PMID- 15909417
OWN - NLM
STAT- MEDLINE
DCOM- 20050715
LR  - 20201209
VI  - 76
IP  - 1
DP  - 2004 Jan-Feb
TI  - [Effect of Ca2+ on induction of the mitochondrial pore opening in the rat 
      myocardium].
PG  - 48-55
AB  - The mitochondrial role opening (MPT) induced by Ca2+ has been studied in isolated 
      rat heart mitochondria. MPT was characterized as cyclosporine A-inhibited 
      swelling accompanied by the loss of membrane potential (deltapsim) and Ca2+ 
      efflux after the Ca2+ -loading which was followed spectrophotometrically after 
      the Ca2+ -arsenaso-III complex formation. It has been shown that in suspension of 
      isolated mitochondria MPT was activated by low (with maximum at about 20 microM 
      Ca2+) and high concentrations of Ca2+ (the concentration curve shows a saturation 
      at about 1.0-1.5 mM). In all the cases an access of Ca2+ ions to the matrix space 
      of the mitochondria was necessary for MPT induction. MPT activated by low 
      concentrations of Ca2+ was accompanied by slow decrease of deltapsim and slow 
      release of Ca2+, enhanced by ruthenium red (RR), and was independent of the 
      substrate used (glutamate or succinate). It had not been observed if the 
      respiratory chain was inhibited, even if the Ca2+ access to the inner 
      mitochondrial membrane was provided by Ca2+ -ionophore A23187. At high Ca2+ 
      concentrations rapid Ca2+ -uptake and release via Ca2+ -uniporter (inhibited by 
      ruthenium red) followed by extensive swelling (pore formation) have been 
      observed. It had been supposed that rapid MPT at high concentrations of Ca2+ was 
      the result of Ca2+ entrance to the mitochondrial matrix and depolarisation of the 
      mitochondrial membrane. The data obtained show two different mechanisms of Ca2+ 
      -induced MPT. The one is sensitive to the redox-state of the electron transport 
      chain and is abolished if the respiration is inhibited. The other is independent 
      of mitochondrial respiration and needs only Ca2+ access to the inner 
      mitochondrial membrane and Ca2+ binding to some specific sites leading to MPT 
      opening.
FAU - Akopova, O V
AU  - Akopova OV
FAU - Sagach, V F
AU  - Sagach VF
LA  - rus
PT  - Journal Article
TT  - Induktsiia otkrytiia mitokhondrial'noi pory pod deistviem Ca2+ v miokarde krys.
PL  - Ukraine
TA  - Ukr Biokhim Zh (1999)
JT  - Ukrains'kyi biokhimichnyi zhurnal (1999 )
JID - 101657175
RN  - 0 (Ion Channels)
RN  - 0 (Ionophores)
RN  - 0 (Mitochondrial Membrane Transport Proteins)
RN  - 0 (Mitochondrial Permeability Transition Pore)
RN  - 37H9VM9WZL (Calcimycin)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - Calcimycin/pharmacology
MH  - Calcium/*metabolism
MH  - In Vitro Techniques
MH  - Ion Channel Gating/drug effects/*physiology
MH  - Ion Channels/*metabolism
MH  - Ionophores/pharmacology
MH  - Membrane Potentials/drug effects/physiology
MH  - Mitochondria, Heart/*metabolism/physiology
MH  - Mitochondrial Membrane Transport Proteins
MH  - Mitochondrial Permeability Transition Pore
MH  - Myocardium/*metabolism
MH  - Rats
EDAT- 2005/05/25 09:00
MHDA- 2005/07/16 09:00
CRDT- 2005/05/25 09:00
PHST- 2005/05/25 09:00 [pubmed]
PHST- 2005/07/16 09:00 [medline]
PHST- 2005/05/25 09:00 [entrez]
PST - ppublish
SO  - Ukr Biokhim Zh (1999). 2004 Jan-Feb;76(1):48-55.