In vitro uncoupling of oxidative phosphorylation in normal liver mitochondria by serum of sarcoma-bearing rats

1961 ◽  
Vol 17 (9) ◽  
pp. 402-404 ◽  
Author(s):  
G. Nanni ◽  
A. Casu
1962 ◽  
Vol 40 (8) ◽  
pp. 1025-1042 ◽  
Author(s):  
J. F. Scaife ◽  
B. Hill

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.


1962 ◽  
Vol 40 (1) ◽  
pp. 1025-1042 ◽  
Author(s):  
J. F. Scaife ◽  
B. Hill

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.


1966 ◽  
Vol 44 (7) ◽  
pp. 983-988 ◽  
Author(s):  
John N. Hathcock ◽  
C. H. Hill ◽  
S. B. Tove

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.


1966 ◽  
Vol 36 (1) ◽  
pp. 63-71 ◽  
Author(s):  
E. BEDRAK ◽  
V. SAMOILOFF

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.


Author(s):  
Nicolay N. Brustovetsky ◽  
Evgeni I. Maevsky ◽  
Stella G. Kolaeva ◽  
Lubov S. Danilova ◽  
Nikita G. Solomonov

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