the aging process, and their loss parallels the decline in respiratory control. Related to the loss of total adenine nucleotides is a dramatic decrease in ADP and ATP translocation (uptake). The decline of respiratory control is due primarily to a decrease in State-3 respiration; loss of this respiratory activity can be related to the decline in ADP translocation. Mitochondrial ATPase activity does not increase significantly until State-4 respiration has increased appreciably. At the time of loss of respiratory control the ATPase activity increases to equal the uncoupler-stimulated activity. The H+/O ratio and P/O ratios do not decrease appreciably until respiratory control is lost. Similarly, permeability of the membrane to the passive diffusion of protons increases only after respiratory control is lost. There observations reinforce our earlier conclusion that there are two main phases in mitochondrial aging. The first phase is characterized by loss of the ability to translocate adenine nucleotides. The second phase is characterized by a decline in the ability of the mitochondrion to conserve energy (i.e. maintain a respiration-driven proton gradient) and to synthesize ATP.

scholarly journals Chloride-dependent uncoupling mediated by oligomycin in rat liver mitochondria

1973 ◽  
Vol 136 (4) ◽  
pp. 911-917 ◽  
Author(s):  
N. Ariel ◽  
Y. Avi-Dor
Keyword(s):  
Rat Liver ◽  
Respiratory Control ◽  
Liver Mitochondria ◽  
Rat Liver Mitochondria ◽  
Anionic Species ◽  
Energy Conserving ◽  
Uncoupling Of Oxidative Phosphorylation ◽  
Triton X ◽  
Energy Dependent ◽  
Stimulation Of

In rat liver mitochondria suspended in KCl medium and containing a low concentration of a K+-specific cationophore (valinomycin or Triton X-100), oligomycin was shown to induce uncoupling of oxidative phosphorylation, stimulation of adenosine triphosphatase activity, release of the respiratory control, decrease of energy-dependent changes in the fluorescence of the dye 8-anilino-1-naphthalenesulphonic acid and rapid swelling of mitochondria. Oligomycin caused none of the above effects when Br-or NO3-was substituted for Cl-as the major anionic species or when Na+replaced the K+. The same concentration of oligomycin that caused uncoupling and swelling slightly improved energy-conserving reactions when the cationophores were omitted. In the presence of KSCN, valinomycin or Triton X-100 by itself caused uncoupling and swelling which was not further enhanced by oligomycin. On the basis of the above results it is suggested that the energy dissipation resulting from the concerted action of the cationophores and oligomycin is connected with the simultaneous transport of K+and its counter ion and that oligomycin plays its role in the uncoupling by facilitating the permeation of Cl-through the cristae membrane of the mitochondria.

scholarly journals The decrease of mitochondrial substrate uptake caused by trialkyltin and trialkyl-lead compounds in chloride media and its relevance to inhibition of oxidative phosphorylation

1975 ◽  
Vol 146 (2) ◽  
pp. 465-471 ◽  
Author(s):  
D N Skilleter
Keyword(s):  
Oxidative Phosphorylation ◽  
Atp Synthesis ◽  
Liver Mitochondria ◽  
Rat Liver Mitochondria ◽  
Substrate Uptake ◽  
O2 Uptake ◽  
Lead Compounds ◽  
Mitochondrial Functions ◽  
Respiration Of Mitochondria

1. In a 100 mM-KCl medium (pH 6.8) containing ATP, triethyltin (1 muM) causes a decrease in the uptake of pyruvate, malate, citrate or β-hydroxybutyrate by rat liver mitochondria, but no decrease is observed in a 100 mM-KNO3 medium. This response is not modified by the presence of rotenone in the incubation medium. 2. In the KCl medium at least 1 muM-triethyltin is required to cause maximum inhibition of pyruvate uptake. 3. Trimethyltin, tributyltin and the trialkyl-lead analogues at 1 muM, to varying degrees, also cause a decrease in pyruvate uptake by mitochondria only in the KCl medium. 4. Triethyltin stimulates resting respiration of mitochondria with all the substrates tested in the KCl medium but not in the KNO3 medium, yet this stimulation of O2 uptake occurs under conditions when substrate uptake is decreased. 5. In contrast, both O2 uptake during state 3 respiration and ATP synthesis when linked to the oxidation of pyruvate, malate or citrate are strongly inhibited by 1 muM-triethyltin in a KCl medium, but O2 uptake and ATP synthesis during the oxidation of β-hydroxybutyrate are only slightly affected. In a KNO3 medium O2 uptake and ATP synthesis linked to the oxidation of all substrates are only slightly affected. 6. The relevance of the decrease in substrate uptake by mitochondria caused by triethyltin in a KCl medium to the greater sensitivity of various mitochondrial functions observed in vitro is discussed. It is concluded that decrease of matrix substrate content is probably not the major cause of the greater sensitivity of oxidative phosphorylation to triethyltin in a KCl medium observed previously.

scholarly journals Theoretical studies on the control of oxidative phosphorylation in muscle mitochondria: application to mitochondrial deficiencies

1996 ◽  
Vol 319 (1) ◽  
pp. 143-148 ◽  
Author(s):  
Bernard KORZENIEWSKI ◽  
Jean-Pierre MAZAT
Keyword(s):  
Oxidative Phosphorylation ◽  
Atp Synthesis ◽  
Threshold Effect ◽  
Liver Mitochondria ◽  
Rat Liver Mitochondria ◽  
Muscle Mitochondria ◽  
Hypoxic Conditions ◽  
Titration Curves ◽  
Flux Control Coefficients ◽  
Control Coefficients

1. The dynamic model of oxidative phosphorylation developed previously for rat liver mitochondria incubated with succinate was adapted for muscle mitochondria respiring on pyruvate. We introduced the following changes considering: (1) a higher external ATP/ADP ratio and an ATP/ADP carrier less displaced from equilibrium; (2) a substrate dehydrogenation more sensitive to the NADH/NAD+ ratio; and (3) the respiratory chain, ATP synthase and phosphate carrier being more displaced from equilibrium. The experimental flux control coefficients already determined in state 3 for respiratory rate and ATP synthesis were used to adjust some parameters. This new oxidative phosphorylation model enabled us to simulate the whole titration curves obtained experimentally in state 3. These curves, which mimic the effect of mitochondrial complex deficiencies on oxidative phosphorylation, show a threshold effect, which is reproduced by the model. 2. The model was also used to simulate other physiological conditions such as: (i) state 3.5, conditions inbetween state 4 and state 3; and (ii) hypoxic conditions. In both cases a profound change in the pattern of the control coefficients was shown. 3. This model was thus found useful in investigating a variety of new conditions, the most interesting of which can then be experimentally studied.

scholarly journals Inhibition of Palmityl Carnitine Oxidation in Rat Liver Mitochondria by Tert-Butyl Hydroperoxide

2008 ◽  
pp. 133-136
Author(s):  
Z Červinková ◽  
H Rauchová ◽  
P Křiváková ◽  
Z Drahota
Keyword(s):  
Oxidative Damage ◽  
Respiratory Chain ◽  
Respiratory Control ◽  
Atp Synthesis ◽  
Liver Mitochondria ◽  
Rat Liver Mitochondria ◽  
Respiratory Chain Complexes ◽  
Butyl Hydroperoxide ◽  
Tert Butyl ◽  
Tert Butyl Hydroperoxide

Mitochondria as an energy generating cell device are very sensitive to oxidative damage. Our previous findings obtained in hepatocytes demonstrated that Complex I of the respiratory chain is more sensitive to oxidative damage than other respiratory chain complexes. We present additional data on isolated mitochondria showing that palmityl carnitine oxidation is strongly depressed at a low (200 µM) tert-butyl hydroperoxide (tBHP) concentration, while oxidation of the flavoproteindependent substrate – succinate is not affected and neither is ATP synthesis inhibited by tBHP. In the presence of tBHP, the respiratory control index for palmityl carnitine oxidation is strongly depressed, but when succinate is oxidized the respiratory control index remains unaffected. Our findings thus indicate that flavoprotein-dependent substrates could be an important nutritional factor for the regeneration process in the necrotic liver damaged by oxidative stress.

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