UNCOUPLING OF OXIDATIVE PHOSPHORYLATION BY VANADATE

1966 ◽  
Vol 44 (7) ◽  
pp. 983-988 ◽  
Author(s):  
John N. Hathcock ◽  
C. H. Hill ◽  
S. B. Tove
Keyword(s):  
Electron Transport ◽  
Oxidative Phosphorylation ◽  
Adenosine Triphosphate ◽  
Adenosine Diphosphate ◽  
Liver Mitochondria ◽  
In Vitro Studies ◽  
Exchange Reactions ◽  
Uncoupling Of Oxidative Phosphorylation

The addition of ammonium metavanadate to the diet of chicks at a level to supply 25 parts per million vanadium uncoupled oxidative phosphorylation in mitochondria isolated from the livers. In vitro studies revealed that 1 mM vanadate uncoupled oxidative phosphorylation in liver mitochondria. This uncoupling was manifest whether succinate or β-hydroxybutyrate was used as the substrate, suggesting that all three phosphorylating sites associated with electron transport were uncoupled.At a concentration of 0.1 mM, vanadate increased the destruction of adenosine triphosphate by mitochondria. As the concentration of vanadate was increased the destruction of adenosine triphosphate became progressively less. The exchange reactions of adenosine triphosphate with orthophosphate and with adenosine diphosphate, catalyzed by liver mitochondria, were inhibited by 0.1 mM vanadate. These results suggest the possibility that the known toxic effects of vanadium in vivo are related to the uncoupling of oxidative phosphorylation.

THE UNCOUPLING OF OXIDATIVE PHOSPHORYLATION BY IONIZING RADIATION

1962 ◽  
Vol 40 (8) ◽  
pp. 1025-1042 ◽  
Author(s):  
J. F. Scaife ◽  
B. Hill
Keyword(s):  
Oxidative Phosphorylation ◽  
Liver Mitochondria ◽  
Cell Suspensions ◽  
Whole Body ◽  
X Rays ◽  
Succinate Oxidation ◽  
Mouse Ascites ◽  
Uncoupling Of Oxidative Phosphorylation

Whole body irradiation of rabbits or rats with X-rays or Co60γ-rays causes uncoupling of oxidative phosphorylation in thymus mitochondria, which is not prevented by the prior administration of AET. Whole body irradiation was not found to affect oxidative phosphorylation in liver or mouse ascites cell mitochondria. The radiation lesion can be repaired in vitro by the addition of cytochrome c, bovine serum albumin, or vitamin K1to mitochondria. Vitamin E and coenzyme Q10 were without effect. Both phosphorylating steps in the electron transport chain associated with succinate oxidation are affected by irradiation. The diphosphopyridine nucleotide dependent steps in the oxidation of α-ketoglutarate by thymus mitochondria are damaged by in vivo irradiation. Diphosphopyridine nucleotide levels of thymus and spleen but not liver or ascites cells are reduced by in vivo irradiation. No effect of in vitro irradiation on oxidative phosphorylation could be found for thymocyte cell suspensions, isolated thymus or liver mitochondria, or ascites or HeLa cell suspensions. Respiration of ascites or thymocyte cells was unaffected by in vitro irradiation.

THE UNCOUPLING OF OXIDATIVE PHOSPHORYLATION BY IONIZING RADIATION

1962 ◽  
Vol 40 (1) ◽  
pp. 1025-1042 ◽  
Author(s):  
J. F. Scaife ◽  
B. Hill
Keyword(s):  
Oxidative Phosphorylation ◽  
Liver Mitochondria ◽  
Cell Suspensions ◽  
Whole Body ◽  
X Rays ◽  
Succinate Oxidation ◽  
Mouse Ascites ◽  
Uncoupling Of Oxidative Phosphorylation

Whole body irradiation of rabbits or rats with X-rays or Co60γ-rays causes uncoupling of oxidative phosphorylation in thymus mitochondria, which is not prevented by the prior administration of AET. Whole body irradiation was not found to affect oxidative phosphorylation in liver or mouse ascites cell mitochondria. The radiation lesion can be repaired in vitro by the addition of cytochrome c, bovine serum albumin, or vitamin K1to mitochondria. Vitamin E and coenzyme Q10 were without effect. Both phosphorylating steps in the electron transport chain associated with succinate oxidation are affected by irradiation. The diphosphopyridine nucleotide dependent steps in the oxidation of α-ketoglutarate by thymus mitochondria are damaged by in vivo irradiation. Diphosphopyridine nucleotide levels of thymus and spleen but not liver or ascites cells are reduced by in vivo irradiation. No effect of in vitro irradiation on oxidative phosphorylation could be found for thymocyte cell suspensions, isolated thymus or liver mitochondria, or ascites or HeLa cell suspensions. Respiration of ascites or thymocyte cells was unaffected by in vitro irradiation.

scholarly journals Mitochondrial damage: a possible mechanism of the “topical” phase of NSAID induced injury to the rat intestine

Gut ◽  
1997 ◽  
Vol 41 (3) ◽  
pp. 344-353 ◽  
Author(s):  
S Somasundaram ◽  
S Rafi ◽  
J Hayllar ◽  
G Sigthorsson ◽  
M Jacob ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Small Intestine ◽  
Electron Transport ◽  
Oxidative Phosphorylation ◽  
In Vivo Studies ◽  
Tolerability Profile ◽  
Marker Enzyme ◽  
Subcellular Organelle

Background—The “topical” effect of non-steroidal anti-inflammatory drugs (NSAIDs) seems to be an important cause of NSAID induced gastrointestinal damage.Aim—To examine the possible mechanism of the “topical” phase of damage in the small intestine.Methods—Electron microscopy and subcellular organelle marker enzyme studies were done in rat small intestine after oral administration of indomethacin (doses varied between 5 and 30 mg/kg). The effect of conventional and non-acidic NSAIDs on rat liver mitochondrial respiration was measured in vitro in a Clarke-type oxygen electrode.Results—The subcellular organelle marker enzymes showed mitochondrial and brush border involvement within an hour of indomethacin administration. Electron microscopy showed dose dependent mitochondrial changes following indomethacin administration consistent with uncoupling of oxidative phosphorylation (or inhibition of electron transport) which were indistinguishable from those seen with the uncoupler dinitrophenol. Parenteral indomethacin caused similar changes, but not in rats with ligated bile ducts. A range of NSAIDs, but not paracetamol or non-acidic NSAIDs which have a favourable gastrointestinal tolerability profile, uncoupled oxidative phosphorylation in vitro at micromolar concentrations and inhibited respiration at higher concentrations. In vivo studies with nabumetone and aspirin further suggested that uncoupling or inhibition of electron transport underlies the “topical” phase of NSAID induced damage.Conclusion—Collectively, these studies suggest that NSAID induced changes in mitochondrial energy production may be an important component of the “topical” phase of damage induction.

ALDOSTERONE AND OXIDATIVE PHOSPHORYLATION IN LIVER MITOCHONDRIA

1966 ◽  
Vol 36 (1) ◽  
pp. 63-71 ◽  
Author(s):  
E. BEDRAK ◽  
V. SAMOILOFF
Keyword(s):  
Oxidative Phosphorylation ◽  
Mouse Liver ◽  
Electrolyte Concentration ◽  
Reaction Medium ◽  
Liver Mitochondria ◽  
Rat Liver Mitochondria ◽  
Male And Female ◽  
Single Intraperitoneal Injection ◽  
Uncoupling Of Oxidative Phosphorylation

SUMMARY A single intraperitoneal injection of 2 μg. d-aldosterone monoacetate/g. body weight produced a rapid, but temporary, uncoupling of oxidative phosphorylation in mouse liver mitochondria. This resulted in low P:O ratios in male and female animals of 1·21 and 1·52, respectively. The P:O ratio of females remained somewhat lower than the control levels but there was a progressive improvement in oxidative phosphorylation during the first 24 hr. after the injection leading to P: O ratios similar to those in the controls. Experiments in vitro showed that the uncoupling effects of aldosterone were related to its concentration in the reaction medium. Aldosterone added to fresh rat liver mitochondria, at concentrations of 10−10, 10−7 and 10−4m inhibited phosphorylation by 9·5, 77·1 and 95·1% and lowered P:O ratios to 2·46, 1·66 and 0·41, respectively. These changes in oxidative phosphorylation were not related to alteration in ATPase activity and were independent of mitochondrial electrolyte concentration.

Conformational Changes of Mitochondria associated with Uncoupling of Oxidative Phosphorylation in vivo and in vitro

Nature ◽  
1970 ◽  
Vol 226 (5242) ◽  
pp. 272-274 ◽  
Author(s):  
P. BUFFA ◽  
V. GUARRIERA-BOBYLEVA ◽  
U. MUSCATELLO ◽  
I. PASQUALI-RONCHETTI
Keyword(s):  
Oxidative Phosphorylation ◽  
Conformational Changes ◽  
Uncoupling Of Oxidative Phosphorylation

Oxidative phosphorylation and adenosine triphosphatase activity in the liver mitochondria of rats administered with phenylhydrazine and hydroiyzed glucose cycloacetoacetate

1969 ◽  
Vol 47 (3) ◽  
pp. 297-300 ◽  
Author(s):  
T. G. Reddi ◽  
M. C. Nath
Keyword(s):  
Oxygen Uptake ◽  
Oxidative Phosphorylation ◽  
Rat Liver ◽  
Adenosine Triphosphatase ◽  
Liver Mitochondria ◽  
Rat Liver Mitochondria ◽  
Partial Restoration ◽  
Atp Formation

The effect of phenylhydrazine and hydroiyzed product of glucose cycloacetoacetate (GCAh) administration on the activity of adenosine triphosphatase (ATPase) in rat-liver mitochondria has been investigated. The results are discussed in relation to the efficiency of mitochondrial oxidative phosphorylation. Phenylhydrazine was found to increase the ATPase activity both in vitro and in vivo. However, preincubation or treatment with hydrolyzed glucose cycloacetoacetate resulted in an appreciable depression of this phenylhydrazine-enhanced enzyme activity. The liver mitochondria from phenylhydrazine-administered rats showed very little difference in milligrams of total protein, but the homogenates had a high protein content as compared to the preparations from normal rats and rats administered with hydrolyzed glucose cycloacetoacetate. With citrate as the substrate, normal rat-liver mitochondria exhibited a P/O ratio of 3.0. With the same substrate, the liver mitochondria from phenylhydrazine-administered rats lowered the oxygen uptake and ATP formation, thereby resulting in a decreased P/O ratio of 2.4, whereas administration of hydrolyzed glucose cycloacetoacetate prior to phenylhydrazine resulted in a partial restoration in oxygen uptake and ATP formation, and thus yielded a P/O ratio of 2.8.

The Venom of the Boomslang (Dispholidus Typus): In Vivo and in Vitro Studies

1969 ◽  
Vol 21 (02) ◽  
pp. 234-244 ◽  
Author(s):  
N Mackay ◽  
J.C Ferguson ◽  
Antonia Bagshawe ◽  
A.T.T Forrester ◽  
G.P Mcnicol
Keyword(s):  
In Vitro Studies

SummaryAn account is given of the effects of boomslang venom in man. Evidence was found of a fibrinolytic state apparently secondary to the coagulant action of the venom. These features rapidly responded to the administration of specific antivenom. In vitro studies, using a homogenate of boomslang parotids, confirmed the coagulant properties of the venom and showed them to be of much greater potency than the proteolytic actions.

Sign in / Sign up

Export Citation Format

Share Document