Data supporting the involvement of the adenine nucleotide translocase conformation in opening the Tl(+)-induced permeability transition pore in Ca(2+)-loaded rat liver mitochondria

There we made available information about the effects of the adenine nucleotide translocase (ANT) ‘c’ conformation fixers (phenylarsine oxide (PAO), tert-butylhydroperoxide (tBHP), and carboxyatractyloside) as well as thiol reagent (4,4′-diisothiocyanostilbene-2,2′-disulfonate (DIDS)) on isolated rat liver mitochondria. We observed a decrease in A(540) (mitochondrial swelling) and respiratory control rates (RCR(ADP) [state 3/state 4] and RCR(DNP) [2,4-dinitrophenol-uncoupled state/basal state or state 4]), as well as an increase in Ca(2+)-induced safranin fluorescence (F(485/590), arbitrary units), showed a dissipation in the inner membrane potential (ΔΨ(mito)), in experiments with energized rat liver mitochondria, injected into the buffer containing 25–75 mM TlNO(3), 125 mM KNO(3), and 100 µM Ca(2+). The fixers and DIDS, in comparison to Ca(2+) alone, greatly increased A(540) decline and the rate of Ca(2+)-induced ΔΨ(mito) dissipation. These reagents also markedly decreased RCR(ADP) and RCR(DNP). The MPTP inhibitors (ADP, cyclosporin A, bongkrekic acid, and N-ethylmaleimide) fixing the ANT in ‘m’ conformation significantly hindered the above-mentioned effects of the fixers and DIDS. A more complete scientific analysis of these findings may be obtained from the manuscript “To involvement the conformation of the adenine nucleotide translocase in opening the Tl(+)-induced permeability transition pore in Ca(2+)-loaded rat liver mitochondria” (Korotkov et al., 2016 [1]).