Tl+ induces both cationic and transition pore permeability in the inner membrane of rat heart mitochondria

2013 ◽  
Vol 45 (6) ◽  
pp. 531-539 ◽  
Author(s):  
Sergey M. Korotkov ◽  
Vladimir P. Nesterov ◽  
Irina V. Brailovskaya ◽  
Viktor V. Furaev ◽  
Artemy V. Novozhilov
2007 ◽  
Vol 415 (1) ◽  
pp. 206-210 ◽  
Author(s):  
S. M. Korotkov ◽  
V. P. Nesterov ◽  
L. V. Emel’yanova ◽  
N. N. Ryabchikov

1987 ◽  
Vol 245 (3) ◽  
pp. 915-918 ◽  
Author(s):  
M Crompton ◽  
A Costi ◽  
L Hayat

Rat heart mitochondria became permeabilized to sucrose when incubated with 100 nmol of Ca2+/mg of protein in the presence of Pi. Ca2+ chelation with EGTA restored impermeability to sucrose, which became entrapped in the matrix space. t-Butylhydroperoxide markedly promoted permeabilization in the presence of Ca2+ but not in its absence, and Ca2+-plus-t-butylhydroperoxide-induced permeabilization was reversed by EGTA. The data suggest that Ca2+ and oxidative stress synergistically promote the reversible opening of an inner membrane pore.


2019 ◽  
Vol 487 (4) ◽  
pp. 460-464
Author(s):  
S. M. Korotkov ◽  
I. V. Brailovskaya ◽  
V. P. Nesterov ◽  
S. I. Soroko

The effect of pinacidil was studied on calcium-loaded rat heart mitochondria (RHM) in the presence of succinate and rotenone. In experiments with pinacidil, the swelling of these mitochondria increased in media with NH4NO3 or K‑acetate, but the inner membrane potential DΨmito and state 3 or 2,4-dinitrophenol-uncoupled respiration of these organelles were decreased due to opening of the mitochondrial permeability transition pore in the inner membrane. These effects were inhibited by cyclosporin A and ADP. It was concluded that the protective effect of pinacidil in the cardiac muscle ischemia/reperfusion may be associated with stimulation mitochondrial swelling and a decrease in RHM calcium overload resulted in a decrease in DΨmito due to the soft uncoupling pinacidil effect.


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