SITES OF ENERGY CONSERVATION IN OXIDATIVE PHOSPHORYLATION

1957 ◽  
Vol 79 (11) ◽  
pp. 2970-2970 ◽  
Author(s):  
Britton Chance ◽  
Gunnar Hollunger
Keyword(s):  
Oxidative Phosphorylation ◽  
Energy Conservation

scholarly journals Effects of the cyanine dye 3,3′-dipropylthiocarbocyanine on mitochondrial energy conservation

1979 ◽  
Vol 180 (3) ◽  
pp. 669-672 ◽  
Author(s):  
P H Howard ◽  
S B Wilson
Keyword(s):  
Membrane Potential ◽  
Electron Transport ◽  
Oxidative Phosphorylation ◽  
Energy Conservation ◽  
Mitochondrial Respiration ◽  
Cyanine Dye

Mitochondrial respiration and oxidative phosphorylation were inhibited by the membrane potential probe 3,3′-dipropylthiocarbocyanine [diS-C3-(5)]. Evidence is presented that suggests that the dye acts as both an inhibitor of electron transport and an uncoupler of oxidative phosphorylation.

scholarly journals Respiration-driven proton translocation by yeast mitochondria with differing efficiencies of oxidative phosphorylation

1973 ◽  
Vol 134 (4) ◽  
pp. 1045-1049 ◽  
Author(s):  
J. A. Downie ◽  
P. B. Garland
Keyword(s):  
Oxidative Phosphorylation ◽  
Energy Conservation ◽  
Candida Utilis ◽  
Proton Translocation ◽  
Yeast Mitochondria

Measurements were made of the stoicheiometry of proton translocation coupled to respiration in mitochondria from Candida utilis where the number of functional energy-conservation sites between intramitochondrial NADH and oxygen was one in a mutant with a novel oxidase (Downie & Garland, 1972), two in sulphate-deficient cells (Haddock & Garland, 1971) or three in glycerol-limited cells (Light & Garland, 1971). The stoicheiometries of protons translocated per atom of oxygen utilized (i.e. →H+/2e− ratio; Mitchell, 1966) were close to 2.0, 4.0 and 6.0 respectively. Thus by using the same substrate (intramitochondrial NADH) and oxygen throughout, the →H+/2e− ratio is shown to be 2.0 per energy-conservation site when the number of such sites is varied from one to three.

Energy conservation in membranes of mutants of Escherichia coli defective in oxidative phosphorylation

1973 ◽  
Vol 325 (1) ◽  
pp. 62-71 ◽  
Author(s):  
F.J.R.M. Nieuwenhuis ◽  
B.I. Kanner ◽  
D.L. Gutnick ◽  
P.W. Postma ◽  
K. Van Dam
Keyword(s):  
Escherichia Coli ◽  
Oxidative Phosphorylation ◽  
Energy Conservation

Oxidative phosphorylation and related reactions in liver mitochondria from diabetic dogs

1961 ◽  
Vol 200 (4) ◽  
pp. 838-840 ◽  
Author(s):  
Robert E. Beyer ◽  
Charles A. Shamoian
Keyword(s):  
Electron Transport ◽  
Oxidative Phosphorylation ◽  
Energy Conservation ◽  
Exchange Reaction ◽  
Liver Mitochondria ◽  
Primary Lesion ◽  
Metabolic Defect ◽  
Electron Transport Rates ◽  
Diabetic Dogs ◽  
Diabetic Syndrome

Oxidative phosphorylation, dinitrophenol- and Mg++-activated adenosinetriphosphatase and the adenosinetriphosphatein-organic orthophosphate exchange reaction were studied in mitochondria isolated from livers of chronic and acutely diabetic dogs. Although such reactions are readily demonstrable in these preparations, no trends indicating a deficiency of the energy-conservation reactions studied in preparations from diabetic dogs were noted. In addition, electron transport rates with glutamate or succinate as substrate were increased in the diabetic preparations, as was the yield of mitochondria from such animals. This is not in agreement with recently published reports concerning related studies on diabetic cats and rats. The above findings indicate that a metabolic defect in the efficiency of oxidative phosphorylation is not a general primary lesion in the diabetic syndrome.

THE EFFECT OF RIBOFLAVIN DEFICIENCY AND GALACTOFLAVIN FEEDING ON OXIDATIVE PHOSPHORYLATION AND RELATED REACTIONS IN RAT LIVER MITOCHONDRIA

1961 ◽  
Vol 39 (1) ◽  
pp. 73-88 ◽  
Author(s):  
Robert E. Beyer ◽  
Stanley L. Lamberg ◽  
M. Arthur Neyman
Keyword(s):  
Electron Transport ◽  
Oxidative Phosphorylation ◽  
Energy Conservation ◽  
Atpase Activity ◽  
Exchange Rates ◽  
Rat Liver ◽  
Liver Mitochondria ◽  
Rat Liver Mitochondria ◽  
Riboflavin Deficiency

The effect of riboflavin deficiency and feeding of galactoflavin on the flavin content of liver mitochondria, oxidative phosphorylation, Pi–ATP exchange, and ATPase activity was studied. Both dietary riboflavin deprivation and galactoflavin feeding resulted in a depressed flavin content of mitochondria, the latter treatment resulting in a more severe flavin loss. P/O ratios under all treatments were normal as were Pi–ATP exchange rates and the oxidation of succinate. Glutamate and β-hydroxybutyrate oxidations were depressed in mitochondria from rats fed galactoflavin for 15 or 28 days. DNP-activated ATPase was elevated in both flavin-deficient and galactoflavin-fed preparations while Mg++-activated ATPase was depressed in the galactoflavin-fed preparations. These results are discussed in relation to the hypothesis that flavin is involved in energy conservation in the diaphorase region of electron transport.

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