Mersalyl prevents the Tl + -induced permeability transition pore opening in the inner membrane of Ca 2+ -loaded rat liver mitochondria.

Autor: Korotkov SM; Sechenov Institute of Evolutionary Physiology and Biochemistry, The Russian Academy of Sciences, Thorez pr. 44, 194223 St. Petersburg, Russia. Electronic address: korotkov@SK1645.spb.edu., Konovalova SA; Sechenov Institute of Evolutionary Physiology and Biochemistry, The Russian Academy of Sciences, Thorez pr. 44, 194223 St. Petersburg, Russia., Nesterov VP; Sechenov Institute of Evolutionary Physiology and Biochemistry, The Russian Academy of Sciences, Thorez pr. 44, 194223 St. Petersburg, Russia., Brailovskaya IV; Sechenov Institute of Evolutionary Physiology and Biochemistry, The Russian Academy of Sciences, Thorez pr. 44, 194223 St. Petersburg, Russia.
Jazyk: angličtina
Zdroj: Biochemical and biophysical research communications [Biochem Biophys Res Commun] 2018 Jan 08; Vol. 495 (2), pp. 1716-1721. Date of Electronic Publication: 2017 Dec 06.
DOI: 10.1016/j.bbrc.2017.12.023
Abstrakt: It was earlier shown that the calcium load of rat liver mitochondria in medium containing TlNO 3 and KNO 3 resulted in the Tl + -induced mitochondrial permeability transition pore (MPTP) opening in the inner membrane. This opening was accompanied by an increase in swelling and membrane potential dissipation and a decrease in state 3, state 4, and 2,4-dinitrophenol-uncoupled respiration. This respiratory decrease was markedly leveled by mersalyl (MSL), the phosphate symporter (PiC) inhibitor which poorly stimulated the calcium-induced swelling, but further increased the potential dissipation. All of these effects of Ca 2+ and MSL were visibly reduced in the presence of the MPTP inhibitors (ADP, N-ethylmaleimide, and cyclosporine A). High MSL concentrations attenuated the ability of ADP to inhibit the MPTP. Our data suggest that the PiC can participate in the Tl + -induced MPTP opening in the inner membrane of Ca 2+ -loaded rat liver mitochondria.
(Copyright © 2017 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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