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Virus‐induced permeability transition in mitochondria
Author(s) -
Zorova Ljubava D.,
Krasnikov Boris F.,
Kuzminova Alevtina E.,
Polyakova Irina A.,
Dobrov Eugeny N.,
Zorov Dmitry B.
Publication year - 2000
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/s0014-5793(99)01709-3
Subject(s) - mitochondrion , mitochondrial permeability transition pore , egta , virus , biophysics , permeability (electromagnetism) , inner mitochondrial membrane , mitochondrial apoptosis induced channel , chemistry , negative stain , mitochondrial membrane transport protein , membrane permeability , calcium , microbiology and biotechnology , membrane , biochemistry , biology , apoptosis , electron microscope , virology , programmed cell death , physics , organic chemistry , optics
Isolated rat liver mitochondria undergo permeability transition after supplementation with a suspension of tobacco mosaic virus. Four mitochondrial parameters proved the opening of the permeability transition pore in the inner mitochondrial membrane: increased oxygen consumption, collapse of the membrane potential, release of calcium ions from mitochondria, and high amplitude mitochondrial swelling. All virus‐induced changes in mitochondria were prevented by cyclosporin A. These effects were not observed if the virus was treated with EGTA or disrupted by heating. Protein component of the virus particle in the form of 20S aggregate A‐protein, or helical polymer, as well as supernatant of the heat‐disrupted virus sample, had no effect on mitochondrial functioning. Electron microscopy revealed the direct interaction of the virus particles with isolated mitochondria. The possible role of the mitochondrial permeability transition pore in virus‐induced apoptosis is discussed.