Ca(2+)-triggered membrane permeability transition in deenergized mitochondria from rat liver.
The opening of the cyclosporin A-sensitive permeability transition pore (MTP) in deenergized mitochondria was induced only at millimolar Ca2+. Pretreatment of the mitochondria with 'inducers', such as duroquinone and phenylarsine oxide, allowed observing the pore opening at 0.01-0.1 mM Ca2+. 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 Ca2+. 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.[1]References
- Ca(2+)-triggered membrane permeability transition in deenergized mitochondria from rat liver. Chernyak, B.V., Dedov, V.N., Chernyak VYa, n.u.l.l. FEBS Lett. (1995) [Pubmed]
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