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Ca 2+ ‐triggered membrane permeability transition in deenergized mitochondria from rat liver
Author(s) -
Chernyak B.V.,
Dedov V.N.,
Chernyak V.Ya.
Publication year - 1995
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(95)00411-2
Subject(s) - phenylarsine oxide , chemistry , nad+ kinase , mitochondrial permeability transition pore , mitochondrion , permeability (electromagnetism) , biophysics , dithiol , membrane , n ethylmaleimide , biochemistry , enzyme , biology , programmed cell death , apoptosis
The opening of the cyclosporin A‐sensitive permeability transition pore (MTP) in deenergized mitochondria was induced only at millimolar Ca 2+ . Pretreatment of the mitochondria with ‘inducers’, such as duroquinone and phenylarsine oxide, allowed observing the pore opening at 0.01–0.1 mM Ca 2+ . Duroquinone caused a rapid (within 20 s) NAD(P)H oxidation which was followed by a slow (20 min) induction of the pore sensitive to low Ca 2+ . Phenylarsine oxide capable of cross‐linking of vicinal SH‐groups caused pore formation without the oxidation of NAD(P)H. The pore opening by both ‘inducers’ was prevented by N ‐ethylmaleimide. We propose that oxidation or cross‐linking of critical dithiol(s) in membrane proteins increase the sensitivity of a putative ‘Ca 2+ ‐sensor’ that regulates the permeability transition pore opening.