A ‘hexokinase effect’ in the inhibition of oxidative phosphorylation in heart muscle mitochondria by Adriamycin

1982 ◽  
Vol 105 (4) ◽  
pp. 1440-1445 ◽  
Author(s):  
H. Muhammed ◽  
T. Ramasarma ◽  
C.K.Ramakrishna Kurup
1957 ◽  
Vol 5 (3) ◽  
pp. 226-229 ◽  
Author(s):  
KATHARINE ARMSTRONG PLAUT ◽  
MENARD M. GERTLER ◽  
G. W. E. PLAUT

1954 ◽  
Vol 14 ◽  
pp. 443-444 ◽  
Author(s):  
Gladys Feldott Maley ◽  
G.W.E. Plaut

Mitochondrion ◽  
2007 ◽  
Vol 7 (6) ◽  
pp. 422-423
Author(s):  
George Kypriotakis ◽  
Bruce H. Cohen ◽  
Sumit Parikh ◽  
Douglas S. Kerr ◽  
Charles L. Hoppel ◽  
...  

1960 ◽  
Vol 198 (1) ◽  
pp. 89-93 ◽  
Author(s):  
Sidney S. Schreiber ◽  
Murray Oratz ◽  
Marcus A. Rothschild

Potassium in the working frog ventricle exists in two physiological compartments and the more slowly exchanging compartment is influenced by the amount of work performed, ventricular failure and ouabain. In the present study, the exchange of potassium in mitochondria is investigated both in the control state and after exposure to ouabain, in order to determine whether mitochondria potassium represents the slowly exchanging compartment. Mitochondria potassium represents only 15% of the total ventricular potassium, while the slowly exchanging phase contains about 50%. Ouabain perfusion is associated with inhibition of entrance of potassium into the slowly exchanging ventricular phase, but no isolated specific effect on the mitochondria potassium is found. Alterations in mitochondria potassium directly reflect changes within the total ventricle. A fraction of mitochondria potassium is found to be inexchangeable under the conditions of the experiment. The results indicate that mitochondria potassium does not represent the major part of the slowly exchanging compartment.


1970 ◽  
Vol 48 (12) ◽  
pp. 1332-1338 ◽  
Author(s):  
K. Wrogemann ◽  
M. C. Blanchaer ◽  
B. E. Jacobson

Skeletal muscle mitochondria were isolated in the presence and absence of the proteinase Nagarse from dystrophic hamsters of the BIO 14.6 strain, aged 45–196 days, and from normal hamsters. Mitochondria from the dystrophic animals prepared by glass-on-glass homogenization without Nagarse in 0.25 M sucrose – 1 mM EDTA, pH 7.4, did not differ from normal in their respiratory rate or capacity for oxidative phosphorylation. However, these functions were subnormal in mitochondria isolated with Nagarse from the same animals, both in the presence and absence of albumin. Respiration measured with an O2 electrode was reduced by 50–70% and the stimulation of O2 uptake normally seen after ADP addition was minimal or absent. This was most marked in mitochondria from young hamsters about 65 days old with muscle necrosis. The defect was ameliorated by addition to the Polarographie test system of an ATP trap or of Mg2+, one of the trap constituents. This ion, when added to the defective mitochondria prior to ADP and substrate, restored respiration and oxidative phosphorylation to values that did not differ significantly from those found with skeletal muscle mitochondria of normal hamsters.


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